Neurons give rise to processes known as dendrites and axons that form a complex network of interconnections throughout the brain at specialized sites called synapses. Around the turn of the nineteenth century, the Italian physician Camillo Golgi (1873) developed a silver staining technique that revealed the full extent of dendritic and axonal arbors. From these images, he proposed the "reticular theory" suggesting that the neurons are not discrete cells, but instead are continuous with each other and form a syncytium. The renowned Spanish neuroscientist Santiago Ramón y Cajal (1891) used Golgi's method to reveal individual neurons in the brain and spinal cord during development and after a variety of experimental manipulations. These experiments led Cajal to conclude that neurons were discrete cells with axons ending on dendrites of different cells, a theory referred to as the "neuron doctrine." The term synapse is derived from the Greek word meaning "to clasp" and was first used by Sir Charles Sherrington (1897) in reference to Cajal's findings to indicate the point of contact between the axons and dendrites. Electron microscopy resolved the controversy in the 1950s by showing that a gap, the synaptic cleft, which is about twenty nanometers wide, separates the pre-synaptic axon from the postsynaptic dendrite, in favor of the neuron doctrine (Peters et al., 1991; Cowan et al., 2001). Scientists widely acknowledge that communication between neurons via signals at synapses provides an important cellular basis for perception, behavior, learning, and memory.
Synapses are characterized presynaptically by an axon that contains membrane bound vesicles and postsynaptically by a thickening in the membrane referred to as the postsynaptic density (see Figure 1). Excitatory synapses contain round vesicles in the pre-synaptic bouton (swelling in the axon) and an asymmetric postsynaptic density along the inside of the postsynaptic membrane (see Figure 1a, b). Depending
[Image not available for copyright reasons]
on the particular synapse, the presynaptic bouton may contain as few as three or as many as 5,000 or more of the synaptic vesicles each having diameters of approximately twenty to sixty nanometers. The other primary organelles in the presynaptic bouton include mitochondria (for production of ATP); smooth endoplasmic reticulum (to store and release calcium); and organelles involved in the recycling of the vesicular membrane called endosomes. The post-synaptic dendrite also contains these organelles in the vicinity of synapses. The internal structure is held together by cytoskeletal elements composed primarily of actin filaments and their linking proteins, and a few microtubules that provide transport of molecules and organelles to and from the cell body. The preand postsynaptic elements are held together by adhesion molecules that span the synaptic cleft.
The presynaptic vesicles of excitatory synapses contain the neurotransmitter glutamate, visualized by antibody labeling of the molecule in the vesicles, or special electrodes that detect glutamate released from the synapses. When an action potential arrives at the synapse, one or more vesicles fuse with the presynaptic membrane, and the contents of the vesicle are released into the synaptic cleft. Glutamate released in this way activates receptors located in the postsynaptic membrane, resulting in a variety of signals to the postsynaptic neuron. Activation of the AMPAergic glutamate receptors causes the postsynaptic membrane to become depolarized. This relieves the magnesium blockade of the calcium channel associated with a second important glutamate receptor, the NMDA receptor. When the NMDA receptor is both activated by glutamate and the postsynaptic membrane is depolarized, calcium enters the postsynaptic neuron through the channels associated with the NMDA receptor. A variety of calcium-dependent signaling molecules are tethered in the postsynaptic membrane and comprise the heavily stained postsynaptic density. Depending on the strength of synaptic activation and the amount of calcium entering the dendrite, the signaling molecules will trigger second messenger cascades that result in temporary changes in synaptic strength through activation of phosphorylation events, or more permanent changes in synaptic strength via the synthesis and insertion of more synaptic proteins thereby enlarging the synapse.
Inhibitory synapses are distinguished morphologically from excitatory synapses by the presence of symmetric pre- and postsynaptic thickenings that are not as wide as the postsynaptic density of excitatory synapses (see Figure 1c). The presynaptic vesicles of inhibitory synapses are typically smaller and are less uniform in shape, often appearing somewhat flattened. These synapses contain glycine or GABA as their primary neurotransmitter, and when they are activated they typically reduce the level of activity at the neuron. These synapses also have a specific set of signaling molecules tethered to their densities, such that depending on the degree of activation their strength can also be modified.
