Hyperphagia and obesity in female rats with temporal lobe lesions

King, Bruce M.; Kass, Jenny M.; Cadieux, Nicole L.; Sam, Hoan; Neville, Katherine L.; Arceneaux, Elizabeth R.

doi:10.1016/0031-9384(93)90088-w

Cited by 36 publications

(23 citation statements)

References 42 publications

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“…The results of the present study confirm our earlier reports of excessive weight gains after electrolytic lesions of the most posterodorsal aspects of the amygdala in rats (50,51,84). Mean daily weight gains ranged from 10.6 to 16.2 g in the first 2-3 days after lesions.…”

Section: Body Weightsupporting

confidence: 93%

“…111), a minimum criterion for weight gain of 10 g/day was used to select animals with bilateral lesions for inclusion in the group to be processed for silver staining. Ten grams per day is at the high end of weight gain in the first few days after PDA lesions (50,51). Animals with unilateral or control lesions were not screened according to this weight gain criterion.…”

Section: Body Weightmentioning

confidence: 99%

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

King

Cook

Rossiter

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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King, Bruce M., Jack T. Cook, Kirk N. Rossiter, and Bethany L. Rollins. Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport. Am J Physiol Regul Integr Comp Physiol 284: R965-R982, 2003. First published November 14, 2002 10.1152/ajpregu.00249.2002.-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 (ϩ21 to ϩ32 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. nucleus accumbens; hypothalamus; stria terminalis SEVERAL RECENT STUDIES have demonstrated that bilateral electrolytic lesions of the amygdala in female rats can result in marked hyperphagia and excessive weight gains. Daily food intake nearly doubles, and weight gains of 20-30 g during the first 3 days after lesions are not unusual (e.g., 45, 50-53, 84). Weight gains of Ն100 g in 20-25 days have been observed (50, 51). The lesions result in a marked preference for carbohydrates (53). Although food intake eventually returns to normal, the excessive weight gain is maintained indefinitely, with a marked increase in adipose tissue (50).These results are similar to those reported many years ago for cats, dogs, and primates (including humans) given amygdaloid lesions or temporal lobectomies (e.g., 9, 32, 37, 70, 103). In the rat, the effective lesion site for hyperphagia and obesity has recently been identified as the posterodorsal part of the medial amygdaloid nucleus (MePD) and the intra-amygdaloid bed nucleus of the stria terminalis (BSTIA), together ...

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Section: Body Weightsupporting

confidence: 93%

Section: Body Weightmentioning

confidence: 99%

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

King

Cook

Rossiter

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Therefore, it is concluded that the effects of the two lesions are not additive and that the weight gain observed after VMH or PDA lesions represents damage at two different points in a common pathway. The mean total weight gain of 82.7 g observed in the unilateral VMH-contralateral PDA group over 40 days is consistent with the typical weight gains of 50 -80 g over 20 days previously observed in female rats with bilateral PDA lesions (15,16,18,20; see also 42).…”

Section: Discussionsupporting

confidence: 89%

“…Thus it can be concluded that female rats with either VMH or PDA lesions, whether bilateral or unilateral, are similar in that both display a dynamic and static phase of weight gain (4). Previous studies, as well as the present one, have demonstrated that the rate of weight gain in rats with PDA lesions is directly reflective of the hyperphagia (e.g., 15,20,23), and the hyperinsulinemia (16) probably helps to maintain the excess body weight. Activity level in rats with PDA lesions has not yet been monitored.…”

Section: Discussionsupporting

confidence: 65%

“…ventromedial hypothalamus; amygdala; stria terminalis; feeding behavior; body weight LESIONS OF THE MOST POSTERODORSAL part of the amygdala result in hyperphagia and excessive weight gain in rats (42). Female rats with bilateral lesions typically gain 50 -80 g in 20 days, and gains of as much as 100 g in 20 days have been observed (15,16,18,20,21). The obesity syndrome resembles that which follows lesions of the ventromedial hypothalamus (VMH) in many respects.…”

mentioning

confidence: 99%

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Combination unilateral amygdaloid and ventromedial hypothalamic lesions: evidence for a feeding pathway

