Site Plan | I. Neurons/nerve cells A neuron is a cell specialized to conduct electrochemical impulses called nerve impulses or action potentials. Neuron is the main cellular component of the nervous system, a specialized type of cell that integrates electrochemical activity of the other neurons that are connected to it and that propagates that integrated activity to other neurons. They are the basic information processing structures in the CNS. There are as many as 10,000 specific types of neurons in the human brain, A.
Types of Neurons a.
Motor neurons >These transmit impulses from the central nervous system to the * muscles and * glands that carry out the response. >Most motor neurons are stimulated by interneurons, although some are stimulated directly by sensory neurons. b. Sensory neurons These run from the various types of stimulus receptors, e. g. , to the central nervous system (CNS), the brain and spinal cord. * touch * odor * taste * sound * vision c.
Interneurons Interneurons >are found exclusively within the spinal cord and brain.
They are stimulated by signals reaching them from * sensory neurons * other interneurons or * both. > also called association neurons. B. Structure of Neurons a. Processes 1. Dendrite Dendritic connections are the basic receiving stations by which neurons form the signaling networks that constitute the brain’s circuitry. . AxonsAll neurons outside the central nervous system (and many within it) conduct impulses along hairlike cytoplasmic extensions, the nerve fibers or axons. The axons connecting your spinal cord to your foot can be as much as 1 m long C. Development of Neurons A. life span D. Kinds of Neurons II. Nerve impulse ConductionFirst, an action potential is generated near the cell body portion of the axon III. Nerve impulse transmission A. Neurotransmitters a. Excitatory AcH b. Inhibitory AcH B. Synaptic transmission A.
Synapse A synapse is where two neurons communicate electrically or chemically. A synapse is the junction point between two neurons. | | | | | | Nerve Cells Nerve cells consist of a body, with branches at one end. The branches are called axons. The axons are positioned near an adjacent nerve or a muscle. Nerve impulses pass from the axons of one nerve to the next nerve or muscle. The impulse transmission speed can be reduced in damaged nerves. Surrounding a nerve is a tough protective coat of a material called myelin.
Nerve damage can involve damage or loss of myelin, damage to the nerve body, or damage to the axon region. The nerve conduction study, which was devised in the 1960s, can detect the loss of nerve function due to these injuries, and, from the nature of the nerve signal pattern that is produced, offer clues as to the nature of the problem. Depending on the nature of the nerve damage, the pattern of signal transmission can be different. For example, in a normal nerve cell, sensors placed at either end of the cell will register the same signal pattern.
But, in a nerve cell that is blocked somewhere along its length, these sensors will register different signal patterns. In another example, in a nerve cell in which transmission is not completely blocked, the signal pattern at the axon may be similar in shape, but reduced in intensity, to that of the originating signal, because not as much of the signal is completing the journey down the nerve cell. Diseases of the nerve itself mainly affect the size of the responses (amplitudes); diseases of the myelin mainly affect the speed of the responses.
Nerve conduction studies are now routine, and can be done in virtually any hospital equipped with the appropriate machine and staffed with a qualified examiner. The nerve conduction study utilizes a computer, computer monitor, amplifier, loudspeaker, electrical stimulator, and filters. These filters are mathematical filters that can distinguish random, background electrical signals from the signal produced by an activated nerve. When the study is done, small electrodes are placed on the skin over the muscles being tested. Generally, these muscles are located in the arms or legs.
Some of the electrodes are designed to record the electrical signal that passes by them. Other electrodes (reference electrodes) are designed to monitor the quality of the signals to make sure that the test is operating properly. If monitoring of the test is not done, then the results obtained are meaningless. After the electrodes are in place, a small electrical current can be applied to the skin. The electrical stimulation is usually done at several points along the nerve, not just at a single point. This is done because conduction of an impulse through a nerve is not uniform.
Some regions of a nerve conduct more slowly than other regions. By positioning the stimulating electrodes at several sites, a more accurate overall measurement of conduction velocity is obtained. The electrical current activates nerves in the vicinity, including those associated with the particular muscle. The nerves are stimulated to produce a signal. This is known as the “firing” of the nerve. The nerve signal, which it also electric, can be detected by some of the electrodes and conveyed to the computer for analysis.
The analysis of the nerve signal involves the study of the movement of the signal through the nerve and from the nerve to the adjacent muscle. Using characteristics such as the speed of the impulse, and the shape, wavelength, and height of the signal wave, an examiner can assess whether the nerve is functional or defective. Risks Mechanism of impulse transmission A nerve impulse travels through a nerve in a long, slender cellular structure called an axon, and it eventually reaches a structure called the presynaptic membrane, which contains neurotransmitters to be released in a free space called the synaptic cleft.
Freely flowing neurotransmitter molecules are picked up by receptors (structures that appear on cellular surfaces that pick up molecules that fit into them like a “lock and key”) located Neurotransmitters are chemicals that transmit messages from one nerve cell (neuron) to another. The nerve impulse travels from the first nerve cell through the axon—a single smooth body arising from the nerve cell— to the axon terminal and the synaptic knobs. Each synaptic knob communicates with a dendrite or cell body of another neuron, and the synaptic knobs contain neurovesicles that store and release neurotransmitters.
The synapse lies between the synaptic knob and the next cell. For the impulse to continue traveling across the synapse to reach the next cell, the synaptic knobs release the neurotransmitter into that space, and the next nerve cell is stimulated to pick up the impulse and continue it. in a structure called the postsynaptic membrane of another nearby neuron. Once the neurotransmitter is picked up by receptors in the postsynaptic membrane, the molecule is internalized in the neuron and the impulse continues. This process of nerve cell communication is extremely rapid.
Once the neurotransmitter is released from the neurotransmitter vesicles of the presynaptic membrane, the normal movement of molecules should be directed to receptor sites located on the postsynaptic membrane. However, in certain disease states, the flow of the neurotransmitter is defective. For example, in depression, the flow of the inhibitory neurotransmitter serotonin is defective, and molecules flow back to their originating site (the presynaptic membrane) instead of to receptors on the postsynaptic membrane that will transmit the impulse to a nearby neuron.
The mechanism of action and localization of neurotransmitters in the brain has provided valuable information concerning the cause of many mental disorders, including clinical depression and chemical dependency, and in researching medications that allow normal flow and movement of neurotransmitter molecules. Neurotransmitters, mental disorders, and medications Schizophrenia Impairment of dopamine-containing neurons in the brain is implicated in schizophrenia, a mental disease marked by disturbances in thinking and emotional reactions.
