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部分边缘系统点燃——大脑、行为与苯二氮䓬受体

Partial limbic kindling--brain, behavior, and the benzodiazepine receptor.

作者信息

Adamec R E

机构信息

Department of Psychology, Memorial University, St. John's, NFLD, Canada.

出版信息

Physiol Behav. 1993 Sep;54(3):531-45. doi: 10.1016/0031-9384(93)90247-d.

DOI:10.1016/0031-9384(93)90247-d
PMID:8415948
Abstract

Partial kindling (PK) of the left perforant path (PP) lastingly increased feline defensiveness. Perforant path PK produced long-term potentiation (LTP) in the amygdalo-ventromedial hypothalamic (AM-VMH) pathways in both hemispheres, and in the ventroamygdalofugal (VAF)-VMH efferents of the amygdala of the left hemisphere. Long-term potentiation paralleled behavioral changes. Perforant path PK did not affect recurrent inhibition in area CA3 of the ventral hippocampus. Long-term potentiation of CA3 EPSP and population spikes appeared, but before behavioral changes. Changes in excitability of the periaqueductal grey also accompanied behavioral changes. After kindling, the benzodiazepine receptor antagonist, flumazenil, reduced defensive response to rats in a drug-dependent manner. Flumazenil also reduced LTP in the AM-VMH pathway, but did not affect LTP in the VAF-VMH pathway. Therefore, flumazenil was acting in the amygdala, and not at the VAF-VMH synapse. Kindling caused flumazenil to act like an agonist on behavior, and in the amygdala, and as an agonist or an inverse agonist in area CA3 depending upon the physiological measure taken.

摘要

左侧穿通通路(PP)的部分点燃(PK)会持久增强猫的防御性。穿通通路PK在两侧半球的杏仁核-腹内侧下丘脑(AM-VMH)通路以及左侧半球杏仁核的腹侧杏仁核传出纤维-腹内侧下丘脑(VAF-VMH)传出纤维中产生了长时程增强(LTP)。长时程增强与行为变化平行。穿通通路PK并未影响腹侧海马CA3区的回返抑制。CA3区兴奋性突触后电位(EPSP)和群体峰电位的长时程增强出现了,但在行为变化之前。导水管周围灰质兴奋性的变化也伴随着行为变化。点燃后,苯二氮䓬受体拮抗剂氟马西尼以药物依赖的方式降低了对大鼠的防御反应。氟马西尼还降低了AM-VMH通路中的LTP,但不影响VAF-VMH通路中的LTP。因此,氟马西尼作用于杏仁核,而不是VAF-VMH突触。点燃使氟马西尼在行为上以及在杏仁核中表现得像一种激动剂,而在CA3区根据所采用的生理指标表现为激动剂或反向激动剂。

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