Grundmann

Pankey

Cook

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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King. Combination unilateral amygdaloid and ventromedial hypothalamic lesions: evidence for a feeding pathway. Am J Physiol Regul Integr Comp Physiol 288: R702-R707, 2005; doi:10.1152/ajpregu.00460.2004.-Previous studies have reported hyperphagia and obesity in female rats with bilateral lesions of the most posterodorsal part of the amygdala. In rats with unilateral posterodorsal amygdaloid lesions, a dense pattern of anterograde degeneration appears in the ipsilateral ventromedial hypothalamus, but not the contralateral nucleus. In the present study, female rats with unilateral ventromedial hypothalamic lesions or sham lesions were given either sham lesions or unilateral lesions of the posterodorsal amygdala (PDA) 20 days later. Unilateral lesions of the ventromedial hypothalamus resulted in hyperphagia and excessive weight gain. Subsequent amygdaloid lesions that were contralateral to the initial hypothalamic lesions resulted in hyperphagia and additional excessive weight gains, but amygdaloid lesions ipsilateral to the initial hypothalamic lesions did not. It is concluded that the effects of the two lesions on body weight are not additive and that the PDA and ventromedial hypothalamus are part of the same ipsilateral pathway regulating feeding behavior and body weight regulation. ventromedial hypothalamus; amygdala; stria terminalis; feeding behavior; body weight LESIONS OF THE MOST POSTERODORSAL part of the amygdala result in hyperphagia and excessive weight gain in rats (42). Female rats with bilateral lesions typically gain 50 -80 g in 20 days, and gains of as much as 100 g in 20 days have been observed (15,16,18,20,21). The obesity syndrome resembles that which follows lesions of the ventromedial hypothalamus (VMH) in many respects. For example, the weight gains are greater in female rats than in male rats (23), and the animals are hyperinsulinemic even when food restricted (16) and do not respond appropriately to caloric challenges (24).Excessive weight gains have been produced with small lesions limited exclusively to the posterodorsal medial amygdaloid nucleus and the intra-amygdaloid bed nucleus of the stria terminalis (42). Examination of anterograde degeneration by the amino-cupric silver method in the brains of rats given unilateral posterodorsal amygdala (PDA) lesions revealed a dense pattern of degenerating terminals in areas that have previously been shown to be involved in various aspects of feeding behavior and/or body weight regulation (17). Particularly dense staining was observed in the VMH ipsilateral to the PDA lesion, but not in the contralateral VMH. There was little to no staining in the paraventricular hypothalamic nucleus.The pattern of anterograde degeneration observed after unilateral PDA lesions suggests an ipsilateral pathway mediating feeding behavior and body weight regulation. The major pathway between the PDA and VMH is the stria terminalis (5, 6, 39), and after unilateral PDA lesions there is dense degeneration in the dorsal component and medial part of the ventral componen...

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Contributions of the hippocampus and medial prefrontal cortex to energy and body weight regulation

Davidson¹,

Chan²,

Jarrard³

et al. 2008

Hippocampus

175

131

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The effects of selective ibotenate lesions of the complete hippocampus (CHip), the hippocampal ventral pole (VP), or the medial prefrontal cortex (mPFC) in male rats were assessed on several measures related to energy regulation (i.e., body weight gain, food intake, body adiposity, metabolic activity general behavioral activity, conditioned appetitive responding). The testing conditions were designed to minimize the nonspecific debilitating effects of these surgeries on intake and body weight. Rats with CHip and VP lesions exhibited significantly greater weight gain and food intake compared to controls. Furthermore, CHip-lesioned rats, but not rats with VP lesions, showed elevated metabolic activity, general activity in the dark phase of the light-dark cycle, and greater conditioned appetitive behavior, compared to control rats without these brain lesions. In contrast, rats with mPFC lesions were not different from controls on any of these measures. These results indicate that hippocampal damage interferes with energy and body weight regulation, perhaps by disrupting higher-order learning and memory processes that contribute to the control of appetitive and consummatory behavior.Much research on the causes of overeating and excessive weight gain has been directed at identifying the brain regions where metabolic and hormonal signals that stimulate or suppress intake are detected and utilized (Benoit et al., 2004;Cummings and Overduin, 2007;Leibowitz and Wortley, 2004;Seeley et al., 2004). Although specification of these physiological substrates will be central to any comprehensive account of food intake regulation, it is now clear that such accounts must also consider the role of learning and memory in the control of eating and appetitive behavior (Davidson et al., 2005;Higgs, 2005;Sclafani, 1997;Woods and Ramsay, 2000). In recent years, the hippocampus, a brain structure long considered critical to the performance of a number of learning and memory functions (Eichenbaum, 2006;Squire, 2004), has received increasing attention related to its potential involvement in energy regulation.This increased interest in possible involvement of hippocampus in energy regulation is based, in part, on findings that neurohormonal signals involved with meal termination (e.g., cholecystokinin), meal initiation, (e.g., ghrelin) and signaling the status of bodily energy Please correspond with: Terry L. Davidson,

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Hyperphagia and obesity in female rats with temporal lobe lesions

Cited by 36 publications

References 42 publications

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

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

Combination unilateral amygdaloid and ventromedial hypothalamic lesions: evidence for a feeding pathway

Contributions of the hippocampus and medial prefrontal cortex to energy and body weight regulation

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