Medications that block dopamine receptors in the brain, such as chlorpromazine and clozapine, have been used to alleviate the symptoms and help patients return to a normal social setting. Depression In depression, which afflicts about 3. 5% of the population, there appears to be abnormal excess or inhibition of signals that control mood, thoughts, pain, and other sensations. Depression is treated with antidepressants that affect norepinephrine and serotonin in the brain. The antidepressants help correct the abnormal neurotransmitter activity.
A newer drug, fluoxetine (Prozac), is a selective serotonin reuptake inhibitor (SSRI) that appears to establish the level of serotonin required to function at a normal level. As the name implies, the drug inhibits the re-uptake of serotonin neurotransmitter from synaptic gaps, thus increasing neurotransmitter action. In the brain, then, the increased serotonin activity alleviates depressive symptoms. Alzheimer’s disease Alzheimer’s disease, which affects an estimated four million Americans, is characterized by memory loss and the eventual inability for self-care.
The disease seems to be caused by a loss of cells that secrete acetylcholine in the basal forebrain (region of brain that is the control center for sensory and associative information processing and motor activities). Some medications to alleviate the symptoms have been developed, but presently there is no known treatment for the disease. Generalized anxiety disorder People with generalized anxiety disorder (GAD) experience excessive worry that causes problems at work and in the maintenance of daily responsibilities. Evidence suggests that GAD involves several neurotransmitter systems in the brain, including norepinephrine and serotonin.
Attention-deficit/hyperactivity disorder People affected by attention-deficit/hyperactivity disorder (ADHD) experience difficulties in the areas of attention, overactivity, impulse control, and distractibility. Research shows that dopamine and norepinephrine imbalances are strongly implicated in causing ADHD. Others Substantial research evidence also suggests a correlation of neurotransmitter imbalance with disorders such as borderline personality disorders, schizotypal personality disorder, avoidant personality disorder, social phobia, histrionic personality disorder, and somatization disorder.
Drug addictions Cocaine and crack cocaine are psychostimulants that affect neurons containing dopamine in the areas of the brain known as the limbic and frontal cortex. When cocaine is used, it generates a feeling of confidence and power. However, when large amounts are taken, people “crash” and suffer from physical and emotional exhaustion as well as depression. Opiates, such as heroin and morphine, appear to mimic naturally occurring peptide substances in the brain that act as neurotransmitters with opiate activity called endorphins.
Natural endorphins of the brain act to kill pain, cause sensations of pleasure, and cause sleepiness. Endorphins released with extensive aerobic exercise, for example, are responsible for the “rush” that long-distance runners experience. It is believed that morphine and heroin combine with the endorphin receptors in the brain, resulting in reduced natural endorphin production. As a result, the drugs are needed to replace the naturally produced endorphins and addiction occurs. Attempts to counteract the effects of the drugs involve using medications that mimic them, such as nalorphine, naloxone, and naltrexone.
Alcohol is one of the depressant drugs in widest use, and is believed to cause its effects by interacting with the GABA receptor. Initially anxiety is controlled, but greater amounts reduce muscle control and delay reaction time due to impaired thinking. Resources BOOKS Tasman, Allan, Kay Jerald, MD, Jeffrey A. Lieberman, MD, eds. Psychiatry. 1st ed. Philadelphia: W. B. Saunders Company, 1997. Laith Farid Gulli, M. D. Mary Finley Source: Duke University Medical Center How The Neuron Sprouts Its Branches, December 11, 2005
Neurobiologists have gained new insights into how neurons control growth of the intricate tracery of branches called dendrites that enable them to connect with their neighbors. Dendritic connections are the basic receiving stations by which neurons form the signaling networks that constitute the brain’s circuitry. Such basic insights into neuronal growth will help researchers better understand brain development in children, as well as aid efforts to restore neuronal connections lost to injury, stroke or neurodegenerative disease, said the researchers. In a paper published in the Dec. , 2005, issue of Neuron, Howard Hughes Medical Institute investigator Michael Ehlers and his colleagues reported that structures called “Golgi outposts” play a central role as distribution points for proteins that form the building blocks of the growing dendrites. Besides Ehlers, who is at Duke University Medical Center, other co-authors were April Horton in Ehlers’ laboratory; Richard Weinberg of the University of North Carolina at Chapel Hill. ; Bence Racz in Weinberg’s laboratory; and Eric Monson and Anna Lin of Duke’s Department of Physics. The research was sponsored by The National Institutes of Health.
The Golgi apparatus is a cellular warehouse responsible for receiving, sorting and shipping cargoes of newly synthesized molecules needed for cell growth and function. Until the new findings, researchers believed that only a central Golgi apparatus played a role in such distribution, said Ehlers. “In most mammalian cells, the Golgi has a very stereotyped structure, a stacked system that resides near the cell nucleus in the middle of the cell,” he said. “But mammalian neurons in the brain are huge, with a surface area about ten thousand times that of the average cell.
So, it was an entirely open question where all the membrane components came from to generate the complex surface of growing dendrites. And we thought these remote structures we had discovered in dendrites called Golgi outposts might play a role. ” The researchers studied the dendritic growth process in pyramidal neurons, which grow a single long “apical” dendrite and many shorter ones. To explore the role of Golgi outposts, they used imaging of living rat brain cells grown in culture, as well as electron microscopy of rat brain tissue.
These studies revealed that the Golgi outposts tended to appear in longer dendrites and also that those Golgi in the main cell body tended to orient toward longer dendrites. And importantly, said Ehlers, the studies in cell culture revealed that the Golgi orientation preceded the preferential growth of long dendrites. “This finding showed us that we weren’t just seeing a correlation between Golgi and longer dendrites,” said Ehlers. “Initially, when these growing dendrites are all essentially uniform in length, they grow at about the same rate.
But later, after the Golgi orient toward one dendrite, it takes off and grows dynamically to become the longest dendrite. ” The researchers also used tracer molecules to track the molecular cargo secreted by the Golgi, said Ehlers. “We saw very clearly that this cargo that originates in the Golgi gets directed towards the one longest dendrite in a highly preferential way,” he said. “As cargo comes out of the Golgi, it does not go randomly to the cell surface. ” Ehlers and his colleagues also found that the Golgi outposts appeared to locate themselves at dendritic branch points. This finding is important because a fundamental problem that neurons must solve is how to sort appropriate cargo molecules in the right amounts down different dendritic branches,” said Ehlers. “After all, different dendritic branches can have different functional properties, molecular composition and electrical properties. So, when a cargo reaches a branch point, it’s like a highway intersection, and the cargo needs to be directed. We’ve found that these dendritic Golgi outposts are located at the strategic points to do just that.
