SEARCH · PubMed Health

Results for “Veratridine”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1977

Effects of neurotoxins (veratridine, sea anemone toxin, tetrodotoxin) on transmitter accumulation and release by nerve terminals in vitro.

Two of the tree toxic compounds used in this work, veratridine and the sea anemone toxin, provoke neurotransmitter release from synaptosomes; the third one, tetrodotoxin, prevents the action of both veratridine and the sea anemone toxin. The half-maximum effects of veratridine and sea anemone toxin actions on synaptosomes are K0.5 = 10 and 0.02 micronM, respectively. Although veratridine and the sea anemone toxin similarly provoke neurotransmitter release, they act on different receptor structures in the membrane. Tetrodotoxin antagonizes the effects of both veratridine and the sea anemone toxin. The half-maximum inhibitory concentration of tetrodotoxin is K0.5 = 4 nM for veratridine and 7.9 nM for ATXII. It is very similar to the dissociation constant measured from direct binding experiments with the radioactive toxin. The analysis of this antagonistic action offers an easy in vitro assay for tetrodotoxin interaction with its receptor.

Animals↗

PubMed1979

Differential effects of veratridine and potassium depolarization on neuronal and glial GABA release.

The effect of veratridine and potassium depolarization on the release of [3H]GABA from neural tissues in which GABA uptake is neuronal (cerebrocortical slices and frog retina) or glial (rat retina, spinal and sympathetic ganglia) was studied. The 'neuronal' but not the 'glial' release of [3H]GABA was greatly increased by KC1 (25 mM) and veratridine (10 microM). The 'neuronal' release of [3H]GABA evoked with KC1 was calcium dependent but the small potassium induced increase in 'glial' release were not reduced in the absence of calcium ions even when additional Mg2+ was included in the medium. Surprisingly, the veratridine induced release of [3H]GABA from cortical slices was greatly potentiated in calcium free medium although the release of [3H]noradrenaline produced by veratridine was calcium dependent. Because of the insensitivity of the glial GABA release mechanism to potassium depolarization, it is concluded that release of endogenous GABA from glial pools in response to physiological increases in extracellular potassium is unlikely to be important.

Animals↗

PubMed1975

Effects of potassium, veratridine, and scorpion venom on calcium accumulation and transmitter release by nerve terminals in vitro.

1. 45-Ca uptake by pinched-off nerve terminals (synaptosomes) of rat brain incubated in standard physiological saline (including 132 mM-Na + 5mM-K + 1-2 mM-Ca) at 30 degrees C averages about 0-5 mumole Ca per g protein per minute. This may be equivalent to a Ca influx of about 0-03 p-mole/cm-2 sec. 2. The rate of 45-Ca uptake is increased when the concentration of K in the medium is increased above 15-20 mM, K replacing Na isosmotically. Maximum stimulation, a three- to six-fold increase in the rate of Ca uptake, occurs when [K]o is about 60 mM. The effect of increased [K]o is reversible. 3. The K-stimulated Ca uptake is associated primarily with the nerve terminal fraction of brain homogenates. The entering Ca is not accompanied by extracellular markers such as mannitol or inulin. Replacement of external chloride by methylsulphate or sulphate does not prevent the stimulation by K. 4. The effects of external K are quantitatively mimicked by Rb. Caesium also stimulates Ca uptake, but is only about one fifth as effective as K or Rb; Li is ineffective. 5. Two other depolarizing agents also stimulate Ca uptake by synaptosomes: veratridine (7-5 times 10- minus 6 to 7-5 times 10- minus 5 M) and scorpion (Leirus quinquestriatus) venom (6-7 times 10- minus 7 to 6-7 times 10- minus g/ml.). The stimulatory effects of veratridine and scorpion venom, but not of increased [K] are blocked by 2 times 10- minus 7 M tetrodotoxin. 6. Internal K also influences the rate of 45-Ca uptake by synaptosomes: lowering [K]i reduces the stimulatory effect of external K and veratridine. 7. Replacement of external Na by choline markedly inhibits the response to veratridine, but has a much smaller effect on the response to increased [K]o. 8. The Ca uptake mechanism has an apparent dissociation constant for Ca (KCa) of about 0-8 mM. Increasing [K]o increases the maximal rate of Ca uptake, but has no effect on KCa. The K-induced 45-Ca uptake is competitively inhibited by Mg-2+, Mn-2+ and La-3+. 9. The release of acetylcholine and noradrenaline was also studied. Increasing [K]o stimulates external Ca-dependent acetylcholine release. Scorpion venom stimulates noradrenaline release from synaptosomes; this effect could be prevented by adding tetrodotoxin or removing external Ca. 10. These results indicate that synaptosomes may increase their permeability to Ca, accumulate Ca and release neural transmitter substances, when stimulated by depolarizing agents under appropriate physiological conditions.

Acetylcholine↗

PubMed1979

Release of catecholamines from perfused cat adrenal gland by veratridine.

Experiments were undertaken to verify the existence of fast sodium channels in the adrenal chromaffin cell membrane and to assess their contribution to the physiological release of catecholamines. We have used veratridine to activate sodium channels. Veratridine causes secretion of catecholamines from perfused cat adrenal gland. Secretory response to veratridine is calcium dependent and abolished by tetrodotoxin. Secretion of catecholamines by acetylcholine is only partially blocked by tetrodotoxin. It is concluded that the adrenal chromaffin cell membrane contains fast sodium channels directly comparable to those of impulse-propagating neurons, but they do not appear to be essential in the secretory response to acetylcholine or splanchnic nerve stimulation.

Acetylcholine↗

PubMed1979

High potassium, veratridine and electrically induced release of taurine from the cerebellar cortex.

In the in vivo superfused cerebellar cortex of anaesthetized rats, the following stimuli were effective in evoking large increases of isotopically labelled taurine from preloaded tissue: high (40 mM) K+; rectangular, 0.1 msec electrical pulses at 1.5 mA and 500 Hz; the depolarizing veratrum alkaloid, veratridine (0.5 x 10(-5) M) and scorpion venom (10(-6) g.ml-1). Both the high K+ and electrically evoked effluxes were markedly Ca2+ dependent; the veratridine response was abolished in the presence of tetrodotoxin (10(-6) g.ml-1). The data indicate that taurine is being released from excitable cells rather than neuroglia and may therefore have some neurotransmitter-like role in the cerebellum.

Animals↗

PubMed1979