Neurotransmission presynaptic nerve terminal

Alpha-2 (ttj) adrenergic receptors inhibit sympathetic neurotransmission by two mechanisms. Postsynaptic receptors inhibit sympathetic neurons that exit the brain. Alpha-2 receptors are also found on presynaptic nerve terminals where they inhibit norepinephrine release. 

Two types of illness are associated with the botulinum toxin, infant and adult botulism. An adult becomes iU by eating spoiled food that contains the toxin. Infants become ill from eating the spores of the botulinum bacterium. One source of these spores comes from the ingestion of honey. Spores are not normally toxic to adults. Botulinum toxins work by binding to the presynaptic nerve terminal at the neuromuscular junction and at cholinergic autononuc sites. They then act to stop the release of acetylchloline presynaptically, thus blocking neurotransmission. 

Abstract Neurotransmission in the nervous system is initiated at presynaptic terminals by fusion of synaptic vesicles with the plasma membrane and subsequent exocytic release of chemical transmitters. Currently, there are multiple methods to detect neurotransmitter release from nerve terminals, each with their own particular advantages and disadvantages. For instance, most commonly employed methods monitor actions of released chemical substances on postsynaptic receptors or artificial substrates such as carbon libers. These methods are closest to the physiological setting because they have a rapid time resolution and they measure the action of the endogenous neurotransmitters rather than the signals emitted by exogenous probes. However, postsynaptic receptors only indirectly report neurotransmitter release in a form modified by the properties of receptors themselves, which are often nonlinear detectors of released substances. Alternatively, released chemical substances... 

Synaptic neurotransmission in brain occurs mostly by exocytic release of vesicles filled with chemical substances (neurotransmitters) at presynaptic terminals. Thus, neurotransmitter release can be detected and studied by measuring efflux of neurotransmitters from synapses by biochemical methods. Various methods have been successfully employed to achieve that, including direct measurements of glutamate release by high-performance liquid chromatography of fluorescent derivatives or by enzyme-based continuous fluorescence assay, measurements of radioactive efflux from nerve terminals preloaded with radioactive neurotransmitters, or detection of neuropeptides by RIA or ELISA. Biochemical detection, however, lacks the sensitivity and temporal resolution afforded by electrophysiological and electrochemical approaches. As a result, it is not possible to measure individual synaptic events and apply quantal analysis to verify the vesicular nature of neurotransmitter release. 

Cholinesterases, e.g., acetylcholinesterase (AChE, EC 3.1.1.7) and butyrylcholi-nesterase (BChE, EC 3.1.1.8), are serine hydrolases that break down the neurotransmitter acetylcholine and other choline esters [5]. In the neurotransmission processes at the neuromuscular junction, the cationic neurotransmitter acetylcholine (ACh) is released from the presynaptic nerve, diffuses across the synapse and binds to the ACh receptor in the postsynaptic nerve (Fig. 1). Acetylcholinesterase is located between the synaptic nerves and functions as the terminator of impulse transmissions by hydrolysis of acetylcholine to acetic acid and choline as shown in Scheme 4. The process is very efficient, and the hydrolysis rate is close to diffusion controlled [6, 7]. 

Other drugs. Penicillamine causes some patients, especially those with rheumatoid arthritis, to form antibodies to the acetylcholine receptor and a syndrome indistinguishable from myasthenia gravis results. Spontaneous recovery occurs in about two-thirds of cases when penicillamine is withdrawn. Phenytoin may rarely induce or aggravate myasthenia gravis, or induce a myasthenic syndrome, possibly by depressing release of acetylcholine. Lithium may impair presynaptic neurotransmission by substituting for sodium ions in the nerve terminal. 

First, consider the processes involved in neurotransmission (Fig. 2.4A and 2.4B) 1) the neurotransmitter is synthesized from chemical precursors, 2) it is packaged into vesicles in the presynaptic terminal, 3) the presyn-aptic nerve is stimulated causing the synaptic vesicles to fuse with the synaptic membrane and release the... 

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