Muscimol-stimulated Cl(-)conductance in brain cortex synaptoneurosomes from Wistar rats decreased 15 min after single intraperitoneal injection of pentylenetetrazole in a subconvulsive dose. These changes reflected a decrease in functional activity of the GABA(A)-receptor/Cl(-)ionophore complex. Muscimol-stimulated Cl(-)conductance in synaptoneurosomes returned to normal 48 h after pentylenetetrazole administration.

Experiments on Wistar rats showed that muscimol-stimulated Cl(-) conduction of synaptoneurosomes, isolated from the cerebral cortex increased after 5-day systemic treatment with subconvulsive doses of pentylene tetrasole during the initial stage of pharmacological pentylene tetrasole kindling, characterized by gradually augmenting convulsive readiness of the brain. This indicates an increase in functional activity of the GABA(A) receptor/Cl(-) ionophore complex.

No abstract

Muscimol-stimulated Cl- conductance of synaptoneurosomes from the cerebral cortex of Wistar rats increased during the early stage of pharmacological kindling not inducing the seizure response in animals. Picrotoxin, bicuculline, and pentylenetetrazole potentiated inhibition of muscimol-dependent 36Cl- entry into synaptoneurosomes, which attested to increased sensitivity of the GABA(A) receptor/Cl- ionophore complex to classic convulsants.

Delta-sleep-inducing peptide (DSIP) is an endogenous substance that regulates the response of the organism to stress. It was found that DSIP, like diazepam and ethanol, activates muscimol-stimulated 36Cl- uptake in the rat brain cortex and partially counteracts the stimulatory action of ethanol on this process. The effect of peptide disappears at the lowering of the incubation temperature. We propose that DSIP is a concordant regulator partly mediating its action through the membrane phospholipids.