Fig 1.

Depicts the noradrenergic elements hypothesized to be involved in behavioral inhibition. LC neuron firing rates are regulated by a variety of afferent inputs including glutamatergic neurons from the PGi (Ennis et al., 1992) and neocortex (Zhu et al., 2004) acting at NMDA receptors (Ennis and Aston-Jones, 1988), CRF from the AMYG (Van Bockstaele et al., 1998), EPI from C1(Pieribone et al., 1988) and NE and possibly DA from recurrent collaterals of the LC itself (Nakamura et al., 1988) or from other brainstem noradrenergic nuclei acting at α₁-, α₂- and β-adrenoceptors (not shown). The LC projects primarily to forebrain regions involved in sensorimotor organization and motivational processes which are assumed to be inhibited during high rates of LC discharge via galanergic and adrenergic receptors (see text). Stress areas of the PVH, BNST and AMYG receive noradrenergic innervation chiefly from the lateral tegmental brainstem nuclei, A1 and A2 (Aston-Jones et al., 1999), and partially from the LC, all via α and β-adrenoceptors (Koob, 1999; Ma and Morilak, 2004) . Stress areas send inhibitory efferents containing CRF and GABA to the sensorimotor and motivational regions and thus convey the noradrenergic signal from A1 and A2 neurons to these areas (see text for details).