And I believe this is the first such specific organelle identified at a dendritic branch point positioned to perform this fundamental neuronal function. ” Finally, the researchers disrupted the orientation, or “polarity,” of the Golgi — thus causing them to move into all the dendrites — without disrupting their function. They found that disrupting the polarity caused all the dendrites to grow at the same rate. Further studies, said Ehlers, will explore how Golgi outposts arise, how they arrive at dendritic branch points and what cargo they distribute.
The researchers also will seek to understand how molecules are selected for import to the distant reaches of the dendrites and which will be locally synthesized in the dendrites. Such studies could give important insights into the machinery of neuronal growth and how it is controlled, he said. “Understanding this machinery has clinical relevance because many disorders of brain development in children manifest abnormal dendritic structures,” said Ehlers. “Also, it turns out that most neurodegenerative diseases, such as Parkinson’s and Alzheimer’s, are disorders of protein processing.
But we know very little about how and where integral membrane proteins are synthesized and processed by neurons. ” NERVE CONDUCTION| | | | | None of our perceptions, thoughts, or memories would be possible without nerve conduction, the process by which nerve impulses are propagated along our neurons. Nerve conduction is an electrochemical process, which means that it uses electricity made with chemical molecules. In other words, the electricity in the brain is not produced by electrons flowing the way they do through a household electrical wire.
Instead, the brain’s electricity is caused by the movements of electrically charged molecules through the neurons’ membranes. The membrane of a neuron, like that of any other cell, contains tiny holes known as channels. It is through these channels that charged molecules pass through the neural membrane. But unlike the channels in other cells, the channels in neurons are so specialized that they can coordinate the movements of these charges across the membrane so as to conduct nerve impulses.
The following diagram shows in simplified form the sequence of events by which a nerve impulse is conducted (click on step numbers 2 and 3 to see the corresponding steps). Scientists know a great deal about the charged molecules that generate nerve impulses and the sequence of their movements. But conduction of a nerve impulse down a single neuron would serve no purpose were it not for the other major component of neuronal communication: the synaptic transmission that lets the impulse pass from one neuron to the next. | | | | | | | | | | | | | | | SYNAPTIC TRANSMISSION| | | | | The brain’s great computational abilities are derived from the communication among its billions of nerve cells. But the process of neural conduction that lets a nerve impulse propagate down a neuron would serve no purpose if it were not coupled with another mechanism: the synaptic transmission that lets the impulse pass from one neuron to the next. At the synapse between two neurons, they do not actually touch each other. They therefore need to secrete chemical messengers that travel from one neuron to the other to regenerate the nerve impulse.
This mechanism of synaptic transmission can be divided into four main steps. (Click on step numbers 2, 3, and 4 in the diagram below to see the corresponding steps). In addition to the chemical messengers and the receptors, the membrane channels play an essential role in each of these four phases of synaptic transmission. | | SYNAPSES| | | | | The term “synapse” designates the point where the axon of one neuron connects to a dendrite of another. This word comes from the Greek syn (together) and haptein (join).
In the animal kingdom, neurons can be connected to each other in two very different ways: * by an electrical synapse, in which the two cells touch and are connected by tiny holes, which lets the nerve impulse pass directly from one neuron to the other; or * by a chemical synapse, where the two cells do not touch and the nerve impulse needs particular molecules to bridge the gap between them. The vast majority of the synapses in the human brain are chemical synapses. Chemical synapses are slower than electrical ones but are also far more flexible.
This valuable flexibility is the foundation of all learning. In a chemical synapse, a nerve impulse can travel in only one direction. In contrast, in an electrical synapse, the impulse travels in both directions. Also, across a chemical synapse, the impulse is transmitted with a 0. 5-millisecond delay, while across an electrical synapse, the delay is almost non-existent. | | On either side of the synapse, the axon and dendrite have evolved specialized molecules to perform their respective tasks. | | | | | | | | | | | | | NEUROTRANSMITTERS| | | | |
Neurotransmitters are chemical molecules that “ferry” nerve impulses across the synapse from one neuron to the next. Each type of neurotransmitter has a molecular form that lets it bind to the right site on the second neuron to produce its particular effect. The neurotransmitter thus acts somewhat like a key. If it is the right shape for the next neuron (shown here as a lock), it will produce an effect on that neuron. | | Neurotransmitters are divided into two categories according to the effect that they have on the second neuron once they are released into the synaptic gap.
Neurotransmitters that help this neuron to propagate the nerve impulse are classified as excitatory neurotransmitters. Neurotransmitters that reduce the likelihood of this neuron’s propagating the impulse are called inhibitory neurotransmitters. | | | CELLULAR LEVEL NEURONS| | | | | The human nervous system is composed of two types of cells: glial cells and neurons. Neurons are the ones that make us so clever. Like all the cells in the human body, every neuron has a membrane that surrounds its cytoplasm and a nucleus that contains its genes.
Neurons also have small organelles that let them produce energy and manufacture proteins. But because the neurons’ main job is to transmit information, they also have two types of highly specialized extensions that distinguish them from other cells. Dendrites, with their tree-like branching structure, gather information and relay it to each neuron’s cell body. Axons are generally very long, and each neuron has only one. This axon carries information away from the neuron’s cell body toward other neurons, with which it makes connections called synapses.
Axons can also directly stimulate other types of cells, such as muscle and gland cells. | | | | | | | | | | | | | | | | GLIAL CELLS| | | | | The human nervous system is composed of two types of cells: glial cells and neurons. You do not usually hear much about glial cells, even though there are 10 to 50 times more of them in the human nervous system than the typical 100 billion neurons. Why do the glial cells languish in such obscurity? Basically, because they do not conduct nerve impulses. But that does not mean they are not essential. In fact, they are so essential that without them, the neurons could not work properly.
The glial cells provide the neurons with nourishment, physical support, and protection. Glial cells also dispose of the waste materials generated when neurons die, and accelerate neural conduction by acting as an insulating sheath around certain axons. Each of these functions is performed by a different specialized type of glial cell. | | | | | | | | | | | | | | | | | | | | | From six to eight weeks after fertilization, the cerebral hemispheres begin to form. Around the seventh week, nerves make connections with some muscles that enable the embryo to make spontaneous movements.
