Synapse chemical changes

To be useful for more than a few minutes stored information must be transferred from the temporary to more permanent forms. We know that even temporary memory depends upon chemical changes in synapses. Long-term memory involves both stable chemical changes and also changes in the physical connections between neurons. Before discussing these... 

FIGURE 17.3 Transmission of a nerve impulse. The neurotransmitter is stored in the vesicles until it is needed. When a nerve impulse arrives, the vesicles move to the cell membrane and join with it so that the neurotransmitter is released. By crossing the synapse and binding to receptors on the surface of the adjacent nerve cell, the neurotransmitter transmits the impulse. The receptors in turn initiate chemical changes that allow the impulse to proceed. 

Figure 5.1 Mechanism of action at a chemical synapse. The arrival of an action potential at the axon terminal causes voltage-gated Ca++ channels to open. The resulting increase in concentration of Ca++ ions in the intracellular fluid facilitates exocytosis of the neurotransmitter into the synaptic cleft. Binding of the neurotransmitter to its specific receptor on the postsynaptic neuron alters the permeability of the membrane to one or more ions, thus causing a change in the membrane potential and generation of a graded potential in this neuron.

It is a measure of the changed outlook among neurophysiologists that it has been thought appropriate to include. ..[here]. .. a discussion on the nature of synaptic transmitter substances other than acetylcholine. A few years ago, the whole hypothesis of the chemical mediation of impulse transmission across central synapses was meeting so much opposition that the energies of those who supported it had to be concentrated on the claims of acetylcholine. ... 

The response of the brain to both acute and chronic stress can be discussed in terms of its capacity to demonstrate its dynamic plasticity. The term plasticity describes almost any change in the brain, from the chemical level to the formation of new neurons and synapses. Prolonged or chronic stress has specific effects on the structure and function of the synapses in different brain regions. The neurons in different regions may show signs of atrophy, cell death, as a result of chronic psychosocial stress, as well as after... 

Urine catecholamines may also serve as biomarkers of disulfoton exposure. No human data are available to support this, but limited animal data provide some evidence of this. Disulfoton exposure caused a 173% and 313% increase in urinary noradrenaline and adrenaline levels in female rats, respectively, within 72 hours of exposure (Brzezinski 1969). The major metabolite of catecholamine metabolism, HMMA, was also detected in the urine from rats given acute doses of disulfoton (Wysocka-Paruszewska 1971). Because organophosphates other than disulfoton can cause an accumulation of acetylcholine at nerve synapses, these chemical compounds may also cause a release of catecholamines from the adrenals and the nervous system. In addition, increased blood and urine catecholamines can be associated with overstimulation of the adrenal medulla and/or the sympathetic neurons by excitement/stress or sympathomimetic drugs, and other chemical compounds such as reserpine, carbon tetrachloride, carbon disulfide, DDT, and monoamine oxidase inhibitors (MAO) inhibitors (Brzezinski 1969). For these reasons, a change in catecholamine levels is not a specific indicator of disulfoton exposure. 

A further intercellular communication mechanism relies on electrical processes. The conduction of electrical impulses by nerve cells is based on changes in the membrane potential. The nerve cell uses these changes to communicate with other cells at specialized nerve endings, the synapses (see chapter 16). It is central to this type of intercellular commimication that electrical signals can be transformed into chemical signals (and vice versa, see chapter 16). 

Once an electrical impulse invades the presynaptic axon terminal, it causes the release of chemical neurotransmitter stored there (Fig. 1—3). Electrical impulses open ion channels, such as voltage-gated calcium channels and voltage-gated sodium channels, by changing the ionic charge across neuronal membranes. As calcium flows into the presynaptic nerve, it anchors the synaptic vesicles to the inner membrane of the nerve terminal so that they can spill their chemical contents into the synapse. The way is paved for chemical communication by previous synthesis and storage of neurotransmitter in the first neuron s presynaptic axon terminal. 

As described in Chapter 4, regulatory G proteins act as an intermediate link between receptor activation and the intracellular effector mechanism that ultimately causes a change in cellular activity. In the case of opioid receptors, these G proteins interact with three primary cellular effectors calcium channels, potassium channels, and the adenyl cyclase enzyme.27 At the presynaptic terminal, stimulation of opioid receptors activates G proteins that in turn inhibit the opening of calcium channels on the nerve membrane.65 Decreased calcium entry into the presynaptic terminal causes decreased neurotransmitter release because calcium influx mediates transmitter release at a chemical synapse. At the postsynaptic neuron, opioid receptors are linked via G proteins to potassium channels, and... 

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