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Verrucotoxin inhibits KATP channels in cardiac myocytes through a muscarinic M3 receptor-PKC pathway.

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Verrucotoxin is the major component of venom from the stonefish (Synanceia verrucosa). Stings from the dorsal spines of the stonefish produce intensive pain, convulsions, hypotension, paralysis, respiratory weakness and collapse of the cardiovascular system, occasionally leading to death. It has

Neurotoxicity of a novel local anesthetic agent, ropivacaine: the possible roles of bursts of potential and cytoplasmic second messenger.

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OBJECTIVE Ropivacaine has been shown to induce convulsion following overdose or accidental intravenous injection, but the mechanisms are poorly understood. Using an identifiable central neuron from giant African snail, the authors studied the mechanism of ropivacaine-elicited bursts of potential and

The role of protein kinase A in acute ethanol-induced neurobehavioral actions in rats.

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BACKGROUND cAMP-dependent protein kinase (PKA) signaling pathways are involved in the regulation of ethanol-induced sedative effects in knockout mouse models. In the present study, we examined the role of PKA on the behavioral action caused by ethanol in Sprague Dawley rats. METHODS A loss of

Kinase-dependent loss of Na+ channel slow-inactivation in rat CA1 hippocampal pyramidal cell dendrites after brief exposure to convulsants.

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Na+ channels in the dendrites of rat CA1 pyramidal neurons display a profound activity-dependent inactivation, termed slow inactivation, that limits excitability in the dendrites even at low physiological rates of firing. The magnitude of this slow inactivation is powerfully modulated by a protein

Caffeine-induced inhibition of the activity of glutamate transporter type 3 expressed in Xenopus oocytes.

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Caffeine has been known to trigger seizures, however, the precise mechanism about the proconvulsive effect of caffeine remains unclear. Glutamate transporters play an important role to maintain the homeostasis of glutamate concentration in the brain tissue. Especially, dysfunction of excitatory

17β-Estradiol attenuates the activity of the glutamate transporter type 3 expressed in Xenopus oocytes.

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Estrogen, a neuroactive sex hormone in the brain, enhances neuronal excitability and increases seizures. Glutamate transporters help in limiting the excitatory neurotransmission by uptaking glutamate from the synapses. We investigated the effects of 17β-estradiol on the activity of a glutamate

Nicotine decreases the activity of glutamate transporter type 3.

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Nicotine, the main ingredient of tobacco, elicits seizures in animal models and cigarette smoking is regarded as a behavioral risk factor associated with epilepsy or seizures. In the hippocampus, the origin of nicotine-induced seizures, most glutamate uptake could be performed primarily by

Activity-dependent phosphorylation of SNAP-25 in hippocampal organotypic cultures.

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Synaptosomal-associated protein of 25 kDa (SNAP-25) is thought to play a key role in vesicle exocytosis and in the control of transmitter release. However, the precise mechanisms of action as well as the regulation of SNAP-25 remain unclear. Here we show by immunoprecipitation that activation of

Cocaine inhibition of GABA(A) current: role of dephosphorylation.

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Acute cocaine toxicity is frequently associated with seizures. The mechanisms underlying the convulsant effect of cocaine are not well understood. Previously, we have shown that cocaine depresses whole-cell current evoked by gamma-aminobutyric acid (GABA) in hippocampal neurons freshly isolated from

D-amphetamine-elicited action potential bursts in central snail neurons: role of second messenger systems.

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OBJECTIVE Neuronal bursts of action potentials are closely related to seizure activity. Amphetamine rarely induces seizures at therapeutic doses, but seizure may occur after the first dose. This study investigated factors affecting d-amphetamine-elicited action potential bursts in isolated central

Cocaine decreases the glycine-induced Cl- current of acutely dissociated rat hippocampal neurons.

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The effects of cocaine on glycine-induced Cl- current (I(GLY)) of single neurons, freshly isolated from the rat hippocampal CA1 area, were studied with conventional whole-cell recording under voltage-clamp conditions. Cocaine depressed I(GLY) in a concentration-dependent manner, with an IC50 of 0.78

Carbamazepine enhances the activity of glutamate transporter type 3 via phosphatidylinositol 3-kinase.

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Glutamate transporters (also called excitatory amino acid transporters, EAAT) participate in maintaining extracellular homeostasis of glutamate, a major excitatory neurotransmitter, and regulating glutamate neurotransmission. EAAT3, the major neuronal EAAT, may also regulate gamma-aminobutyric

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