At the end of the eighth week, all of the body’s essential internal and external structures are present. The second and third trimesters of pregnancy are devoted essentially to growth of these structures that have already been put in place. | | | | | | | | In the epithelium of the neural tube, proliferation takes place at specific locations called germinal zones. The germinal zones from which most parts of the nervous system will develop are located near the surface of one of the cavities that will become the ventricular system of the brain. | | | | HOW THE NERVOUS SYSTEM BEGINS| | | | | | |
About three weeks after conception, the human brain is nothing more than a single layer of flattened cells located in the ectoderm and known as the neural plate. Next, a furrow forms that extends from the rostral portion to the caudal portion of this plate. The sides of this neural furrow then form the neural groove. The sides of this groove then close over, starting from the middle of the groove and moving outward rostrally and caudally, to form the neural tube. Certain cells in the dorsal portion of the neural tube will become the neural crest, the structure that is the origin of the neurons of the peripheral nervous system.
The part of the neural plate located just above the notochord differentiates into the floor plate. The inductive signals from this floor plate induce the development of the spinal motor neurons and the motor neurons of the medulla and the pons from the most ventral cells of the neural tube. The most dorsal cells will give rise to the sensory neurons. | | | | | | | | | The process of formation of the neural tube, which often begins before the mother even knows she is pregnant, is called neurulation. It is from this tube that the brain and the spinal cord will develop.
At this stage they will be the largest organs in the embryo, resulting in its characteristic curved form. At the end of the third week, the eyes and the ears will also have begun to form. | | | | | After the segmentation and gastrulation phases are completed, organogenesis begins. In this phase, the groups of cells are laid down that will become the various organs of the human body. Organogenesis starts with a process called metamerization, in which the mesoderm divides into a series of identical segments called metameres along the embryo’s longitudinal axis.
At this stage, the mesoderm develops masses called somites on either side of the neural tube. It is from these somites that the 33 vertebrae of the spinal column and the corresponding skeletal muscles will develop. Source: Dr. K. Tosney, University of Michigan At the start of the 4th week after fertilization, the neural tube closes entirely, completing the first stage of the development of the brain and the spinal cord. The next stage, histogenesis, in which the stem cells differentiate to form the various nerve tissues, can now begin in earnest.
At the same time, the major subdivisions of the brain will form, and the cell populations will be rearranged accordingly. | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | | HOW THE MAJOR SUBDIVISIONS OF THE BRAIN ARE FORMED| | | | | | | The encephalon begins to form when the neural tube swells and subdivides, first into the three primary vesicles (the prosencephalon, mesencephalon and rhombencephalon), and then into the five secondary vesicles (the telencephalon, diencephalon, mesencephalon, metencephalon and myelencephalon).
The telencephalon is the most rostral of the secondary vesicles. Two buds emerge from either side of its rostral portion to form the two telencephalic vesicles. These two vesicles grow rapidly to form the two cerebral hemispheres. First they grow back over the diencephalon, then they grow down to cover its sides. | | | | | General diagram of a sagittal section of the brain (applicable to all mammals) | Another pair of vesicles will also sprout from the ventral surface of these cerebral hemispheres to become the olfactory bulbs and other structures that contribute to the sense of smell.
Various structures will then emerge from the walls of the telencephalon while the white matter that connects these structures develops as well. The neurons of the telencephalon wall proliferate to form three distinct regions—the cerebral cortex, the basal telencephalon, and the olfactory bulb. | The axons of these neurons will also gradually elongate to make connections with the other parts of the nervous system. Some of these axons will constitute the cortical white matter that arises from and projects to neurons in the cortex. Others will form the corpus callosum, the band of nerve fibres that connects the two hemispheres of the brain.
Still others—those of the internal capsule—will connect the cortical white matter to the brain stem, generally by way of the thalamus. For example, the axons arising from the motor cortex will pass through the internal capsule to connect to the motor neurons in the spinal cord. In the the remaining space between the telencephalon and the diencephalon on either side, the two cerebral ventricles (also known as the lateral ventricles or the first and second ventricle) form, while the third ventricle forms in the space at the centre of the diencephalon.
The diencephalon also differentiates into distinct areas: the thalamus and the hypothalamus. | | | On either side of the diencephalon, two secondary vesicles also develop—the optic vesicles. The optic vesicles lengthen and fold inward to form the optic peduncles and optic cups, which will give rise to the retinas and the optic nerves. The retinas and the optic nerves are therefore not part of the peripheral nervous system, but rather they are integral parts of the brain! | Compared with the prosencephalon (telencephalon and diencephalon), the mesencephalon undergoes far less transformation.
Its dorsal surface forms the tectum, while its floor forms the tegmentum. While these structures are differentiating, the cavity that separates them shrinks to a narrow channel called the cerebral aqueduct. The rostral portion of this aqueduct opens into the third ventricle of the diencephalon. | | The mesencephalon serves as the passageway for the bundles of fibres that connect the cortex to the spinal cord—both those that arise from the sensory system and those that descend to participate in movement control. The tectum differentiates into two structures.
One, the superior colliculus, receives information directly from the eye and controls eye movements. The other, the inferior colliculus, receives information from the ear and serves as an important relay in the auditory pathways. The tegmentum is one of the most colourful areas of the brain. It contains the substantia nigra (“black matter”) and the red nucleus, two structures that are involved in controlling voluntary movement. Other groups of cells in the mesencephalon project their axons diffusely into large areas of the brain and influence a wide variety of functions, such as consciousness, mood, pleasure and pain. Caudal to the mesencephalon lies the metencephalon, which is the rostral portion of the hindbrain and differentiates into two major structures: the cerebellum and the pons. The cerebellum arises from the thickening of the tissue covering the lateral walls of the neural tube at this location. The two masses thus formed ultimately fuse dorsally to form the cerebellum. During this time, a swelling develops on the ventral side of the metencephalon and forms the pons.
