Amygdaloid lesion-induced obesity: relation to sexual behavior, olfaction, and the ventromedial hypothalamus

2006 ◽  
Vol 291 (5) ◽  
pp. R1201-R1214 ◽  
Author(s):  
Bruce M. King
Keyword(s):  
Sexual Behavior ◽  
Nodal Point ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Male Rats ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Normal Feeding ◽  
Medial Amygdaloid Nucleus

Lesions of the amygdala have long been known to produce hyperphagia and obesity in cats, dogs, and monkeys, but only recently have studies with rats determined that the effective site is the posterodorsal amygdala (PDA)—the posterodorsal medial amygdaloid nucleus and the intra-amygdaloid bed nucleus of the stria terminalis. There is a sex difference; female rats with PDA lesions display greater weight gain than male rats. In the brains of female rats with obesity-inducing PDA lesions, there is a dense pattern of axonal degeneration in the capsule of the ventromedial hypothalamus (VMH) and other targets of the stria terminalis. Transections of the dorsal component of the stria terminalis also result in hyperphagia and obesity in female rats. Similar to rats with VMH lesions, rats with PDA lesions are hyperinsulinemic during food restriction and greatly prefer high-carbohydrate diets. The PDA is also a critical site for some aspects of rodent sexual behavior, particularly those that depend on olfaction, and the pattern of degeneration observed after obesity-inducing PDA lesions is remarkably parallel to the circuit that has been proposed to mediate sexual behavior. Medial amygdaloid lesions disrupt the normal feeding pattern and result in impaired responses to caloric challenges, and there is evidence that these behavioral changes are also due to a disruption of olfactory input. With its input from the olfactory bulbs and connections to the VMH, the PDA may be a nodal point at which olfactory and neuroendocrine stimuli are integrated to affect feeding behavior.

Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport

2003 ◽  
Vol 284 (4) ◽  
pp. R965-R982 ◽  
Author(s):  
Bruce M. King ◽  
Jack T. Cook ◽  
Kirk N. Rossiter ◽  
Bethany L. Rollins
Keyword(s):  
Weight Gain ◽  
Grid Point ◽  
Retrograde Transport ◽  
Ventromedial Hypothalamus ◽  
Lateral Septum ◽  
Female Rats ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Medial Amygdaloid Nucleus

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 h after surgery (+21 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 intra-amygdaloid 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. A dense pattern of degenerating terminals was found in the lateral septum, amygdala, ventral striatum, and ventromedial hypothalamus. Degeneration in the paraventricular nucleus of the hypothalamus was scarce or absent. Small retrograde tracer injections made in either the intra-amygdaloid 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. The data suggest that subdivisions of the posterodorsal amygdala participate in the regulation of feeding in a manner that is similar to the better-known role of this part of the brain in mediating reproductive behavior. Although topographical differences may exist within the amygdaloid and hypothalamic subdivisions regulating these two sexually dimorphic behaviors, the relays engaged by feeding-related connections and those related to reproduction are remarkably parallel.

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

2000 ◽  
Vol 279 (4) ◽  
pp. R1348-R1356 ◽  
Author(s):  
Bethany L. Rollins ◽  
Bruce M. King
Keyword(s):  
Female Rats ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Common Area ◽  
Weight Gains ◽  
Bilateral Lesions ◽  
Medial Amygdaloid Nucleus ◽  
Amygdaloid Nuclei

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.

scholarly journals Sex-Specific Effects of Relaxin-3 on Food Intake and Brain Expression of Corticotropin-Releasing Factor in Rats

Endocrinology ◽  
2014 ◽  
Vol 156 (2) ◽  
pp. 523-533 ◽  
Author(s):  
Christophe Lenglos ◽  
Juliane Calvez ◽  
Elena Timofeeva
Keyword(s):  
Food Intake ◽  
Plasma Corticosterone ◽  
Corticotropin Releasing Factor ◽  
Female Rats ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Specific Effects ◽  
Male And Female Rats

This study compared the effects of relaxin-3 (RLN3) on food intake, plasma corticosterone, and the expression of corticotropin-releasing factor (CRF) in male and female rats. RLN3 was injected into the lateral ventricle at 25, 200, and 800 pmol concentrations. RLN3 at 25 pmol increased food intake (grams) at 30 and 60 minutes after injection in female but not male rats. Female rats also showed higher increase in relative to body weight (BW) food intake (mg/g BW) for all RLN3 concentrations at 30 minutes and for 800 pmol of RLN3 at 60 minutes. Moreover, RLN3 at 800 pmol significantly increased 24-hour BW gain in female but not male rats. At 60 minutes after administration, 800 pmol of RLN3 produced a significant increase in plasma corticosterone and in the expression of CRF and c-fos mRNAs in the parvocellular paraventricular hypothalamic nucleus (PVN) in male but not female rats. The levels of c-fos mRNA in the magnocellular PVN were increased by RLN3 but did not differ between the sexes. Conversely, expression of CRF mRNA in the medial preoptic area was increased in female rats but was not sensitive to 800 pmol of RLN3. In the bed nucleus of the stria terminalis, 800 pmol of RLN3 significantly increased CRF mRNA expression in female but not male rats. Therefore, female rats showed more sensitivity and stronger food intake increase in response to RLN3. The differential effects of RLN3 on CRF expression in the PVN and bed nucleus of the stria terminalis may contribute to the sex-specific difference in the behavioral response.

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