Two actions of vasopressin on neurons in the rat ventral hippocampus: A microiontophoretic study

Long-lasting enhancement of synaptic excitability of CA1/subiculum neurons of the rat ventral hippocampus by vasopressin and vasopressin(4–8)

“…In vitro, micromolar concentrations of VP are usually needed to demonstrate this excitatory action of VP in a significant population of neurons, suggesting that these short-lasting excitations are presumably not the action by which the picogram quantities of VP or its active metabolites facilitate memory. Most of the lateral septum and ventral hippocampal neurons that were not excited by iontophoretically applied VP exhibited a marked increase in their responses to iontophoretically released glutamate, an effect which lasted for tens of minutes after the termination of peptide application [29,67]. Also, the synaptic responses of lateral septum neurons to stimulation of the fimbria fibers, that are presumably mediated by glutamate [30,73], were markedly potentiated by iontophoretically applied VP [29].…”

“…The notion that VP in very low concentrations potentiates the responses of brain neurons to excitatory, glutamatergic input came from earlier field potential [66] and microiontophoretic studies [29,67], and from recent intracellular experiments. Bath-applied 0.1-0.001 nM VP increased the amplitude of the EPSPs in lateral septum neurons, evoked by stimulation of the fimbria fibers, in nearly the same fashion as that described here.…”

“…These results and the recenl finding of specific binding sites for VP (4)(5)(6)(7)(8) in synaptosomal membrane preparations from the anterior cortex [22] strongly suggest that many of the central effects of VP and its metabolites are mediated by specific receptor complex(es) distinct from the peripheral V l, V~ or OT receptors. The observation that many of the VP effects on the brain neurons are prevented by pretreatment of the neurons with d(CH2)5-Tyr(Me)-arg inines VP [38,45,47,67,70], shown to be a selective antagonist at the periheral V~ pressor VP receptor [36], might be misleading as this antagonist acts as a general neurodepressant agent [49]. Thus, further studies with various ligands for VP and for OT types of receptors might be a better approach for characterization of the receptors mediating the VP effect on EPSPs.…”

“…The action of microiontophoretically or bath-applied micromolar concentrations of VP on hippocampal and other brain neurons is predominantly an excitatory one, characterized by a reversible increase in the firing rate that vanishes immediately or within several minutes after the termination of peptide administration [28,38,43,45,62,67]. In vitro, micromolar concentrations of VP are usually needed to demonstrate this excitatory action of VP in a significant population of neurons, suggesting that these short-lasting excitations are presumably not the action by which the picogram quantities of VP or its active metabolites facilitate memory.…”

Role of Arginine Vasopressin V1 and V2 Receptors for Brain Damage After Transient Focal Cerebral Ischemia

“…This effect, if present, seems to be restricted to penumbral tissue, because inhibition of AVP V 1 receptors does not affect CBF in the infarct core (Figure 1). Another explanation for AVP V 1 receptor-mediated neuroprotection might be that AVP V 1 receptors are widely expressed in the brain parenchyma (Brinton et al, 1984;Pearlmutter et al, 1988;Phillips et al, 1988;Young et al, 1999;Tribollet et al, 1999;Fernandez et al, 2001) where they have been implicated in intracellular calcium mobilization, activation of NMDA receptors, and superoxide anion generation (Urban and Killian, 1990;Hess et al, 1991;Gouzenes et al, 1999;Armstead, 2001), all conditions well known to be associated with neuronal cell death after cerebral ischemia (Lo et al, 2003). Accordingly, the positive effect AVP V 1 receptor inhibition on cell death might also be explained by a reduction of glutamate-and superoxide anion-mediated toxicity, as also discussed previously (Tanaka et al, 1994).…”