Peptidergic transmission in the brain. I. Vasopressin-like signal in the hippocampus

Abstract

Studies of the action of arginine vasopressin (AVP) in the rat hippocampal slice have produced a model of the peptide's neural action. AVP excites local circuit inhibitory interneurons and causes consequent inhibition of pyramidal cells that is apparent as a reduction in the amplitude of the evoked population spike in field potential recording. Here we show that applied AVP does the same thing to the evoked population spike in the whole animal. Then we show that stimulation of the source of hippocampampal AVP, the medial amygdaloid nucleus, also inhibits the evoked population spike. Analysis of the synaptic potential indicates that the same mechanisms are employed by exogenously applied and endogenously released peptide. The inhibition can only be obtained by stimulating those brain structures known to project vasopressin fibers to the hippocampus. The stimulus-response characteristics and kinetics of the endogenous signal correspond to the properties of peptidergic signals in simple systems. The results are taken to support a transmitter role for AVP in the rat hippocampus.