Amygdala-lesion obesity: what is the role of the various amygdaloid nuclei?

Abstract

Anatomic descriptions of amygdaloid lesions resulting in hyperphagia and obesity in rats, cats, and dogs have been inconsistent and often contradictory, frequently resulting in failures to replicate. The present study attempted to reconcile these differences by examining common areas of overlap among differently placed lesions in female rats. Small bilateral lesions of the most posterodorsal aspects of the amygdala resulted in substantial weight gains (mean = 45.4 g/10 days). The smallest lesions caused damage limited to the posterodorsal medial amygdaloid nucleus and the bed nucleus of the stria terminalis and were directly in the area where axons are collecting to form the stria terminalis. Larger lesions that extensively damaged the central and/or anterodorsal medial amygdaloid nuclei sometimes resulted in excess weight gains, as did very large lesions of the basolateral nuclei, but substantial weight gains occurred only when the lesions extended (unilaterally or bilaterally) into the posterodorsal amygdala. Examination of previously published brain sections indicated that the hyperphagia and obesity that have been observed after widely differing lesion placements in cats and dogs were also the result of damage to a common area of overlap (i.e., the bed nucleus and/or stria terminalis). In rats, the critical area producing weight gain has extensive reciprocal relations with the medial hypothalamus.

Glutamate Microinjected in the Posterodorsal Medial Amygdala Induces Subtle Increase in the Consumption of a Three‐Choice Macronutrient Self‐Selection Diet in Male Rats

“…As evidenced by electrophysiological recordings, not all hypothalamic neurons sampled responded to MeA stimulation but, when it occurred, both excitatory and inhibitory responses were evoked in different target areas (Carrer et al, 1978;Choi et al, 2005;Bian et al, 2008). It is also conceivable that lesions involving the ''posterodorsal amygdala'' and that induced hyperphagia (King et al, 1998(King et al, , 1999(King et al, , 2003Rollins and King, 2000;Grundmann et al, 2005) have affected other amygdaloid nuclei or transition areas besides the MePD (Rollins and King, 2000;King et al, 2003;Moscarello et al, 2009). In effect, excessive weight gains in lesioned females might be more related to damage the intra-amygdaloid division of the bed nucleus of the ST than to the MePD itself (King et al, 1998).…”

“…Lesions also promoted anterograde degeneration in the ipsilateral hypothalamic ventromedial nucleus (Rollins and King, 2000;Grundmann et al, 2005), an integrated area for the central control of food intake and energy balance (Berthoud, 2002). Damage to the posterodorsal aspect of the MeA (MePD) and the intraamygdaloid bed nucleus of the ST or to the ST promoted an increase in the rat weight gain (Rollins and King, 2000;Rollins et al, 2006). Altogether, these data suggest that the distinct components of the amygdaloid ''posterodorsal region,'' probably using the ST as its connecting pathway with hypothalamic nuclei (Dong et al, 2001;Petrovich et al, 2001), respond to feeding stimuli and elicit and/or regulate ingestive behavior and energy balance in female rats (Grundmann et al, 2005).…”

“…Previous reports involved the ''posterodorsal region'' of the amygdala with feeding behavior in rats (King et al, 1998(King et al, , 1999(King et al, , 2003Rollins and King, 2000;Grundmann et al, 2005). This wide area is neither an anatomical nor a functional unit; rather, it involves different amygdaloid components, such as the medial nucleus of the amygdala (MeA), the stria terminalis (ST), and the bed nucleus of the ST among others.…”

“…Unilateral or bilateral electrolytic lesions of this ''posterodorsal region'' led Long-Evans adult female rats to display a marked preference for carbohydrate consumption, hyperphagia, and an abnormal increase in body weight (King et al, 1998(King et al, , 1999(King et al, , 2003. Lesions also promoted anterograde degeneration in the ipsilateral hypothalamic ventromedial nucleus (Rollins and King, 2000;Grundmann et al, 2005), an integrated area for the central control of food intake and energy balance (Berthoud, 2002). Damage to the posterodorsal aspect of the MeA (MePD) and the intraamygdaloid bed nucleus of the ST or to the ST promoted an increase in the rat weight gain (Rollins and King, 2000;Rollins et al, 2006).…”

“…Similar to gustatory information, olfactory inputs can generate representations of food environment, its emotional valence and memory for the condition experienced. However, no other MeA subnuclei than the MePD appear to be involved with feeding behavior in rats (Stanley et al, 1993;Rollins and King, 2000). It participates in the interpretation of olfactory/vomeronasal information and remarkable projections leave this subnucleus via the ST to reach the hypothalamic ventromedial nucleus, the anteroventral periventricular nucleus, the preoptic area, and the ventral premammillary nucleus in the hypothalamus (Newman, 1999;Dong et al, 2001;Petrovich et al, 2001).…”