Infusion of NMDA antagonists into the nucleus reticularis pontis oralis inhibits the maximal electroshock seizure response

doi:10.1016/0006-8993(95)01026-2

Brain Research

Volume 702, Issues 1–2, 8 December 1995, Pages 101-109

https://doi.org/10.1016/0006-8993(95)01026-2 Get rights and content

Abstract

The nucleus reticularis pontis oralis (RPO) is necessary for the expression of tonic hindlimb extension (THE) in maximal electroshock (MES) seizures of rats. Previous work in this laboratory has demonstrated that both systemic administration and focal RPO microinfusion of d-cycloserine inhibits THE. The purpose of the present study was to characterize specific components of the NMDA receptor/ionophore complex that regulate the anticonvulsant activity mediated by the RPO. Bilateral RPO microinfusion of the competitive NMDA antagonists (−)AP7 and D-CPP as well as the uncompetitive antagonist dizocilpine ((+)MK-801) inhibited THE in a dose-related fashion. Bilateral RPO microinfusion of NMDA did not affect the THE response to MES but did induce convulsions resembling audiogenic seizures in genetically epilepsy prone rats. Bilateral RPO microinfusion of the strychnine-insensitive glycine site partial agonist d-cycloserine and the antagonist 5,7-dichlorokynurenic acid inhibited THE. The strychnine-insensitive glycine partial agonists (+)HA-966 and ACPC, as well as the agonists glycine and d-serine, did not significantly affect the THE response. Strychnine microinfusions in the RPO had no effect on THE. The results support a hypothesis that the RPO is a site of anticonvulsant drug action in MES and indicate that either competitive or uncompetitive NMDA antagonist action regulates the anticonvulsant activity mediated by the RPO. The role of the strychnine-insensitive glycine site in the regulation of the anticonvulsant activity medicated by the RPO is uncertain.

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Infusion of NMDA antagonists into the nucleus reticularis pontis oralis inhibits the maximal electroshock seizure response

Abstract

Epilepsy Res.

Eur. J. Pharmacol.

Eur. J. Pharmacol.

Eur. J. Pharmacol.

Neurosci. Lett.

Brain Res.

Life Sci.

Brain Res.

Behav. Neural Biol.

Eur. J. Pharmacol.

Neurosci. Lett.

Eur. J. Pharmacol.

Neurosci. Lett.

Neurosci. Lett.

Neuropharmacology

Pharmacol. Biochem. Behav.

Pharmacol. Biochem. Behav.

Brain Res.

Neuroscience

Eur. J. Pharmacol.

Epilepsy Res.

Epilepsy Res.

Eur. J. Pharmacol.

Neuropharmacology

Brain Res.

J. Neurosci. Methods

Brain Res.

Life Sci.

Epilepsy Res.

Eur. J. Pharmacol.

Brain Res.

Eur. J. Pharmacol.

Neurosci. Lett.

Eur. J. Pharmacol.

Brain Res.

Eur. J. Pharmacol.

Activity of 5,7-dichlorokynurenic acid, a potent antagonist at the NMDA receptor-associated glycine binding site

Mol. Pharmacol.