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Am J Physiol Regul Integr Comp Physiol (November 14, 2002). doi:10.1152/ajpregu.00249.2002
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Articles in PresS, published online ahead of print November 14, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00249.2002
Submitted on May 6, 2002
Accepted on November 11, 2002

Obesity-Inducing Amygdala Lesions: Examination of Anterograde Degeneration and Retrograde Transport

Bruce M King1*, Jack T Cook1, Kirk N Rossiter1, and Bethany L Rollins1

1 Psychology, University of New Orleans, New Orleans, LA, USA

* To whom correspondence should be addressed. E-mail: bmking{at}uno.edu.

Small lesions centered in the posterodorsal region of the medial amygdala resulted in excessive weight gains in female rats. Unilateral lesions were nearly as effective as bilateral lesions in the first 48 hrs after surgery (+21 g to +32 g). Assessment of lesion damage was done by both qualitative evaluation and by a quantitative grid-point counting method. The critical sites for weight gain were the intraamygdaloid bed nucleus of the stria terminalis and the posterodorsal medial amygdaloid nucleus. Incidental damage to the overlying globus pallidus was negatively related to weight gain. The cupric silver method for demonstrating axonal degeneration was applied to brains with obesity-inducing lesions. Degenerating terminals were found in the lateral septum, amygdala, ventral striatum, and medial hypothalamus in targets that are likely participants in the regulation of food intake. Degeneration in the paraventricular nucleus of the hypothalamus was scarce or absent. Small retrograde tracer injections made in either the intraamygdaloid bed nucleus of the stria terminalis or in the posterodorsal medial amygdaloid nucleus labeled cells in the amygdala, lateral septum, and hypothalamus, reciprocating the anterograde projections from the amygdala to these areas. In addition, afferent neurons were noted in the thalamic subparafascicular nucleus and in the superior lateral subnucleus of the parabrachial complex, likely viscero-sensory relays to the forebrain and hypothalamus. Overall, the data suggest that subdivisions of the posterodorsal amygdala participate in the regulation of feeding in a manner that is in some respects similar to the better-known role of this part of the brain in mediating social behaviors. Although topographical differences may exist within the amygdaloid and hypothalamic subdivisions regulating these diverse, sexually dimorphic behaviors, the relays engaged by feeding-related connections and those related to reproduction are remarkably parallel. The direct projections and indirect relays of the posterodorsal region of the medial amygdala afford the opportunity for these structures to influence a broad pattern of regulatory and social behaviors that encompass somatomotor, autonomic, and neuroendocrine aspects of behavioral control.




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