The effect of amygdaloid lesions on feeding, grooming and reproduction in rats

Schwartz, Neena B.; Kling, Arthur

doi:10.1007/bf01227295

Cited by 29 publications

(4 citation statements)

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“…Numerous studies have examined the effects of amygdaloid lesions on food intake and body weight in rats, resulting in a similar collection of inconsistent and contradictory results. Initial studies that employed large lesions that destroyed most of the amygdala reported hypophagia and weight loss (4,12,41,56,61,64,65). Subsequent studies of rats with smaller lesions aimed at the basolateral and/or lateral nuclei reported weight gain (8,23,43), no change in body weight (18,28,40,45,58,60), or even weight loss (14).…”

mentioning

confidence: 99%

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

Rollins

King

2000

American Journal of Physiology-Regulatory, Integrative and Comp

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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.

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mentioning

confidence: 99%

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

Rollins

King

2000

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The result was hypophagia and weight loss (e.g., Refs. 5,26,111,179,197,207,208). Subsequent studies that used smaller lesions to target specific amygdaloid nuclei reported inconsistent and conflicting results regarding daily food intake and body weight.…”

Section: Lesion Studies With Ratsmentioning

confidence: 99%

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

King¹

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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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.

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“…In a laboratory environment, rats with complete ablations of neocortex and hippocampal formation eventually eat, drink, and maintain energy and hydromineral balance (Schwartz & Kling, 1964;Sorenson & Ellison, 1970;Vanderwolf, Kolb, & Cooley, 1978). Indeed, a neodecorticate rat is able not only to respond to deficit signals (salt deprivation), it can also utilize learned information to redress the deficit (Wirsig & Grill, in press).…”

Section: Constructing Hunger In the Brainmentioning

confidence: 99%

The Physiological Mechanisms of Motivation

Pfaff¹

1982

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The effect of amygdaloid lesions on feeding, grooming and reproduction in rats

Cited by 29 publications

References 37 publications

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

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

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

The Physiological Mechanisms of Motivation

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