In addition to the excitatory and inhibitory synapses some synapses are modulatory, containing neuropeptides and hormones that act to modify the strength of the excitatory or inhibitory synaptic input. These neuromodulatory substances, along with growth factors, are often found co-localized in the same presynaptic boutons that form excitatory or inhibitory synapses. Their release also depends on the rate or intensity of presynaptic activation. In addition, there are electrical synapses (often called gap junctions) that form very close appositions between neurons such that channels in the adjacent membranes are aligned and current passes directly between the cells, without the need for a chemical neurotransmitter. If one of the two neurons that are coupled via electrical synapses is depolarized by chemical synaptic transmission at other synapses along its dendrites, then the current generated will also depolarize the coupled cell.
The third important partner at a synapse is the glial cell process (see Figure 1b). Astrocytic glia form long processes that end in numerous tiny projections. Some of these processes form end feet on the blood capillaries of the brain and through these end feet pass glucose and other substances from the blood. The glia store the glucose in the form of glycogen and provide the neuron with glucose or lactate as a form of energy to make ATP. Neurons usually do not store their own glucose, and hence are dependent on the glia for this metabolic energy. Glia also extend tiny processes to surround or partially surround synapses. In some brain regions, such as the cerebellar cortex, nearly all of the synapses are completely ensheathed with the astrocytic glia. In other brain regions, such as hippocampus and cortex, the glial processes end at the edge of the synaptic cleft, but rarely completely surround the synapse. Glia are critical for regulating ionic conditions in the extracellular milieu. If, for example, a glutamatergic neuron fires rapidly, it is the glia that remove the potassium that is extruded into the extracellular space, and also the glia that take up the excess glutamate that is released during neuronal firing. The glutamate stimulates the glia to break down glycogen and provide glucose or lactate to the neuron to replenish its energy. Removal of glutamate and potassium returns the neuron's environment to its normal resting state, thereby readying the neuron to respond to the next activation.
Synapses occur in many different locations on the neurons. The majority of excitatory synapses are distributed along the dendrites and are located up to one millimeter away from the cell body. More than 90 percent of the neurons in the brain have tiny protrusions called dendritic spines emanating from the postsynaptic surface (see Figure 1b). Most of the excitatory synapses are located on these dendritic spines and the neurons are referred to as spiny or sparsely spiny neurons depending on the number of dendritic spines they have. Nonspiny neurons comprise about 1 percent to 10 percent of the neurons in a particular brain region and these often have excitatory synapses distributed directly onto the dendritic shaft. Most inhibitory synapses are located on the neuronal cell body. The axon leaves the neuron from the cell body at a specialized site called the axonal hillock and travels millimeters to meters to make synapses with different neurons. Therefore, inhibitory synapses located between the excitatory inputs on the dendrites and the output axon can dampen the total amount of excitation and prevent the neuron from firing too rapidly. In this way, the inhibitory synapses serve to put the "brakes" on rapidly firing neurons before their activity can spread to other cells and cause a seizure. Neuromodulatory synapses are also widely distributed along the dendrites and cell bodies, but usually at a lower frequency than the excitatory and inhibitory inputs. Gap junctions also occur at a lower density and it remains to be determined whether all neurons are coupled in this way to one or more other neurons or the surrounding glia.
The remainder of this section focuses on the structure and function of dendritic spines because many scientists agree that the dendritic spines are crucial elements for learning and memory. Dendritic spines vary greatly in their structure. Some spines are short and stubby. Other spines, called thin or sessile spines, are short or long with a constricted neck and a slightly enlarged head. Yet other spines have a constricted neck with a very large head and are referred to as "mushroom" spines. Spines range in length from about 0.3 to 2 μ m; volume from 0.01 to 0.6 μ m3; and in synapse area from 0.03 to 0.5 μ m2, both within and across brain regions. There is a near perfect correlation between the number of presynaptic vesicles and the size of the synapse on a spine head, as well as the spine's volume, suggesting that larger spines have greater synaptic activity at them. The full range in spine diversity can be found along a single short segment of dendrite suggesting that each spine has a unique history of activation.
Like other excitatory synapses, spines contain a postsynaptic density. Some spines contain smooth endoplasmic reticulum (SER) in proportion with their volume, presumably to regulate internal calcium. Due to the very small volume of some spines, they appear not to need SER and cytoplasmic calcium buffers are sufficient. Spine cytoskeleton is primarily made up of actin, and microtubules are not found in the spine compartment, though they run extensively in the neighboring dendritic shaft beneath the spines.
