Amygdaloid N-methyl-D-aspsraate and γ-aminobutyric ACIDA receptors regulate sensorimotor gating in a dopamine-dependent way in rats
Amygdaloid N-methyl-D-aspsraate and γ-aminobutyric ACIDA receptors regulate sensorimotor gating in a dopamine-dependent way in rats
复制标题
DOI：
10.1016/s0306-4522(00)00086-5
复制
发表时间：
2000-01-01
期刊：
影响因子：
3.3
通讯作者：
Koch, M
中科院分区：
文献类型：
--
作者：
Fendt, M;Schwienbacher, I;Koch, M
感觉运动门控可以通过人类和大鼠惊吓反应的前脉冲抑制来测量。由于精神分裂症患者的前脉冲抑制受到损害，因此人们对了解前脉冲抑制的神经元基础非常感兴趣。神经病理学结果表明精神分裂症患者皮质边缘区域的谷氨酸能和 GABA 能系统存在功能障碍。我们测试了基底外侧杏仁核中 N-甲基-D-天冬氨酸或 GABA(A) 受体的阻断是否会影响大鼠的前脉冲抑制。局部输注 N-甲基-D-天冬氨酸受体拮抗剂地佐西平 (0, 6.25 μg/0.5 μl) 或 GABA(A) 受体拮抗剂印防己毒素 (0, 5.0, 10.0 ng/0.5 μl) 可减少前脉冲抑制。 6.25 μg 地佐环平或 10.0 ng 印防己毒素的前脉冲抑制干扰作用可通过全身联合给予多巴胺拮抗剂氟哌啶醇（0.1 mg/kg 腹腔注射）而逆转。这些数据表明，感觉运动门控通过 N-甲基-D-天冬氨酸和 GABA(A) 以多巴胺依赖性方式调节 基底外侧杏仁核中的受体。我们的研究结果是针对精神分裂症患者的神经病理学发现进行讨论的。 (C) 2000 国际广播组织。由爱思唯尔科学有限公司出版。保留所有权利。
Sensorimotor gating can be measured as prepulse inhibition of the startle response in humans and rats. Since prepulse inhibition is impaired in schizophrenics there is considerable interest in understanding the neuronal basis of prepulse inhibition. Neuropathological findings indicate a dysfunction of the glutamatergic and GABAergic system in cortico-limbic areas in schizophrenics. We tested whether blockade of N-methyl-D-aspartate or GABA(A) receptors in the basolateral amygdala affects prepulse inhibition in rats. Local infusion of the N-methyl-D-aspartate receptor antagonist dizocilpine (0, 6.25 mu g/0.5 mu l), or of the GABA(A) receptor antagonist picrotoxin (0, 5.0, 10.0 ng/0.5 mu l) reduced prepulse inhibition. The prepulse inhibition-disrupting effect of 6.25 mu g dizocilpine or 10.0 ng picrotoxin was reversed by systemic co-administration of the dopamine antagonist haloperidol (0.1 mg/kg i.p.).These data indicate that sensorimotor gating is regulated in a dopamine-dependent way by N-methyl-D-aspartate and GABA(A) receptors in the basolateral amygdala. Our findings are discussed with respect to neuropathological findings in schizophrenics. (C) 2000 IBRO. Published by Elsevier Science Ltd. All rights reserved.