Nerve, action potential

Lowenstein (27) found an approximate correlation between the nerve action potential produced by 1.6% pyrethrins applied externally and 0.3% pyrethrins applied directly to the nerve cord. 

All transmitters (except NO) are released by the following cascade arrival of the nerve action potential at the terminal - opening of voltage-sensitive Ca2+... 

Action potentials, self-propagating. Action potentials of smooth muscle differ from the typical nerve action potential in at least three ways. First, the depolarization phases of nearly all smooth muscle action potentials are due to an increase in calcium rather than sodium conductance. Consequently, the rates of rise of smooth action potentials are slow, and the durations are long relative to most neural action potentials. Second, smooth muscle action potentials arise from membrane that is autonomously active and tonically modulated by autonomic neurotransmitters. Therefore, conduction velocities and action potential shapes are labile. Finally, smooth muscle action potentials spread along bundles of myocytes which are interconnected in three dimensions. Therefore the actual spatial patterns of spreading of the action potential vary. 

Veratridine is a complex lipophilic alkaloid that also binds to sodium channels, causing them to stay open and thereby disrupting the transmission of nerve action potential. It is found in the seeds of a member of the Liliaceae, Schoenocaulon... 

Pyrethroids, such as p,p -DDT, are toxic because they interact with Na+ channels of the axonal membrane, thereby disturbing the transmission of nerve action potential (Eldefrawi and Eldefrawi 1990, and Chapter 5, Section 5.2.4 of this book). In both cases, marked hydrophobicity leads to bioconcentration of the insecticides in the axonal membrane and reversible association with the Na+ channel. Consequently, both DDT and pyrethroids show negative temperature coefficients in arthropods increasing temperature brings decreasing toxicity because it favors desorption of insecticide from the site of action. 

The effects of neurotoxic chemicals upon nerve action potential have been measured both in vertebrates and insects. Of particular interest has been the comparison... 

The effects of DDT on nerve action potential are illustrated in Figure 16.1. In nerves poisoned by the insecticide, there is a prolongation of the sodium current and a consequent delay in returning to the resting potential. This can result in the... 

There is ample precedent for a modulatory role of K channels in behavior. The K channel blocker, 4-AP, selectively blocks component T (Bartschat and Blaustein 1985a). prolongs nerve action potentials, and enhances neurotransmitter release (Llinas et al. 1975). In man, intoxication with this agent may lead to dissociative behavior, agitation, confusion, convulsions, and coma (Spyker et al. 1980). However, the behavioral aberrations induced by 4-AP differ qualitatively from those induced by PCP. This implies that block of various types of presynaptic K channels may modify behavior and mental activity however, the precise nature of the behavioral manifestations is likely to depend upon the specific type of K channel that is affected. 

A decrease in the amplitude of the sensory nerve action potential has also been observed in a group of 20 asymptomatic workers exposed to -hexanc (Pastore et al. 1994). The subjects of this study were selected on the basis of urinary levels of the n-hexane metabolite 2,5-hexanedione (See Sections 2.3 and 2.7) exceeding 5 mg/L and compared to a group of unexposed laboratory workers. Mean years worked was 8.13 (range, 1.5—23 years). Sensory and motor nerve conduction velocities and distal latencies were normal in all nerves tested. However, significant decreases were found in sensory nerve action potential amplitude in the median, sural, and ulnar nerves. Neither the level of 2,5-hexanedione in urine nor age correlated with the changes in amplitude however, there was a significant correlation between years worked and amplitude. 

Neuromuscular transmission involves the events leading from the liberation of acetylcholine (ACh) at the motor nerve terminal to the generation of end plate currents (EPCs) at the postjunctional site. Release of ACh is initiated by membrane depolarization and influx of Ca++ at the nerve terminal (Fig. 28.1). This leads to a complex process involving docking and fusion of synaptic vesicles with active sites at the presynaptic membrane. Because ACh is released by exocytosis, functional transmitter release takes place in a quantal fashion. Each quantum corresponds to the contents of one synaptic vesicle (about 10,000 ACh molecules), and about 200 quanta are released with each nerve action potential. 

The aminopyridines (4-aminopyridine 3,4-diaminopyri-dine) accelerate spontaneous exocytosis at central and peripheral synapses. There is also an increase in the number of transmitter quanta released by a nerve action potential. This is probably the result of increased Ca++ inflow at the terminals due to a reduction of K+ conductance and prolongation of the nerve action potential. Muscle strength is increased in patients with the Lambert-Eaton myasthenic syndrome and in others poisoned with botuUnum E toxin (discussed later). Improvement in uncontrolled spasms, muscle tone, and pulmonary function is noted in patients with multiple sclerosis or long-standing spinal cord damage. Side effects that limit clinical utility include convulsions, restlessness, insomnia, and elevated blood pressure. Of the two agents, 3,4-diaminopyridine is the more potent and crosses the blood-brain barrier less readily. 

Guanidine hydrochloride is the drug of choice in the management of patients with myasthenic syndrome and may be of use in the treatment ofbotulinum intoxication. Its ability to enhance transmitter release may involve a block of K+ channels and prolongation of the nerve action potential. 

What hypnosis now needs to advance as a science is the application of the scientific principles and techniques that other Huxleys developed, from Thomas Henry Huxley (1825-1895), who championed the theory of evolution as Darwin s Bulldog, to Andrew Fielding Huxley (1917- ), who advanced the ionic hypothesis of the nerve action potential and won... 

At the neuromuscular junction, the electrical changes following the action of the neurotransmitter substance acetylcholine on the muscle cell were investigated by Katz and Fatt in 1951. It was reasonable to suppose that the ionic currents passed through channels that were activated by acetylcholine. Both here and with the nerve action potential only the currents produced by flow through some hundreds or thousands of channels at once could be measured. 

The 1952 Hodgkin-Huxley model for membrane electrical potential is perhaps the oldest and the best known cellular kinetic model that exhibits temporal oscillations. The phenomenon of the nerve action potential, also known as excitability, has grown into a large interdisciplinary area between biophysics and neurophysiology, with quite sophisticated mathematical modeling. See [103] for a recent treatise. 

Deterioration of the sensory nerve action potentials more than 40% from baseline may predict the development of neuropathy (51). 

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