The constricted spine neck imparts several important properties (Harris and Kater, 1994). In most brain regions the spine necks are just long and thin enough to elevate the postsynaptic response to activation of the glutamatergic synapse during synaptic transmission without choking off the signal to the parent dendrite. This elevation in postsynaptic potential facilitates the opening of the voltage-dependent channels on the spine head, such as the calcium channel associated with the NMDA glutamatergic receptor discussed above. The spine necks are also constricted enough to concentrate and compartmentalize the calcium and possibly other signaling molecules in the head near to the specific synapses that were activated. In this way, only those synapses will be modified during particular patterns of activity that lead to elevated or depressed synaptic responses underlying different forms of learning and memory. In addition, by concentrating the calcium in the spine head, spines protect the neuron from excitotoxicity by isolating the calcium near the synapse and away from the rest of the neuron where high concentrations would damage key structural elements, such as microtubules, in the dendrite.
Neurons are born without spines. As an animal matures, more dendritic spines are acquired. Dendritic spine number is affected by experience, such that an enriched environment results in more dendritic spines along the dendrite, compared to animals raised in an impoverished environment. Animals given extensive training also have more dendritic spines. An open question among scientists is whether learning, memory, and other experiences induce the formation of new spines and synapses, or if instead experience preserves spines from an ongoing production and loss of spines and synapses.
See also:APLYSIA: MOLECULAR BASIS OF LONG-TERM SENSITIZATION; GLUTAMATE RECEPTORS AND THEIR CHARACTERIZATION; GUIDE TO THE ANATOMY OF THE BRAIN: NEURON; LONG-TERM POTENTIATION: SIGNAL TRANSDUCTION MECHANISMS AND EARLY EVENTS; MORPHOLOGICAL BASIS OF LEARNING AND MEMORY: INVERTEBRATES; MORPHOLOGICAL BASIS OF LEARNING AND MEMORY: VERTEBRATES; NEUROTRANSMITTER SYSTEMS AND MEMORY
Cowan, W. M., Sudhof, T. C., and Stevens, C. F. (2001). Synapses. Baltimore, MD: The Johns Hopkins University Press.
Harris, K. M., and Kater, S. B. (1994). Dendritic spines: Cellular specializations imparting both stability and flexibility to synaptic function. Annual Review of Neuroscience 17, 341-371.
Revised byKristen M.Harris
Synapses serve as one-way communication devices, transmitting information in one direction only, from the fibre ending to the next cell. They come in two varieties, known as chemical and electrical, according to the mechanism by which the signal is transmitted from the presynaptic to the postsynaptic cell. At electrical synapses, which are relatively rare in vertebrates, the membranes of the two cells are in tight contact, producing electrical coupling, which enables a nerve impulse (or action potential) arriving at the presynaptic nerve ending to pass swiftly and reliably to the next cell. Chemical synapses are more complex, because the presynaptic and postsynaptic cells are physically separated by a minute gap (the synaptic cleft), which prevents simple electrical transmission of the action potential to the postsynaptic cell. Instead, transmission is accomplished by the release of a chemical neurotransmitter substance from the presynaptic fibre.
The cytoplasm of the presynaptic nerve terminal (in a chemical synapse) is packed full of small vesicles, each containing a few thousand molecules of neurotransmitter. When an action potential arrives in the terminal it stimulates the opening of calcium channels in the terminal membrane. As a consequence, calcium ions flood into the cell and cause the synaptic vesicles to release their contents into the synaptic cleft. The neurotransmitter molecules that are liberated diffuse across the cleft and interact with specialized protein receptor molecules in the postsynaptic cell membrane. The molecular structure of the neurotransmitter and its receptor are matched, so that they fit one another like a lock and key. At nerve–muscle synapses, and in many nerve–nerve synapses, the receptors have a double function, since they also serve as ion channels. Binding of a neurotransmitter molecule produces a change in the three-dimensional shape of the receptor that opens a tiny intrinsic pore in the protein. In the case of neurotransmitters that excite the postsynaptic membrane, the pore permits positively-charged sodium ions to move into the cell, making the potential across its membrane less negative. This local depolarization is known as an excitatory synaptic potential, and its amplitude is determined by the number of vesicles released from the presynaptic cell. If it is sufficiently large, the synaptic potential initiates an action potential in the cell. If the target cell is a neuron, the action potential sweeps along its fibre. If it is a muscle, it also propagates over the surface of the muscle cell and causes it to contract.