This structure is an important information pathway between the brain, the cerebellum, and the spinal cord. | In the the myelencephalon (the caudal portion of the hindbrain) the changes are less spectacular. The ventral and lateral regions of this structure swell to form the medulla oblongata. Along the ventral aspect of the medulla, the two medullary pyramids will also develop, formed by the passage of the corticospinal bundles responsible for voluntary movement. Lastly, the central canal, which persists while the medulla is forming, becomes the fourth ventricle. | | The entire portion of the neural tube that lies caudal to the five secondary vesicles becomes the spinal cord through a fairly direct process of differentiation consisting in the thickening of the tube walls. This thickening gradually reduces the diameter of the neural tube until it becomes the very narrow spinal canal . As the cross-section shown here illustrates, the cell bodies of the neurons in the spinal cord are concentrated in the grey matter at the centre (the butterfly-shaped area), while the white matter at the periphery is composed of bundles of axons. The grey matter of the spinal cord is in turn divided into the dorsal horn, which receives sensory inputs, and the ventral horn, whose neurons innervate the skeletal muscles. Likewise, within the white matter, there develop dorsal columns composed of sensory axons that ascend to the brain and lateral columns composed of corticospinal axons that descend to transmit signals for controlling movement. Between the dorsal and ventral horns, a large number of interneurons also develop that are involved in various types of reflexes as well as in establishing networks that perform initial processing of the information received in the spinal cord. | SYNAPSES| | | | | A synapse is the junction point between two neurons. However, a nerve impulse can also be transmitted from a sensory receptor cell to a neuron, or from a neuron to a set of muscles to make them contract, or from a neuron to an endocrine gland to make it secrete a hormone. In these last two cases, the connection points are called neuromuscular and neuroglandular junctions. In a typical chemical synapse between two neurons, the neuron from which the nerve impulse arrives is called the presynaptic neuron. The neuron to which the neurotransmitters (chemical messengers) bind is called the postsynaptic neuron. | A presynaptic neuron has several specialized structures that distinguish it from a postsynaptic neuron. The terminal button of the presynaptic neuron’s axon contains mitochondria as well as microtubules that transport the neurotransmitters from the cell body (where they are produced) to the tip of the axon. (click on 2. Axonal Transport)This terminal button also contains spherical vesicles filled with neurotransmitters. These neurotransmitters are secreted into the synaptic gap by a process called exocytosis, in which the vesicles’ membranes fuse with that of the resynaptic button. The synaptic gap that the neurotransmitters have to cross is very narrow–on the order of 0. 02 micron. Across the gap, the neurotransmitters bind to membrane receptors: large proteins anchored in the cell membrane of the post-synaptic neuron. At this location, under an electron microscope, you can observe an accumulation of opaque material which consists of the cluster of receptors and other signalling proteins that are essential for chemical neurotransmission. | Any given neurotransmitter has several sub-types of receptors that are specific to it.
It is the presence or absence of certain of these sub-types that causes a cascade of specific chemical reactions in the postsynaptic neuron. These reactions result in the excitation or inhibition of this neuron. | | | | | | | | | | | A neurotransmitter’s agonist is a molecule that has the same effect on the postsynaptic neuron as the neurotransmitter itself does. An antagonist is a molecule that blocks the effect that the neurotransmitter normally has on the post-synaptic neuron. | It was long thought that a given neuron released only one kind of neurotransmitter.
But today, many experiments show that a single neuron can produce several different neurotransmitters. | Neurons that use GABA and glutamate as neurotransmitters are used by more than 80% of the neurons in the brain and constitute the most important inhibition and excitation systems, respectively, of the substantia nigra pars compacta (SNc). | | | | NEUROTRANSMITTERS| | | | | This section describes a few of the best known neurotransmitters that are involved in many functions in both the central and the peripheral nervous systems.
Apart from acetylcholine, they all belong to the family of amines or amino acids. Neurotransmitter| | Example of Disorder Involving It| | Molecular Structure| Acetylcholine is a very widely distributed excitatory neurotransmitter that triggers muscle contraction and stimulates the excretion of certain hormones. In the central nervous system, it is involved in wakefulness, attentiveness, anger, aggression, sexuality, and thirst, among other things. | | Alzheimer’s disease is associated with a lack of acetylcholine in certain regions of the brain. | | Dopamine is an inhibitory neurotransmitter involved in controlling movement and posture. It also modulates mood and plays a central role in positive reinforcement and dependency. | | The loss of dopamine in certain parts of the brain causes the muscle rigidity typical of Parkinson’s disease. | | | GABA (gamma-aminobutyric acid) is an inhibitory neurotransmitter that is very widely distributed in the neurons of the cortex. GABA contributes to motor control, vision, and many other cortical functions.
It also regulates anxiety. | | Some drugs that increase the level of GABA in the brain are used to treat epilepsy and to calm the trembling of people suffering from Huntington’s disease. | | | Glutamate is a major excitatory neurotransmitter that is associated with learning and memory. | | It is also thought to be associated with Alzheimer’s disease, whose first symptoms include memory malfunctions. | | | Norepinephrine is a neurotransmitter that is important for attentiveness, emotions, sleeping, dreaming, and learning.
Norepinephrine is also released as a hormone into the blood, where it causes blood vessels to contract and heart rate to increase. | | Norepinephrine plays a role in mood disorders such as manic depression. | | | Serotonin contributes to various functions, such as regulating body temperature, sleep, mood, appetite, and pain. | | Depression, suicide, impulsive behaviour, and agressiveness all appear to involve certain imbalances in serotonin. | | | Scientists have now identified some 60 different molecules that meet the criteria for being regarded as neurotransmitters. | INSERT FIGURE OF A SYNAPSE Figure 11a illustrates the site where information is conveyed from one neuron to the next. At this junction, called the , chemicals are used to transmit the electrical neuronal impulse. The structures (magnification approximately 93,000X) and substances involved in synaptic transmission at a are identified, and the sequence of events in chemical transmission are described. A directed synapse is one in which the neurotransmitter release sites and receptor sites are close, but not touching.
The cleft or space between these structures is typically 0. 02-0. 05 microns wide. A greater distance between the site of neurotransmitter release and the site of reception characterizes another type of synapse. In this so-called , the neurotransmitters are released from variscosities (called “string-of-beads”) along a neuron’s axon. synapse directed synapse non-directed synapse Synapses occur between different neuronal structures, and are named based on the site of neurotransmitter release (presynaptic membrane) nd site of receptor binding (postsynaptic membrane). The most common synapses are (between axon and dendrite), (between axon and soma), or (between two axons). The basic process of information exchange at axodendritic and axosomatic synapses is the primary topic of this tutorial. Axoaxonic synapses modulate neuronal transmission by either inhibiting or facilitating depolarization at the presynaptic membrane. Dendrodendritic synapses appear to be unique in their ability to transmit in either direction, allowing for reciprocal effects.
