Reappearance of dynamic hyperphagia during the static phase in medial hypothalamic lesioned rats

King, Bruce M.; Gaston, Michael G.

doi:10.1016/0031-9384(77)90205-0

Cited by 10 publications

(2 citation statements)

References 33 publications

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“…The weight gains were less than those generally observed after lesions of the ventromedial hypothalamus (e.g., 34). Weight gain in rats with posterodorsal amygdaloid lesions generally plateaus 15 to 20 days after surgery, compared with 3 to 6 wk for rats with well-placed lesions of the ventromedial hypothalamus (34).…”

Section: Discussionmentioning

confidence: 94%

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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Section: Discussionmentioning

confidence: 94%

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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“…A major role for the stria terminalis, the direct pathway between the PDA and VMH, has also been established (22). However, it should be noted that the weight gain typically observed after bilateral VMH lesions is much greater than that observed after bilateral PDA lesions or stria terminalis transections (e.g., 4,19), and thus the PDA-stria terminalis pathway is most certainly only one of many influences upon the VMH affecting feeding behavior and body weight regulation. The amygdala itself can influence hypothalamic function by means other than the direct pathway of the stria terminalis.…”

Section: Discussionmentioning

confidence: 99%

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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Ventromedial hypothalamic lesions and weight gain in rats: Absence of a static phase

Hallonquist

Brandes

1981

Physiology & Behavior

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Reappearance of dynamic hyperphagia during the static phase in medial hypothalamic lesioned rats

Cited by 10 publications

References 33 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?

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

Ventromedial hypothalamic lesions and weight gain in rats: Absence of a static phase

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