Nerve signals

The influx of Ca(Il) across the presynaptic membrane is essential for nerve signal transmission involving excitation by acetylcholine (26). Calcium is important in transducing regulatory signals across many membranes and is an important secondary messenger hormone. The increase in intracellular Ca(Il) levels can result from either active transport of Ca(Il) across the membrane via an import channel or by release of Ca(Il) from reticulum stores within the cell. More than 30 different proteins have been linked to regulation by the calcium complex with calmoduhn (27,28). 

Selectivity of ion channels for metal ions is of great current interest (66), as it relates to conduction of nerve signals, maintenance of the appropriate metal ion distribution in the intracellular and extracellular... 

Transection or severing of the axon disrupts nerve signals completely and irreversibly.8 There is growing evidence that cytotoxic (CD8+) T cells cause axonal injury.5 Axonal transection begins as early as 2 weeks after diagnosis and continues throughout the course of the disease.9... 

Nerve agents, which interfere with nerve signaling such as Sarin (GB), Soman (GD), Tabun (GA), or methylphosphonothioic acid, S-[2-diethylamino)ethyl]0-2-methylpropyl ester (VX). 

Nerve signals from the thalamus and the reticular formation are transmitted to the limbic system as well as the hypothalamus. Together, these regions of the brain are responsible for behavioral and emotional responses to pain. The limbic system, in particular, may be involved with the mood-altering and attention-narrowing effect of pain. 

In any signalling process, it is essential that the signal travels only in one direction (e.g. action potential in a nerve, signalling in hormone action). To do this, non-equilibrium reactions must be included in the sequence. 

Blocks transmission of nerve signals by interactions with glutamate-gated chloride channels Depolarization and spastic paralysis... 

Other types of insecticides have been developed and used over the past several decades. To discuss them all requires an entire course. There is an ASIDE which illustrates the halogenated hydrocarbons most of which are not in current use because of their effects on the environment (DDT) and toxicity to humans (Dieldrin/Aldrin). Estrogenic acivity of DDT led to fatal fragility in the eggs of certain predatory birds. All of these compounds are lipophilic and interfere with nerve signal transmission. 

There is a space that exists between neurons known as the synapse. The transmission of the nerve signal across this synaptic cleft is a chemical phenomenon. Molecules generically referred to as neurotransmitters are produced in the neuron and released from the axonal membrane into the synapse. They diffuse to the dendrites of the next nerve cell and combine with receptors. This combination of neurotransmitter (agonist) and receptor produces a response which results in the propagation of the nerve signal down the next neuron. We will discuss this activity in much more detail shortly. 

The white matter is a covering for the nerve fiber known as the myelin sheath. Myelin is a sphingolipid produced by oligodendrocytes (Schwann cells). It acts as a special type of insulation which allows for a much more rapid transmission of the nerve signal. The myelin cover is interrupted periodically. This "bare" area is called a node of Ranvier. It is very important to rapid nerve conduction. See Figure 21. 

The next event in the generation of a nerve signal involves the opening of sodium channels within the membrane. What will happen considering the imbalance of sodium ions Of course, they will rush into the cell The sodium channel opening is following after a brief interval by the opening of... 

Atropine is an antagonist for the naturally occurring neurotransmitter (nerve signal carrier) acetylcholine. Its structural similarity to acetylcholine makes it very specific for acetylcholine receptors. How about its effects ... 

Thalamus—A region in the brain that serves as a relay station for nerve signals from the brain stem to the cortex. 

The chemical connection between brain cells is by means of neurotransmitters—chemicals such as dopamine that convey nerve signals. In normal brain connections a neuron fires (discharges electrical potential). This in turn releases a small quantity of the neurotransmitter, which attaches itself to a receptor molecule in an adjacent neuron, causing it to fire in turn. Eventually the dopamine is returned to the cells until the ne.xt signal comes along. 

The enzymatic catalysis of reactions is essential to living systems. Under biologically relevant conditions, uncatalyzed reactions tend to be slow—most biological molecules are quite stable in the neutral-pH, mild-temperature, aqueous environment inside cells. Furthermore, many common reactions in biochemistry entail chemical events that are unfavorable or unlikely in the cellular environment, such as the transient formation of unstable charged intermediates or the collision of two or more molecules in the precise orientation required for reaction. Reactions required to digest food, send nerve signals, or contract a muscle simply do not occur at a useful rate without catalysis. 

Because molecules slow down with decreasing temperature, the rate at which neurotransmitters are able to diffuse across the synaptic cleft decreases with temperature. This is one of the reasons cold-blooded animals become sluggish at colder temperatures. As neurotransmitters take longer to diffuse across the synaptic cleft, the rate at which nerve signals can reach target muscles slows down. 

In most instances the arrival of a nerve signal at the presynaptic end of a neuron causes the release of a transmitter substance (neurohormone). Tire transmitter passes across the 10-50 nm (typically 20 nm) synaptic cleft between the two cells and induces a change in the electrical potential of the postsynaptic membrane of the next neuron (Fig. 30-10).149 401 Excitatory transmitters usually cause depolarization of the membrane. By this we mean that the membrane potential, which in a resting neuron is -50 to -70 mv (Chapter 8), falls to nearly zero often as a consequence of an increased permeability to Na+ and a resultant inflow of sodium ions. The resulting postsynaptic... 

Consider a message originating with a nerve receptor in the skin or in another sense organ. A nerve signal passes via a sensory neuron (afferent fiber)... 

Methadone and opiates were first used for pain relief, and are still chiefly used in that area of medicine. It is important to remember that methadone and other opiates do not exert their pain control by altering a person s sensitivity to pain. Rather, methadone and other opiates interfere with the transmission of pain impulses from the nervous system to the brain. They accomplish this by a variety of methods. First, they decrease the transmission of nerve signals that conduct pain messages from various parts of the body to the spine. Secondly, they prevent production of neurochemicals that transfer this pain information to the spine. Finally, they mimic the actions of endorphins, which are the body s own pain-controlling chemicals. While methadone and other opiates work quite well to control pain, they do not affect touch, vision, or hearing. 

Methaqualone affects muscle movement and proper functioning of nerve sensation. Users experience paresthesia, which is a numb tingling, or pins and needles sensation, most commonly in the fingers and face. Individuals who take heavy doses of methaqualone also have a heightened pain threshold. The coordination of brain and body becomes disconnected, and nerve signals are slowed or stopped on their way to the brain s command center. While under the influence of methaqualone, users may hurt themselves without realizing it. 

Alkali metal transport in biochemistry is a vital process in maintenance of cell membrane potentials of use, for example, in nerve signal transduction and is at the core of some of the early work on artificial ionophores that mimic natural ion carriers such as valinomycin. Ionophore mediated ion transport is much slower than transport through cation and anion ion channel proteins, however. 

There are no quantitative data on the number of L chains required to intoxicate a nerve terminal. In Aplyisa califomica cholinergic neurons, few molecules of toxin appear to be sufficient to block neuroexocytosis within an hour at room temperature (Poulain, personal communication). It is even more likely that few copies of L chain are sufficient in warm-blooded animals. It is evident that as long as the toxin is present in an active form, the nerve signal cannot be transmitted. 

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