All effects were mediated by V1aR, without involvement of the V1bR (Allaman-Exertier et al., 2007). As a result AVP would lead to a disinhibition

of target structures among which are the hypothalamic nuclei involved in behavioral tasks (Risold and Swanson, 1997) important for social recognition. The direct excitatory effects of AVP on GABAergic neurons may possibly also modulate the theta rhythm that is known to originate in the septal area and propagate to the hippocampus (Urban, 1998). No effects of OT in the dorsal LS seem to have been reported. In addition to these acute neuromodulatory effects, long-lasting selleck compound facilitating effects of AVP on evoked postsynaptic potentials that persist well beyond the period of AVP administration have been reported. As in the hippocampus, these effects of AVP appeared at low concentrations (1 pM). This long-lasting effect could not be blocked by a V1 receptor antagonist ( Van den Hooff and Urban, 1990). Taken together, these findings indicate that in the hippocampus and LS, AVP and OT can exert reversible neuromodulatory effects as well as long-lasting potentiating effects on synaptic transmission. It is possible that neuromodulation of oscillatory rhythms may in addition

affect synaptic plasticity and memory processing, such as required for social memory and cognition. In view of the adjacent expressions of V1aR and OTR in both these reciprocally connected regions, it remains to be explored to what extent OT and AVP can complement each other’s click here functions. Both OT and V1aRs have been found in the spinal cord, with a striking segregation of OTRs in the dorsal and AVPRs in the ventral part (Figure 5E). This is matched by OT projections from the hypothalamus terminating in lamina I-II (Breton et al., 2008) and AVP projections to the ventral

parts (Hallbeck and Blomqvist, 1999). The specific OT-agonist [Thr4Gly7] OT (TGOT) activates here a subpopulation of lamina II glutamatergic interneurons that project onto GABAergic interneurons. OT thereby elevates inhibition of the nociceptive afferent messages that originate from C and Aδ primary afferents. These findings could explain the analgesic effects that have been reported for OT in both humans and rodents (Schorscher-Petcu et al., 2010). Expression of V1aRs is particularly high Aldehyde dehydrogenase in the spinal cord of young rats, declining in older individuals (Liu et al., 2003). AVP excites motoneurons via a postsynaptic mechanism involving suppression of a resting K+ conductance and activation of a cationic conductance in laminae VIII and IX of the lumbar spinal cord and in the sexually dimorphic pudendal motoneurons in segments L5 and L6, which play a critical role in sexual and eliminative functions (Ogier et al., 2006). AVP can also excite glycinergic interneurons that innervate these motoneurons, thereby indirectly increasing inhibition (Kolaj and Renaud, 1998; Oz et al., 2001).