Abstract
The effects of vasopressin on neurons of the rat dorso‐lateral septum (DLS) was studied in brain slices with intracellular microelectrodes. Two out of 13 neurons showed a small depolarization, spontaneous activity, and increased input resistances following a 15 min exposure to 10^‐6^ to 10^‐8^ M vasopressin (VP). These membrane effects disappeared completely within 3–5 min after the application. The remaining DLS neurons treated with these vasopressin concentrations showed an increase in glutamate‐mediated excitatory postsynaptic potentials (EPSP~s~), evoked by stimulation of the fimbria fibers. As little as 10^‐12^ M VP increase these EPSP~s~ markedly in nearly 80% of the cells studied. This increase in most of the cells disappeared within 15 min after the application period, whereas the increase in EPSP~s~ induced by 10^‐10^ M VP outlasted the peptide application period for more than 30 min. Neither the blockade of GABA‐ergic synaptic inhibition nor the pre‐treatment of the neurons with d(CH~2~)~5~‐Tyr(Me)‐arginine vasopressin or 2‐amino‐5‐phosphonovaleric acid (2‐APV), antagonists for the V1 type of vasopressin receptor and NMDA receptors, respectively, interfered with the EPSP~s~ potentiating effect of the peptide. It is concluded that a type of vasopressin receptor other then the V1 type is involved in the long‐lasting potentiation of the primarily non‐NMDA receptor mediated transmission in DLS neurons.