Synaptic deft

Neurotransmitten Any of a group of substances that are released on excitation from the axon terminal of a presynaptic neuron of the central or peripheral nervous system and travel across the synaptic deft to either excite or inhibit the target cell. Among the many substances that have the properties of a neurotransmitter are acetylcholine, norepinephrine, epinephrine, dopamine, glycine, y-aminobutyrate, glutamic add, substance P, enkephalins, endorphins, and serotonin. [EU]... 

Most but not all neuron connections rely on the passage of neurotransmitters across a synaptic deft. The neurons that connect to musdes controlling eye movement, however, are different in that they have what are called electrical synapses, which are direct connections between the neurons and the musdes (there s no gap). The high speeds of these direct connections provide for eye motion that is quick and jerky—a useful trait. Some fish have electrical synapses in their tails, an arrangement that provides for rapid escape from predators. 

In 1973, Solomon Snyder and Candace Pert proved the existence of opiate receptors in the brain. Snyder had been a postgraduate student of Nobel Prize wiimer Julius Axelrod, at the National Institute of Mental Health in Bethesda, MD. Axelrod s research was concerned with the chemical events that occurred in the synaptic deft that coimerts all neurons. 

Acetylcholinesterase (AChE) is responsible for acetylcholine degradation in the synaptic deft. Therefore, inhibitors of AChE are increasing cholinergic... 

Alterations in the release, inactivatioti, or i itake of neurotraitsmitters at the synaptic deft can impair transfer of information to postsynaptic neurons. 

FIGURE 5.5 A simple model of synaptic transmission. The pres)fnaptic neuronal membrane (green) releases the netirotransmitter (triangles) in the synaptic deft. The neurotransmitter travels through the synapse and eventually binds to a receptor (blue) expressed by the postsynaptic neuronal membrane. If the neurotransmifter is soluble in water, it will bind to a surface-accessible region of its receptor. The postsynaptic membrane is represented with a lipid bUayer (cholesterol in red, phospholipids in green). 

Amphetamines and cocaine work the same way in the body, but cocaine is much more vigorous at blocking the reuptake of dopamine. How cocaine works is illustrated in Figure 14.26. The great buildup of dopamine in synaptic clefts in the brains reward center is the source of cocaines euphoric effect. As cocaine keeps dopamine from being reabsorbed by the presynaptic neuron, the dopamine remains active in the synaptic cleft, and as a result the reward center stays stimulated. This euphoric state is only temporary, however, because enzymes in the deft metabolize, and hence deactivate, the dopamine. Once the cocaine is metabolized by enzymes, dopamine reuptake is again permitted. By this time, however, there is very little dopamine in the deft to be reabsorbed. Nor is there an adequate supply of dopamine in the presynaptic neuron, which is unable to make sufficient quantities of dopamine without the recycling process. The net result is a depletion of dopamine that causes severe depression. 

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