The multiple modes of communication provided by the varied synaptic connections underlie the complex structure of communication in the nervous system. Synaptic communication Objectives: – explain the differences between an electrical and chemical synapse – describe the steps involved in synaptic communication at a chemical synapse – design an experiment to test the dependence of chemical synapses on Ca+2 influx – describe the quantal analysis experiments and their significance – describe the SNARE hypothesis in general terms and design an experiment to test this hypothesis in vivo
Reading: Shephard (Neurobiology) Chapter 6 pp: 102 – 108, 115-131. Hall (Introduction to Molecular Neurobiology) Chapter 5. Kelly, R. B. (1993) Storage and release of neurotransmitters. Cell 72/Neuron 10 (suppl. ): 43-53. Jessell, T. M and Kandel, E. R. (1993) Synaptic transmission: a bidirection and self-modifiable form of cell-cell communication. Cell 72/Neuron 10 (suppl. ): 1-30. Nonet et al. (1998) Synaptic Transmission Deficits in Synaptobrevin Mutants Journal of Neuroscience 18: 70-80 Goda (1997) SNAREs and regulated vesicle exocytosis
Caenorhabditis elegans Proc. Natl. Acad. Sci. 94: 769 – 772. Links: Synaptic communication 04/11/02 14:56 http://www. zoology. ubc. ca/%7Eauld/bio455/lectures/synaptic. html Page 1 sur 7 Sherrington (1890) studied reflex functions of spinal cord – coined the word synapse = a functional connection between surfaces – synapse (from the Greek: to clasp, to connect or join) – sites of interaction between neurons and neurons and their targets – cells connect via gap junctions: -membranes are separated by 2 nm – gap junction channels have a large conductance synaptic delay (current spread from cell to cell is instantaneous) – important in some reflexes – commonly found in other cell types as well i. e. glia – can be modulated by intracellular Ca+2, pH, membrane voltage, calmodulin – clusters of proteins that span the gap such that ions and small molecules can pass directly from one cell to another – gap junctions: -made up of 6 protein subunits arranged around a central pore, made up of the connexin protein – cloned from many tissues and organisms and are extremely well conserved – what is a way to test if your clone does indeed encode the right protein? injection of the cloned connexin protein into Xenopus oocytes – results in formation of gap junctions between two oocytes – most common type of synapse – electrical signal in the presynaptic cell is communicated to the postsynaptic cell by a chemical (the neurotransmitter), – separation between presynaptic and postsynaptic membranes is about 20 to 30 nm – a chemical transmitter is released and diffuses to bind to receptors on postsynaptic side – bind leads (directly or indirectly) to changes in the postsynaptic membrane potential (usually by opening or closing transmitter sensitive ion channels) the response of the neurotransmitter receptor can depolarizes (excitatory postsynaptic potential; epsp) or hyperpolarizes (inhibitory postsynaptic potential; ipsp) the post-synaptic cell and changes its activity – significant delay in signal (1 msec) but far more flexible than electrical synapse – synaptic delay is NOT due diffusion of the neurotransmitter across the cleft (happens in about 50 msec) – delay is in the release of neurotransmitter due to a lag in the opening of Ca+2 channels i) Excitatory – excite (depolarize the postsynaptic cell) i) Inhibitory – inhibit (hyperpolarize the postsynaptic cell) iv) Modulatory – modulates the postsynaptic cells response to other synapses Lecture Notes: 2 types of synapses 1) Electrical NO 2) Chemical Some types of chemical synapse include: NMJ – neuromuscular junction: Synaptic communication 04/11/02 14:56 http://www. zoology. ubc. ca/%7Eauld/bio455/lectures/synaptic. html Page 2 sur 7 – motor nerve terminal branches run in shallow grooves on surface of muscle – nerve terminal contains many mitochondria and vesicles vesicles can be seen lined up in double rows along a region of dense material attached to presynaptic membrane => active zone – the dense material could be Ca+ channels – used fluorescently tagged omega-conotoxin (used by sea snails to paralyze their prey) that binds specifically to Ca+ channels and saw concentrated binding in! active zone – synaptic cleft very structured (basal lamina) – many postjunctional folds (motor endplate), grooves and fold particular to skeletal muscle synapses – acetylcholine is the neurotransmitter for the mammalian NMJ – glutamate is the neurotransmitter for the insect NMJ usually in the form of swellings called boutons – also contains many mitochondria and vesicles – boutons also include electron dense active zones with vesicles clustered in rows along side – less postsynaptic specializations – sometimes see thickening of membrane 1. Nerve impulse arrives at presynaptic terminal Synapses on Nerve cells: Basic Function of Chemical Synapse 2. Depolarization causes voltage-gated Ca+2 channels to open – increases Ca+2 influx, get a transient elevation of internal Ca+2 ~100 mM 3.
Vesicle exocytosis – increase in Ca+2 induces fusion of synaptic vesicles to membrane – vesicles contain neurotransmitters 4. Vesicle fusion to membrane releases stored neurotransmitter 5. Transmitter diffuses across cleft to postsynaptic side 6. Neurotransmitters bind to receptor either: i) ligand-gated ion channel or ii) receptors linked to 2nd messenger systems 7. Binding results in a conductance change – channels open or close or – binding results in modulation of postsynaptic side 8.
