The morphology of postnatal development of rat MCs has been previously described (Malun and Brunjes 1996; Treloar et al. type that is often targeted by -adrenergic modulation. The absence of -adrenergic modulation on either electrical or calcium signaling at ON-MC synapses of neonatal rats and mice excludes the involvement of this mechanism in early odor preference learning. Early odor preference learning is observed in neonatal rats when they form a preference to an odor that is paired with a reinforcing stimulus (Sullivan et al. 1989; Sullivan and Wilson 1994; Wilson and Sullivan 1994). This form of learning depends on noradrenergic neurotransmission in the main olfactory bulb (MOB) that receives noradrenergic input Exherin (ADH-1) exclusively from the locus coeruleus (Shipley et al. 1985; McLean et al. 1989; McLean and Shipley 1991). Both – and -adrenoceptors are localized in the MOB (Wanaka et al. 1989; Nicholas et al. 1993a,b; Woo and Leon 1995; Day et al. 1997; Winzer-Serhan et al. 1997; Yuan et al. 2003) and might therefore contribute differentially to early odor preference learning. Although work in vitro (Trombley 1992, 1994; Trombley and Shepherd 1992) and in vivo (Jiang et al. 1996) has indicated norepinephrine (NE)-mediated disinhibition via -adrenoceptors, a role of -adrenoceptors in early odor preference learning has only been recently proposed (McLean et al. 2003). On the other hand, activation of -adrenoceptors has been shown to promote learning-dependent behavioral and neural changes (Wilson and Sullivan 1994; Coopersmith and Leon 1995). Early odor preference learning in Exherin (ADH-1) the MOB is blocked by -adrenoceptor antagonists; and the effect of reinforcing stimulus required for early odor preference learning can be provided by application of -adrenoceptor agonists. On the basis of these findings, it has been proposed that -adrenoceptor activation is both necessary and sufficient for early odor preference learning (Sullivan et al. 2000; but see McLean et al. 2003). In a recent cellular model for early odor preference learning, Yuan et al. (2003) proposed that 1-adrenoceptor activation triggers an intracellular cAMP cascade, whereas ON input triggers an influx of Ca2+ in MC dendrites. The coincident activation of Exherin (ADH-1) the cAMP cascade and increased Ca2+ levels facilitates Ca2+/calmodulin phosphorylation of cAMP response element (CRE)-binding protein (CREB) and CRE-regulated gene transcription. In this model, the cAMP-UCS (unconditioned stimulus) and Ca2+-CS (conditioned stimulus) pathways are hypothesized to converge at the level of CREB phosphorylation/dephosphorylation. There are several possible scenarios, however, for an interaction of the two pathways at an earlier stage. First, the Ca2+ pathway may enhance the cAMP cascade. This possibility has been excluded because odor input itself did not change the cAMP level. Furthermore, odor plus stroking (tactile stimulation) did Exherin (ADH-1) not provide an additional increase to the cAMP level compared with stroking alone (Yuan et al. 2003). The second possibility for an interaction of the cAMP and the Ca2+ pathways at an early stage is the direct enhancement of the odor-induced Ca2+ signaling via the 1-adrenoceptor. In both the hippocampus and the amygdala, the modulation of Ca2+ signaling by -adrenoceptors has been proposed to play a critical role during long-term memory formation (Gray and Johnston 1987; Huang et Exherin (ADH-1) al. 1993, 1996). The pairing of CS and Mouse monoclonal to SUZ12 UCS inputs during fear conditioning leads to Ca2+ entry through both NMDA receptors and L-type Ca2+ channels in lateral amygdala principal neurons (Bauer et al. 2002). Activation of -adrenoceptors has been reported to facilitate glutamate release in the amygdala by increasing presynaptic Ca2+ influx (Huang et al..