In both mitral and granule cell layers OTR mRNA and OT-immunoreactive fibers have been found (Knobloch et al., 2012; Vaccari et al., 1998; Yoshimura et al., 1993). Neuromodulation by both OT and AVP increased excitability of mitral cells via a V1a receptor (Osako et al., 2000, 2001). Furthermore, the AVP effects could be endogenously triggered

by AVP-producing cells that are locally present in the MOB (Tobin et al., 2010). Specific OTR activation caused a decrease of the inhibitory input from GC on MC LY294002 in vivo neurons through a presynaptic mechanism, an effect that seemed important for the induction of maternal behavior (Yu et al., 1996; Osako et al., 2001). It thus appears that in the MOB and AOB, AVP and OT may reinforce each other’s actions, AVP by increasing excitation, OT by decreasing inhibition. It has been proposed that, through these concerted actions, both AVP and OT applications to the olfactory bulb also lengthen the retention interval for short-term social odor recognition in male rats (Dluzen et al., 1998). Of interest in this context, OT can lower the threshold for LTP induction

at excitatory synapses between mitral cells and granule cells in the AOB (Fang et al., 2008). The MOB sends projections to the anterior olfactory nucleus, the piriform cortex, some subdivisions of the cortical amygdala, and the medial amygdala. Most projections to the MeA, however, originate from the AOB (Switzer and DeOlmos, 1985; Swanson and Petrovich, 1998). The AOB also projects to the posterior medial subdivision of the cortical amygdala (COApm) and to the bed nucleus of the stria terminalis (BST)

with which http://www.selleckchem.com/products/Dasatinib.html the MeA is reciprocally connected (Alheid and Heimer, 1988). This is the major pathway for processing pheromonal cues and important for social interactions (Brennan and Zufall, 2006; Swanson and Petrovich, 1998), and the MeA is for that reason also called the “vomeronasal amygdala.” In the MeA of male rats, mRNA for V1aR, V1bR, and OTRs is present and binding of specific OTR antagonists has been demonstrated (Arakawa et al., 2010; Veinante and Freund-Mercier, 1997). Male OT knockout mice lack short-term conspecific Metalloexopeptidase social recognition, which can be rescued by local microinjections in MeA of OT prior to the first exposure (Ferguson et al., 2001) and mimicked by antisense oligonucleotides targeting the OTR (Choleris et al., 2007). Interestingly, an OT antagonist injected in the MeA blocked approach behavior to odors of healthy conspecifics, whereas a V1a antagonist blocked avoidance of odor to sick conspecifics, suggesting nonoverlapping, but contrasting, roles for these peptides in this region (Arakawa et al., 2010). In the MeA and the BST, local AVP-producing neurons have been found (Caffé and van Leeuwen, 1983; van Leeuwen and Caffé, 1983) and in the MeA OTergic fibers that originate from the PVN and SON (Knobloch et al., 2012).