Postsynaptic response – change in membrane potential (e. g. muscle contraction in the case of a motorneuron at a neuromuscular junction) 9. Neurotransmitter is removed from the cleft by two mechanisms i) transmitter is destroyed by an enzyme such as acetylcholine esterase ii) transmitter is taken back up into the presynaptic cell and recycled e. g. – acetylcholine esterase, breaks down acetylcholine in cleft, choline is recycled back into the presynaptic terminal Synaptic communication 04/11/02 14:56 ttp://www. zoology. ubc. ca/%7Eauld/bio455/lectures/synaptic. html Page 3 sur 7 i) non-peptide neurotransmitters a) broken down by enzymes – many nerve gases and insecticides work by blocking acetylcholine esterase – prolongs synaptic communication b) recycled by uptake into presynaptic terminal – due to a specific neurotransmitter transporter c) recycled by uptake into other cells – glial cells will take up neurotransmitters (GABA in crustacean NMJ, mammalian CNS) the concentration of neurotransmitter within the vesicle is pretty constant (for example ~ 3000 molecules of Ach per vesicle at the NMJ) – neurotransmitter are released in packets or quanta = the contents of 1 vesicle – can record the effect of the release of one quanta on the extracellular membrane – for instance, the Ach neurotransmitter in one vesicle opens about 1500 acetylcholine receptors at the NMJ – some vesicles contain only enough neurotransmitter to open 20 channels (depends on the neurotransmitter) one vesicle (or quantum) of Ach depolarizes the muscle ~1 mV – increases in a step wise manner, i. e. 2 vesicles depolarize the postsynaptic membrane by about twice as much and 3 vesicles about three times as much etc. – a normal depolarization at the NMJ is made up of over 200 quantal units 2 types of secretory vesicles – responsible for modulatory signalling and distant signalling – contain neuropeptide transmitters (small peptides cleaved from large precursor proteins) – exocytosis is NOT restricted to active zones exocytosis is triggered by trains of action potentials – these transmitters are produced and packaged into vesicles at the cell body and transported to nerve terminal Removal of neurotransmitter ii) peptide transmitters – don’t appear to be broken down or recycled – diffuse away and are broken down by nonspecific peptidases – explains prolonged actions on synapses One vesicle = one quantum Presynaptic Vesicles 1) large dense-core vesicles: 2) synaptic vesicles: Synaptic communication 04/11/02 14:56 http://www. zoology. ubc. a/%7Eauld/bio455/lectures/synaptic. html Page 4 sur 7 – responsible for fast synaptic signalling – store and secrete non-peptide neurotransmitters, e. g. acetylcholine, glycine, glutamate – enough vesicles in the typical nerve terminal to transmit a few thousand impulses – exocytosis only occurs after an increase of internal Ca+2 (due to depolarization) and at active zones (regions in the presynaptic membrane adjacent to the cleft) – neurotransmitters can be divided into two groups i) low molecular weight, non-peptide e. g. acetylcholine, glycine, glutamate i) peptide (over 40 identified so far and counting) – same transmitters found widely distributed through out diverse organisms – many of the molecules that involved in vesicle exocytosis are now known – related to other vesicle fusion systems such as Golgi or secretory procedures – a group of 6 to 7 proteins work together to respond to Ca+2 influx and regulate vesicle fusion – many of these proteins are common to other secretory pathways – in yeast: mutations that affect the homologues of these exocytosis mediating proteins have been made and all impair exocytosis after exocytosis the synaptic vesicle membranes are reinternalized by endocytosis and reused (reloaded Processing of different neurotransmitter vesicles Neurotransmitter – goes through a number of separate stages in its actions 1. Synthesis – all transmitters except peptides are made in the nerve terminal i) non-peptide transmitters – responsible for fast synaptic signalling – synthetic enzymes + precursors transported into nerve terminal – subject to feedback inhibition (from recycled neurotransmitters) – can be stimulated to increase activity (via Ca+2 stimulated phosphorylation) ii) peptide transmitters peptide neurotransmitters are made from large precursor proteins in the cell body – specific proteases cleave the precursor into the appropriate peptides (this can occur in the cell body, in the vesicle during transport or at the nerve terminal) – responsible for modulatory signalling and distant signalling 2. Packaging into vesicles – neurotransmitters packaged into vesicles i) for small non-peptide neurotransmitters – packaged in small “classical” vesicles – involves a pump powered by a pH gradient between outside and inside of vesicle – pump blocked by drugs and these block neurotransmitter release ii) for peptide neurotransmitters packaged into vesicles in the cell body and transported to terminals (anterograde transport) – found the large dense core vesicles Vesicle Exocytosis Synaptic communication 04/11/02 14:56 http://www. zoology. ubc. ca/%7Eauld/bio455/lectures/synaptic. html Page 5 sur 7 with neurotransmitter by a transmitter transporter system) – vesicles are also transported from the cell body to the nerve terminal – transmitter is synthesized in the terminal and loaded into the vesicles – enzymes and substrates necessary are present in the terminal – i. . acetylcholine, acetyl-CoA + choline used by choline acetyltransferase i) non-peptide transmitters – exocytosis only occurs after an increase of internal Ca+2 (due to depolarization) – at active zones (regions in the presynaptic membrane adjacent to the cleft) – many of the molecules that involved in vesicle exocytosis are now know – a group of 6 to 7 proteins work together to respond to Ca+2 influx and regulate vesicle fusion Lambert-Eaton Syndrome: – muscle weakness and reduction in transmitter release autoimmune disease – antibodies to own Ca+2 channels, block voltage-gated Ca+2 channels Black Widow Spider Venom ( -latrotoxin): – induces a massive release of transmitter by interacting with one of the complex of proteins that mediate the Ca+2 induced fusion of vesicles with the presynaptic membrane – depletes the store of vesicles Botulinus and Tetanus Toxins: (food poisoning) – blocks the fusion of vesicles by interfering with another of the proteins involved in mediating fusion of vesicles – respiratory paralysis i) peptide-transmitters (same as for non-peptide transmitters except:) – exocytosis is NOT restricted to active zones – exocytosis is triggered by trains of action potentials – four components i) V-SNARE – a vesicle membrane protein ii) T-SNARE – a target membrane protein iii) a cytosol protein NSF required for membrane fusion iv) adaptors for the NSF protein called SNAPs – vescile docking occurs between the V-SNARE and T-SNARE proteins – the combined proteins act as a receptor for the SNAPs which then bind NSF – this complex is called the SNARE complex SNARE hypothesis NSF is an ATPase that hydrolyzes ATP to drive membrane fusion – now thought that after ATP hyrolysis the complex is in a new stable form that will fuse only once Ca+2 influx occurs – this process is known to be fast as vesicle fusion occurs 60 microseconds after Ca+2 influx – found associated with vesicle membrane – site of botulinum and tetanus toxin action will cleave this protein – binds to syntaxin (T-SNARE) – mutants in this protein in C. elegans have abnormal synaptic communication (J. Neursci. 18: 70-80, 1998) V-SNARE synaptobrevin synaptotagmin – associated with the vesicle membrane
Synaptic communication 04/11/02 14:56 http://www. zoology. ubc. ca/%7Eauld/bio455/lectures/synaptic. html Page 6 sur 7 – binds NSF, SNAP and SNAP25 – a Ca+2 sensor for transmitter release – mutants in Drosophila and C. elegans: no synaptotagmin result in severe dysfunction in secretion (Cell 74: 1125-1134 (1993); Neuron 12: 909-920 (1994); Cell 73: 1291-1305 (1993)) – associated with target membrane – binds synaptobrevin – binds to Ca+2 channels to localize the t-snare close to the Ca+2 channels for more efficient vesicle fusion T-SNARE syntaxin – synaptosome associated protein 25K not be confused with the SNAPs which are different proteins SNAP25 Intracellular transport A guide to axon transport in the squid giant axon transport of vesicles from the nerve terminal to cell body – retrograde transport transport of vesicles from the cell body to nerve terminal – anterograde transport the motor is not the microtubules or MAPs two major motor proteins, both bind to vesicles and move them along the microtubules but in different directions. Kinesin: 350 kD protein that moves along the microtubules towards the nerve terminal (orthograde transport),
Dynein: 1200 kD protein that moves along the microtubules towards the cell body (retrograde transport) (dynein family also involved in cilia and flagella microtubule movement) two types of axon transport i) slow transport – 1 mm per day, ii) fast or rapid transport – 100 to 400 mm per day NEURAL COMMUNICATION| | | | | All of our sensations, movements, thoughts, and emotions are the result of communication between neurons. This communication is carried out by two complementary processes: electrical conduction and chemical transmission.
