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    • br The amygdala complex The amygdala complex

    2020-03-11


    The amygdala complex The amygdala complex is composed of distinct nuclei and subdivisions including the lateral (LA), basolateral (BL), and basomedial (BM) amygdala; the medial (Imp), lateral paracapsular (lpc), and main intercalated cell cluster (IN); and the lateral and medialcentral amygdala (CeA) (Pitkanen and Amaral, 1994, Sah et al., 2003). The main flow of information follows a lateral-to-medial path, with sensory information from the thalamus and cortex entering the amygdala by afferents synapsing in the LA, which sends glutamatergic projections throughout the amygdala, including to the BM, lateral CeA, and to the Imp. The BM then sends glutamatergic projections to the medial CeA, while the Imp sends GABAergic projections to the lateral CeA, which forms an inhibitory microcircuit with the medial CeA. Both the lateral and medial CeA function as major output nuclei, sending projections to downstream regions regulating rewarding and/or aversive behaviors. The BLA is primarily composed of glutamatergic neurons that are under precisely regulated inhibitory control by lpc neurons and local interneurons (Marowsky et al., 2004, McDonald, 1982, McDonald and Betette, 2001, Muller et al., 2003). Although interneurons make up a small percentage of BLA neurons, the multiple levels of inhibitory control of pyramidal neurons demonstrate that interneurons have significant effects on output of the BLA. In contrast, the CeA is predominately GABAergic cells, (McDonald, 1985, McDonald and Augustine, 1993), which compose the vast majority of both projection neurons and interneurons. The circuitry of the amygdala has been implicated in a number of important Irsogladine functions, but is best known for its role in emotional processing, specifically in the interpretation of emotionally relevant stimuli or the attachment of emotional relevance to otherwise neutral stimuli (Pitkanen & Amaral, 1994). In particular, the amygdala nuclei mediate the negative association processing behind the acquisition and expression of conditioned fear (for review, see Ehrlich et al., 2009) and recent evidence suggests that amygdala microcircuits are also critical for the coding of both positive- and negative-valence cues (Beyeler et al., 2016, Beyeler et al., 2018). The high degree of interconnectivity in the amygdala underlies the complex information processing that takes place as multi-modal input is received, integrated, and processed to produce relevant behavioral output.
    CRF and amygdala microcircuitry Corticotropin releasing factor (CRF) is a neuropeptide that has a well-established role in the stress response of the mammalian central nervous system. CRF is one of the principal activators of the hypothalamic-pituitary-adrenal (HPA) axis, which is responsible for a host of physiological and behavioral responses to stress, including alterations in heart rate, blood flow, reactivity, locomotion, and motivated behavior (Keller, McCluskey, Morgan, & O\'Connor, 2006). CRF activation produces behaviors similar to those seen following acute and chronic stress. Transgenic mice with constitutive overproduction of CRF exhibit reduced locomotor activity in a novel environment and decreased time spent in the open arm of the elevated plus maze, consistent with an anxiogenic phenotype, an effect, which was reversed with the intra-ventricular infusion of a CRF antagonist (Stenzel-Poore, Heinrichs, Rivest, Koob, & Vale, 1994). Similarly, intraventricular infusion of CRF produces a variety of pro-anxiety behavioral responses in rodent models, including novelty reactivity (Britton, Koob, Rivier, & Vale, 1982), social conflict (Britton, Morgan, Rivier, Vale, & Koob, 1985), acoustic startle (Swerdlow, Geyer, Vale, & Koob, 1986), and reduced time in the open arms on an elevated plus maze (Adamec, Sayin, & Brown, 1991). In human participants, CRF levels in the cerebrospinal fluid are elevated in patients with anxiety disorders relative to healthy controls (Baker et al., 1999, Bremner et al., 1997). Two G-protein coupled receptors for CRF have been identified in the mammalian brain, CRF-1 and CRF-2. CRF and the CRF receptors are expressed throughout the amygdala (Van Pett et al., 2000) and have been implicated in neuroplastic changes related to fear (Hubbard, Nakashima, Lee, & Takahashi, 2007), anxiety (Overstreet et al., 2004, Rainnie et al., 2004) and alcohol exposure (Herman, Contet et al., 2013, Lovinger and Roberto, 2013, Nie et al., 2004, Roberto et al., 2010).