Modulation by arginine vasopressin of glutamate excitation in the ventral septal area of the rat brain.

Abstract

Arginine vasopressin is hypothesized to act as a neurotransmitter or neuromodulator in the ventral septal area of the rat brain. To examine this role of vasopressin further, it was applied by microiontophoresis or micropressure from multiple-barrelled micropipettes onto spontaneously active or glutamate-activated neurons. Applied in this manner, vasopressin reduced glutamate-evoked excitation in 32 of the 47 cells studied. Further, micropressure application of the vasopressin antagonist d(CH2)5Tyr(Me)AVP reversed the vasopressin effects. In contrast, administration of vasopressin had no effect on excitations evoked by acetylcholine iontophoresis or on the spontaneous activity of the majority of the ventral septal neurons studied. These observations suggest that vasopressin may be acting on a V1-like receptor on specific neurons in the ventral septal area as a modulator of glutamate actions. Evoked responses were also obtained in the same population of ventral septal cells following stimulation of a variety of limbic areas. Inhibitory input onto most of the vasopressin responsive neurons studied was obtained following electrical stimulation of the paraventricular nucleus and bed nucleus of the stria terminalis, two cell groupings that are potential sources of vasopressin to the ventral septal area. Thus, the similarity in action of exogenously applied vasopressin and the evoked responses following paraventricular nucleus and bed nucleus stimulation suggests that vasopressin may be a neurotransmitter in this pathway.