Electrical conduction lets nerve impulses travel rapidly within a neuron. It involves a brief electrical fluctuation that propagates down the neuron’s dendrites, then through its cell body and out to the tip of its axon. Electrical conduction is what gives the nervous system the rapid-response capability that is lacking in the body’s other major means of communication, the hormonal system. | | Chemical transmission takes place in the synapses between neurons, enabling nerve impulses to be transmitted from one neuron to the next.
This process is called “chemical transmission” because the diffusion of chemical molecules from one neuron to the next is what enables the electrical impulse to be reconstituted in that second neuron. Chemical transmission gives the brain the flexibility that is required for learning. | However, not all of the thousands of connections that a neuron receives are designed to facilitate the transmission of nerve impulses. Some may even make this transmission more difficult. The neuron must therefore find a way of integrating these various commands. | | | | | | | | | | | | AXON MYELINATION| | | | | Neurons need to send nerve impulses rapidly from one end of the human body to the other. To speed up neural conduction along their axons, neurons often receive help from surrounding glial cells. These glial cells wrap themselves around the axon, forming an insulating sheath somewhat like the insulation that covers electrical wires. This sheath, made of a fatty substance called myelin, enables nerve impulses to travel along the axon more quickly.
It is something like wrapping tape around a garden hose that is full of holes, in order to increase the water pressure. Similarly, the myelin sheath wrapped around the axon accelerates neural conduction. | | | This sheath is wrapped around the axon in segments that make it look like a string of sausages. | | SYNAPTIC TRANSMISSION| | | | | The main steps in synaptic transmission–synthesis, secretion, binding, and inactivation–are well known for several “classical” neurotransmitters that have been studied for quite some time, such as dopamine.
On this page we describe these steps using the example of acetylcholine, a neurotransmitter that is very common in the central and peripheral nervous systems as well as in all neuromuscular junctions. | Credit: Dr. Fred E. Hossler et Dr. Roger C. Wagner, University of Delaware| In this photo: the three black arrows identify synaptic vesicles where neurotransmitters are stored in the terminal button of an axon, the letters PC identify two post-synaptic neurons, the black triangle indicates the thickening of the post-synaptic neuronal membrane, and the white triangle that of the pre-synaptic neuronal membrane. | | 1. Synthesis“Classical” neurotransmitters are small molecules that are synthesized locally in the terminal button of the axon. The precursors of these molecules are converted into active neurotransmitters by means of one or more enzymes present in the axon. To produce acetylcholine, for example, the enzyme choline acetyltransferase combines choline with acetyl coenzyme A. Other neurotransmitters, such as neuropeptides (a category that includes endogenous opioids) are far bigger molecules, so they must be synthesized in the neuron’s cell body, where the organelles needed to assemble the amino acids are located. | 2. Excretion Most of the synaptic vesicles where neurotransmitters are stored are attached to cytoskeleton components in the axon’s terminal button, near the active zones where these vesicles will fuse with the button’s membrane. When an action potential reaches the axon’s terminal button, it is accompanied by a massive influx of calcium ions. These generate a cascade of reactions that cause the vesicles to detach from the cytoskeleton components and migrate rapidly to these active zones. | In a process called exocytosis, the vesicles then merge briefly with the terminal button membrane, release their neurotransmitters into the synapse, then close up again and retreat inward, ready to be filled with neurotransmitters again. | (click on 6. Neaurotransmitter Release) 3. Binding | | If the neurotransmitter released into the synapse is acetylcholine, for example, it then binds to acetylcholine-specific receptors on sodium channels in the post-synaptic neuronal membrane, causing these channels to open and let sodium ions enter this neuron.
The neuron’s membrane then becomes depolarized, causing the neuron to become excited. In contrast, when a neurotransmitter such as GABA or glycine binds to receptors on chloride channels in the postsynaptic membrane, it becomes hyperpolarized, and the neuron is inhibited. | (click on 7. Postsynaptic Mechanisms) 4. Inactivation In this final step, the neurotransmitters break their bond with the receptors and return into the synaptic gap, where they must be inactivated for their effects to cease.
Neurotransmitters can be inactivated by one or a combination of the following processes: 1) they can simply diffuse out of the synaptic gap; 2) they can be broken down by enzymes present in the gap, such as acetylcholinesterase, which breaks acetylcholine down into choline and acetate; 3) they can be reabsorbed by the terminal button of the presynaptic neuron (as happens with dopamine, serotonin, and norepinephrine); 4) they can be removed from the gap by glial cells known as astrocytes. (click on 8. Removal of Neurotransmitter)
Ion channels in neuronal membranes can be classified into two major categories: channels that are always open and that help to establish the neuron’s resting potential, and channels that open and close in response to specific stimuli such as neurotransmitters, second messengers, and fluctuations in the membrane’s electrical potential (voltage). Action potentials (nerve impulses) are accompanied by the opening of ion channels that are termed “voltage-dependent” because they react to changes in membrane potential.
These channels are found only on axons. | Site Plan | Anatomy by Level of Organization| | | | | | | Synapses| | | Neuro- transmitters| | | Neurons| | | Glial Cells| | | The Brain| | | The Nervous System| | | Individual Behaviour| | | Social Groups| | | | | | | Function by Level of Organization| | | | | | | Nerve Conduction| | | Synaptic Transmission| | | Neural Communication| | | Axons Myelination| | | The Wired Brain| | | The Hormonal Brain| | | Choosing Behaviours| | | Group Dynamics| | |
Cite this Medical Essay – Nerve Cells
Medical Essay – Nerve Cells. (2018, Jun 11). Retrieved from https://graduateway.com/medical-essay-nerve-cells/