Not all synaptic transmission is excitatory. Inhibitory transmitters also exist which render the post-synaptic cell less excitable and thus less likely to generate an action potential. They often act on receptors that act as channels for chloride ions, and generally make the interior of the postsynaptic cell even more negative (hyperpolarization). Acetylcholine is the excitatory transmitter at nerve–muscle synapses, and glutamate is the main excitatory transmitter in the central nervous system. Examples of inhibitory neurotransmitters include glycine and gamma aminobutyric acid (GABA).
The action of ‘fast’ neurotransmitters is brief, because they unbind quickly from their receptors and are then rapidly cleared from the synaptic cleft, usually by breakdown into inactive substances or reuptake into the cell. Because the receptor channels remain open only as long as neurotransmitter is bound, and because binding is only transient, the synaptic potential is also brief and the membrane potential returns rapidly to its resting level. Many other transmitters, sometimes called modulators (including serotonin, dopamine, noradrenaline, and many small peptide molecules), act more slowly and for much longer periods of time. In general, their receptors do not act as channels but instead activate messenger molecules inside the cell, which can initiate a variety of responses, even including the switching-on of genes in the chromosomes. It used to be thought that each nerve fibre releases only one neurotransmitter (‘Dale's principle’, after the British pharmacologist, Henry Dale), but it is now known that two or more transmitters and/or modulators can be produced by individual nerve terminals.
Each skeletal muscle fibre is innervated by a single excitatory nerve fibre, which discharges 100–300 vesicles for each arriving nerve impulse (enough to produce an action potential in the muscle cell). In contrast, a single nerve cell may have tens, or hundreds, of thousands of synapses. These are not only inhibitory as well as excitatory, but may involve many different type of transmitters and post-synaptic receptors (it is thought there may be more than 100 different neurotransmitters). Each pre-synaptic input may release just a few vesicles in response to a nerve impulse, so that the synaptic potential may be far smaller than that of a muscle fibre and many simultaneous or closely-successive inputs are needed to elicit one action potential. The output of the post-synaptic neuron will therefore be an integrated response to all of its many different inputs.
Most drugs that work on the brain, as well as drugs of abuse, act on synapses. One of the best known is nicotine, which activates acetylcholine receptors (its effect is mediated primarily at neuronal synapses in the brain). Curare, traditionally used by South American Indians as an arrow poison, paralysed the prey because it is an antagonist of the acetylcholine receptor and therefore blocks neuromuscular transmission. Morphine and heroin act on opiate receptors, and cannabis (unsurprisingly) on cannabinoid receptors. Cocaine works differently. It blocks the uptake system that clears the neurotransmitter dopamine from the synaptic cleft: consequently, dopamine hangs around for longer, which explains why cocaine acts as a stimulant. Some nerve gas poisons work in a similar fashion, by blocking the removal of the transmitter acetylcholine at nerve–muscle synapses.
A range of human diseases result from disorders of synaptic function. For instance, the inherited neuromuscular disorder, myasthenia gravis, occurs when the body produces antibodies to the acetylcholine receptors on muscle fibres. This causes them to be taken in by the cell, and the reduced number at the cell surface means that neurotransmission is compromised. Consequently, the patient is easily fatigued. Other myasthenias may result from a deficiency of the enzyme that breaks down acetylcholine, from presynaptic abnormalities that influence the amount of transmitter released, or from postsynaptic abnormalities associated with a reduction in the number or function of the acetylcholine receptors. Epilepsy is sometimes due to a decrease in the efficiency of inhibitory transmission in the brain, leading to over-excitability of networks of neurons. There is some evidence that the major psychiatric conditions, depression and schizophrenia, involve disorders of synapses in which serotonin and dopamine, respectively, act as neurotransmitters.
Frances M. Ashcroft
See also action potentials; motor neurons; nerves; nervous system; neuromuscular junction; neurotransmitters.
Nerve impulses are transmitted through a functional gap or intercellular space between neural cells (neurons) termed the synapse (also termed the synaptic gap). Although nerve impulses are conducted electrically within the neuron , in the synapse they are continued (propogated) via a special group of chemicals termed neurotransmitters.
The synapse is more properly described in structural terms as a synaptic cleft. The cleft is filled with extra cellular fluid and free neurotransmitters.
The neural synapse is bound by the presynaptic terminal end of one neuron, and the dendrite of the postsynaptic neuron. Neuromuscular synapses are created when neurons terminate on a muscle. Neuroglandular synapses occur when neurons terminate on a gland. The major types of neural synapses include axodendritic synapses, axosomatic synapses, and axoaxonic synapses—each corresponding to the termination point of the presynaptic neuron.
