向大鼠丘脑内注射γ-羟基丁酸会增加遗传性失神发作。

Intrathalamic injections of gamma-hydroxybutyric acid increase genetic absence seizures in rats.

作者信息

Liu Z, Snead O C, Vergnes M, Depaulis A, Marescaux C

机构信息

Département de Neurophysiologie et Biologie des Comportements, Centre de Neurochimie du CNRS, Strasbourg, France.

出版信息

Neurosci Lett. 1991 Apr 15;125(1):19-21. doi: 10.1016/0304-3940(91)90119-e.

DOI:10.1016/0304-3940(91)90119-e

PMID:1857553

Abstract

The effects of intrathalamic injections of gamma-hydroxybutyric acid (GHB) and of NCS 382 85, a specific antagonist of GHB receptors, were evaluated in rats with spontaneous generalized absence epilepsy. Bilateral injections of GHB (25 and 50 micrograms/side) into the mediolateral thalamus increased spontaneous spike and wave discharges (SWD) in a dose-dependent fashion. This effect was suppressed by administration of NCS 382 85 (50 micrograms/side). Bilateral injection of NCS 382 85 alone (50 and 100 micrograms/side) into the same sites had no effect on SWD duration. Injection of GHB or NCS 382 85 into the midline thalamus and the area of reticular nuclei did not modify the SWD. These data suggest that GHB receptors in the mediolateral thalamus may be involved in the control of spontaneous SWD in this rat model of petit mal epilepsy.

摘要

在自发性全身性失神癫痫大鼠中，评估了丘脑内注射γ-羟基丁酸（GHB）和GHB受体特异性拮抗剂NCS 382 85的作用。向丘脑中外侧双侧注射GHB（每侧25和50微克）以剂量依赖性方式增加了自发性棘波和慢波放电（SWD）。给予NCS 382 85（每侧50微克）可抑制此效应。单独向相同部位双侧注射NCS 382 85（每侧50和100微克）对SWD持续时间无影响。向中线丘脑和网状核区域注射GHB或NCS 382 85不会改变SWD。这些数据表明，在该小儿失神癫痫大鼠模型中，丘脑中外侧的GHB受体可能参与了自发性SWD的控制。