Depolarization, of nerves

Rapid-acting paralytic neurotoxins that blocks transient sodium channels and inhibits depolarization of nerve cells. They are some of the causative agents of paralytic shellfish poisoning (PSP). They are obtained from dinoflagellates (Gonyaulax spp., Alexandrium spp.) and cyanobacteria (Anabaena circinalis). 

Histamine is stored within and released from neurons but a neuronal transporter for histamine has not been found. Newly synthesized neuronal histamine is transported into TM neuronal vesicles by the vesicular monoamine transporter VMAT2 [16]. Both in vivo and in vitro studies show that depolarization of nerve terminals activates the exocytotic release of histamine by a voltage- and calcium-dependent mechanism. Once released, histamine activates both postsynaptic and presynaptic receptors. Unlike the nerve terminals from other amine transmitters, however, histaminergic nerve terminals do not exhibit a high-affinity uptake system for histamine [5, 9, 23]. Astrocytes may contain a histamine transport system. 

Physiological studies show that monensin is a sodium ionophore (15), that induces inotropic effect on guinea pig atria (17). The polyether toxins including ciguatoxin, okadaic acid, and the recently characterized brevetoxin (5, 16) also induce inotropic effect on guinea pig atrial tissue in vitro (17). Additionally, partially purified CTX has been implicated in the depolarization of nerve cells in vitro, which can be reversed by high concentrations of Ca tetrodotoxin and saxitoxin (18). 

Physiological studies have identified both post- and presynaptic roles for ionotropic kainate receptors. Kainate receptors contribute to excitatory post-synaptic currents in many regions of the CNS including hippocampus, cortex, spinal cord and retina. In some cases, postsynaptic kainate receptors are codistributed with AMPA and NMDA receptors, but there are also synapses where transmission is mediated exclusively by postsynaptic kainate receptors for example, in the retina at connections made by cones onto off bipolar cells. Extrasynaptically located postsynaptic kainate receptors are most likely activated by spill-over glutamate (Eder et al. 2003). Modulation of transmitter release by presynaptic kainate receptors can occur at both excitatory and inhibitory synapses. The depolarization of nerve terminals by current flow through ionotropic kainate receptors appears sufficient to account for most examples of presynaptic regulation however, a number of studies have provided evidence for metabotropic effects on transmitter release that can be initiated by activation of kainate receptors. The hyperexcitability evoked by locally applied kainate, which is quite effectively reduced by endocannabinoids, is probably mediated preferentially via an activation of postsynaptic kainate receptors (Marsicano et al. 2003). 

Sodium With potassium and chloride, helps maintain electrochemical and water balance across cell membrane initiates depolarization of nerve and muscle tissues Men women 1.5 g/d... 

In some types of rhythm disorders, antiar-rhythmics of the local anesthetic, Na+-channel blocking type are used for both prophylaxis and therapy. These substances block the Na+ channel responsible for the fast depolarization of nerve and muscle tissues. Therefore, the elicitation of action potentials is impeded and impulse conduction is delayed. This effect may exert a favorable influence in some forms of arrhythmia, but can itself act arrhythmogenically. Unfortunately, antiarrhythmics of the local anesthetic, Na+-channel blocking type lack suf -cient specificity in two respects (1) other ion channels of cardiomyocytes, such as K1 and Ca+ channels, are also affected (abnormal QT prolongation) and (2) their action is not restricted to cardiac muscle tissue but also impacts on neural tissues and brain cells. Adverse effects on the heart include production of arrhythmias and lowering of heart rate, AV conduction, and systolic force. CNS side effects are manifested by vertigo, giddiness, disorientation, confusion, motor disturbances, etc. 

Pyrethroids can be classified as type I or type II depending on their effects on sensory neurons in American cockroaches. Type I compounds induce repetitive discharges in sensory neurons in vitro but not neurotransmitter release, so these processes are not related to the toxic action of pyrethroids. In contrast, type II pyrethroids, which typically contain the cyano group, do not induce repetitive discharges. Type II pyrethroids cause slow depolarization of nerve membrane, which reduces the amplitude of the action potential, leading to a loss of electrical excitability (Bloomquist, 1999). In addition, type I pyrethroids exhibit a negative temperature coefficient of toxicity, i.e., they are more toxic at low temperatures than at high temperatures, whereas type II pyrethroids exhibit a positive temperature coefficient of toxicity (Corbett et al., 1984 Matsumura, 1985). 

Palytoxin CAS 11077-03-5 respiratory distress, diarrhea, convulsions, shock, low body temperature, and death. causes irreversible depolarization of nerve and muscle tissue. It has a very potent effect on the coronary artery and may also cause delayed effects including disintegration of red blood cells. corals. Palytoxin is soluble in water and alcohol. It is stable to heat, and both low and high pH. 

Like other nenrotransmitters, newly synthesized neuronal histamine is stored within the nerve terminal vesicle. Depolarization of nerve terminals activates the exocytotic release of histamine by voltage-dependent as well as a calcium-dependent mechanism. 

D. Neurotoxic shellfish poisoning is caused by ingestion of brevetoxins, which are produced by red tide dinoflagellates. The mechanism appears to involve stimulation of sodium channels, resulting in depolarization of nerve fibers. 

The rather strong heterocyclic base, 4-aminopyridine 7.47) similarly blocks potassium channels thereby enhancing the influx of calcium ions during the depolarization of nerve terminals (Thesleff, 1980). Substances that can block calcium channels in muscle (e.g. verapamil, nifedipine) were introduced during the last decade as vasodilatory drugs (see Section 14.2). 

Release. The effect of experimental stimulus which simulate physiological depolarization of nerve terminals on the release of taurine has been extensively examined. In pioneer experiments, Jasper and Koyama demonstrated a taurine release from the exposed cat cerebral cortex in vivo, after electrical stimulation of the midbrain reticular formation. An increase in the resting release of endogenous taurine from the rat visual cortex in vivo was demonstrated under electrical stimulation or by topical application of depolarizing KCl concentrations, 13, in vitro, an increase in the efflux of labeled taurine, recently taken up by the tissue, has been reported to occur in rat cerebral cortex37,38. However, in a... 

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