The arrival of an action potential (a moving wave of electrical changes resulting from rapid exchanges of ions across the neural cell membrane ) at the presynaptic terminus of a neuron, expels synaptic vesicles into the synaptic gap.
The four major neurotransmitters found in synaptic vesicles are noradrenaline, actylcholine, dopamine , and serotoin. Acetylchomine is derived from acetic acid and is found in both the central nervous system and the peripheral nervous system. Dopamine, epinephrine, and norepinephrine are catecholamines derived from tyrosine. Dopamine, epinephrine, and norepinephrine are also found in both the central nervous system and the peripheral nervous systems. Serotonin and histamine neurotransmitters are indolamines that primarily function in the central nervous system. Other amino acids, including gama-aminobutyric acid (GABA), aspartate, glutamate, and glycine along with neuropeptides containing bound amino acids also serve as neurotransmitters. Specialized neuropeptides include tachykinins and endorphins (including enkephalins) that function as natural painkillers.
Neurotransmitters diffuse across the synaptic gap and bind to neurotransmitter specific receptor sites on the dendrites of the postsynaptic neurons. When neurotransmitters bind to the dendrites of neurons across the synaptic gap they can, depending on the specific neurotransmitter, type of neuron, and timing of binding, excite or inhibit postsynaptic neurons.
After binding, the neurotransmitter may be degraded by enzymes or be released back into the synaptic cleft where in some cases it is subject to reuptake by a presynaptic neuron.
A number of neurons may contribute neurotransmitter molecules to a synaptic space. Neural transmission across the synapse is rarely a one-to-one direct diffusion across a synapse that separates individual presynapticpostsynaptic neurons. Many neurons can converge on a postsynaptic neuron and, accordingly, presynaptic neurons are often able to affect the many other postsynaptic neurons. In some cases, one neuron may be able to communicate with hundreds of thousands of postsynaptic neurons through the synaptic gap.
Excitatory neurotransmitters work by causing ion shifts across the postsynaptic neural cell membrane. If sufficient excitatory neurotransmitter binds to dendrite receptors and the postsynaptic neuron is not in a refractory period, the postsynaptic neuron reaches threshold potential and fires off an electrical action potential that sweeps down the post synaptic neuron.
A summation of chemical neurotransmitters released from several presynaptic neurons can also excite or inhibit a particular postsynaptic neuron. Because neurotransmitters remain bound to their receptors for a time, excitation or inhibition can also result from an increased rate of release of neurotransmitter from the presynaptic neuron or delayed reuptake of neurotransmitter by the presynaptic neuron.
Bridge junctions composed of tubular proteins capable of carrying the action potential are found in the early embryo. During development, the bridges degrade and the synapses become the traditional chemical synapse.
Cooper, Geoffrey M. The Cell—A Molecular Approach. 2nd ed. Sunderland, MA: Sinauer Associates, Inc., 2000.
Gilbert, Scott F. Developmental Biology. 6th ed. Sunderland, MA: Sinauer Associates, Inc., 2000.
Guyton, Arthur C., and John E. Hall. Textbook of MedicalPhysiology. 10th ed. Philadelphia: W.B. Saunders Co., 2000.
Kandel, E.R., J.H. Schwartz, and T.M. Jessell., eds. Principles of Neural Science. 4th ed. New York: Elsevier, 2000.
Lodish, H., et. al. Molecular Cell Biology. 4th ed. New York: W. H. Freeman & Co., 2000.
Thibodeau, Gary A., and Patton, Kevin T. Anatomy & Physiology. 5th ed. Mosby, 2002.
Cowan, W.M., D.H. Harter, and E.R. Kandel. "The Emergence of Modern Neuroscience: Some Implications for Neurology and Psychiatry." Annual Review of Neuroscience 23: 343–39.
Abbas L. "Synapse Formation: Let's Stick Together." CurrentBiology 8 13 (January 2003): R25–7.
K. Lee Lerner
Nerve impulses are transmitted through a functional gap or intercellular space between neural cells (neurons) termed the synapse (also termed the synaptic gap). Although nerve impulses are conducted electrically within the neuron, in the synapse they are continued (propogated) via a special group of chemicals termed neurotransmitters.
The synapse is more properly described in structural terms as a gap that is filled with extra cellular fluid and free neurotransmitters. The neural synapse is bound by a terminal end of one neuron and the dendrite of an adjacent neuron.
