Rinaman L, Maldovan V (2005) Experimental dissociation of neural circuits underlying anorexic and conditioned avoidance responses to LiCl in rats. Neuroscience 2005 Abstracts 529.7. Society for Neuroscience, Washington, DC.
Summary: The central nucleus of the amygdala (CeA) receives viscerosensory input from noradrenergic (NA) neurons in the nucleus of the solitary tract (NST) and from peptidergic non-NA neurons in the lateral parabrachial nucleus (laPBN). A previous study (J. Neurosci. 23:10084-92) demonstrated that NA neurons in the caudal NST are necessary for cholecystokinin (CCK) to inhibit food intake in rats, but are unnecessary for CCK to activate Fos expression in the laPBN and CeA. The laPBN and CeA are integral components of central neural circuits that underlie the formation and expression of conditioned flavor avoidance (CFA). Thus, the neural substrates for treatment-induced anorexia may be separable from those for CFA. To test this idea, saporin toxin conjugated to an antibody against dopamine β hydroxylase was microinjected bilaterally into the caudal NST in adult male rats in order to selectively lesion NA neurons. Three weeks later, lesioned and sham control rats were tested for the ability of 0.15M LiCl (2% BW, i.p.) to inhibit food intake and to support conditioned flavor avoidance (CFA). Anorexia after LiCl was significantly blunted in lesioned rats compared to sham controls, similar to our previous findings in lesioned rats after CCK treatment. However, LiCl still supported robust CFA in lesioned rats, and its magnitude was similar to that seen in sham controls. A terminal Fos study revealed intact LiCl-induced activation of neural Fos expression in the laPBN and CeA in lesioned rats, despite significant loss of NA neurons in the caudal NST. These new findings support the view that NA neurons in the caudal NST are unnecessary for laPBN and CeA neural responses to viscerosensory stimulation, and also are unnecessary for the learning and expression of conditioned flavor avoidance.
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