PARTIAL LIMBIC KINDLING - BRAIN, BEHAVIOR, AND THE BENZODIAZEPINE RECEPTOR

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.