There are different kinds of synapses, depending on the location of the particular neuron. Neuromuscular synapses are created when neurons terminate on a muscle. Neuroglandular synapses occur when neurons terminate on a gland. The major types of neural synapses include axodendritic synapses, axosomatic synapses, and axoaxonic synapses—each corresponding to the termination point of the presynaptic neuron.
The arrival of an action potential (a moving wave of electrical changes resulting from rapid exchanges of ions across the neural cell membrane) at the end of a neuron expels vesicles (spheres created by the rounding up of a membrane) into the synapse.
The vesicles contain neurotransmitters, which are ferried to the adjacent neuron. Four major neurotransmitters found in synaptic vesicles are noradrenaline, actylcholine, dopamine, and serotoin. Acetylchomine is derived from acetic acid and is found in both the central nervous system and the peripheral nervous system. Dopamine, epinephrine, and norepinephrine, which are catecholamines derived from tyrosine, are also found in both the central nervous system and the peripheral nervous systems. Serotonin and histamine neurotransmitters primarily function in the central nervous system. Other amino acids, including gama-aminobutyric acid (GABA), aspartate, glutamate, and glycine along with neuropeptides containing bound amino acids also serve as neurotransmitters. Specialized neuropeptides include tachykinins and endorphins (including enkephalins) that function as natural painkillers.
Neurotransmitters diffuse across the synaptic gap and bind to neurotransmitter specific receptor sites on the dendrites of the adjacent neuron. This binding can, depending on the specific neurotransmitter, type of neuron, and timing of binding, excite or inhibit the neuron.
After binding, the neurotransmitter may be degraded by enzymes or be released back into the synapse where it can be available for another impulse transmission.
A number of neurons may contribute neurotransmitter molecules to a synaptic space. Neural transmission across the synapse is rarely a one-to-one direct diffusion across a synapse that separates individual presynaptic-postsynaptic neurons. Many neurons can converge on a postsynaptic neuron and, accordingly, presynaptic neurons are often able to affect the many other postsynaptic neurons. In some cases, one neuron may be able to communicate with hundreds of thousands of postsynaptic neurons through the synaptic gap.
Excitatory neurotransmitters work by causing ion shifts across the postsynaptic neural cell membrane. If sufficient excitatory neurotransmitter binds to the dendrities of a neuron, the neuron can fire off an electrical action potential that sweeps down the neuron. At the next neuron, the process is repeated, and so on, which transmits the impulse to its ultimate destination.
Drislane, Frank, Michael Benator, Bernard Chang, Juan Acosta, and John Croom. Blueprints Neurology. New York: Lippincott Williams & Wilkins, 2006.
Rapport, Richard. Nerve Endings :The Discovery of the Synpase. New York: W.W. Norton & Company, 2005.
Ropper, Allan H., and Robert H. Brown. Adams and Victor’s Principles of Neurology. 8th ed. New York: McGraw-Hill Professional, 2005.
K. Lee Lerner
The tiny gap through which communication between two neurons takes place.
Every thought, movement, and sensation occurs due to communication between different neurons, which provide information throughout the nervous system . Within a single neuron , information proceeds through electrical signals, but when information must be transmitted from one neuron to a succeeding neuron, the transmission is chemical.
For two neurons to communicate, chemical messengers, or neurotransmitters, are released into the synaptic cleft (a tiny gap about one thousandth of a millimeter between neurons), at which point they migrate to the next neuron and attach themselves to locations called receptor sites. The result is an initiation of electrical current that moves through that neuron toward the next one. After the neurotransmitter exerts its effect, it is either destroyed by other chemicals in the synaptic cleft or is reabsorbed into the original neuron. This action prevents the neurons from becoming overstimulated.
When neurons communicate, the effect can be either stimulation or inhibition of the next neuron. For example, when a person pays attention to one conversation and ignore others, the neurons in the brain are actively seeking out that information (stimulation) and actively ignoring the rest (inhibition). Neurons come in different shapes and sizes, affecting many other neurons, and can have different numbers of synapses. Some neurons, called Purkinje cells, may have as many as 100,000 synapses.
Synapse ★★ 1995 (R)
Black-marketeer Andre (Makepeace) is doublecrossed by a partner and arrested by Life Corp., which runs this futuristic civilization. As an experimental punishment, his mind is implanted into the body of Celeste (Duffy), who manages to escape and join up with a band of revolutionaries determined to destroy the evil corporation. Fast-paced story and good special effects. 89m/C VHS, DVD . Karen Duffy, Saul Rubinek, Matt McCoy, Chris Makepeace; D: Allan Goldstein.