The perifornical area: the major focus of (a) patchily distributed hypothalamic neuropeptide Y-sensitive feeding system(s)

Stanley, B. Glenn; Magdalin, William; Seirafi, A.; Thomas, William J. W.; Leibowitz, Sarah F.

doi:10.1016/0006-8993(93)90382-w

Cited by 237 publications

(106 citation statements)

References 63 publications

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“…Interestingly, these key feeding-regulatory molecules, leptin and NPY, exert opposite influences on eating. Leptin is linked to inhibition of eating (Friedman and Halaas, 1998;Schwartz et al, 2000), whereas NPY is implicated in the initiation of feeding (Leibowitz, 1994;Schwartz et al, 2000), including the induction of eating in food-satiated rats (Stanley et al, 1993). Thus, the BLA could mediate potentiation of eating by learned cues through activation of NPY, inhibition of leptin-mediated mechanisms, or regulation of both of these components of feeding systems.…”

Section: Discussionmentioning

confidence: 99%

Amygdalo-Hypothalamic Circuit Allows Learned Cues to Override Satiety and Promote Eating

et al. 2002

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Organisms eat not only in a response to signals related to energy balance. Eating also occurs in response to "extrinsic," or environmental, signals, including learned cues. Such cues can modify feeding based on motivational value acquired through association with either rewarding or aversive events. We provide evidence that a specific brain system, involving connections between basolateral amygdala and the lateral hypothalamus, is crucial for allowing learned cues (signals that were paired with food delivery when the animal was hungry) to override satiety and promote eating in sated rats. In an assessment of second-order conditioning, we also found that disconnection of this circuitry had no effect on the ability of a conditioned cue to support new learning. Knowledge about neural systems through which food-associated cues specifically control feeding behavior provides a defined model for the study of learning that may be informative for understanding mechanisms that contribute to eating disorders and more moderate forms of overeating.Key words: amygdala; hypothalamus; eating; feeding behavior; learning; goal-directed behavior; motivation Mild to severe obesity, estimated to affect ϳ60% of the adult population in developed countries, is a risk factor for a range of diseases (United States Department of Health and Human Services, 1999). Despite adverse health consequences, difficulties in achieving and maintaining weight control are common. Overeating is attributable, at least in part, to the fact that food consumption is powerfully influenced by a variety of environmental factors that are unrelated to energy requirements (Rodin, 1981;Booth, 1989). Eating can be socially facilitated (De Castro, 1997), and cues that become associated with food when hunger prevails can increase eating in satiated states (Weingarten, 1983).Recent research is beginning to define the neural systems through which such psychological processes influence eating. Under conditions that strongly potentiate feeding, laboratory rats with neurotoxic lesions of the basolateral amygdalar area (BLA) [including basolateral ("basal"), basomedial ("accessory basal"), and lateral nuclei] fail to increase eating in the presence of a conditioned stimulus (CS) that was previously paired with food (Gallagher, 2000;Holland et al., 2002). The BLA has anatomical connections with neural circuits in the hypothalamus that control feeding behavior (Elmquist et al., 1999;Swanson, 2000;DeFalco et al., 2001;Petrovich et al., 2001). It sends substantial, topographically organized projections to the lateral hypothalamic area (LHA) (Petrovich et al., 2001), which forms part of the feeding circuit and historically has been linked to initiation of feeding (Elmquist et al., 1999).The current investigation examined potentiation of feeding by a CS in rats with a preparation that disconnects the BLA and the LHA. Here we report that the BLA-LHA system is crucial for allowing learned cues to override satiety signals and stimulate eating in sated states. We further show that t...

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Section: Discussionmentioning

confidence: 99%

Amygdalo-Hypothalamic Circuit Allows Learned Cues to Override Satiety and Promote Eating

et al. 2002

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“…Dopamine has a strong inhibitory effect on feeding when applied to the perifornical hypothalamic area, where it also functions to antagonize the stimulatory effects of NPY on feeding. 32 We have recently demonstrated that BCaSKF treatment dramatically reduces elevated hypothalamic NPY mRNA and protein concentrations in obaob mice, 33,34 which may be expected to facilitate a reduction in hyperphagia and an improvement in glucose homeostasis. 35 Furthermore, BC treatment of hamsters normalizes the obese, glucose intolerant condition, while reducing elevated metabolism of noradrenaline and serotonin within the ventromedial hypothalamus, 36 increases in which function to stimulate lipolysis and hepatic glucose output.…”

Section: Dopaminergic Agonists Improve Diabetes In Obaob Micementioning

confidence: 97%

Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists

et al. 1999

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OBJECTIVE: We previously reported that a two week treatment with SKF 38393 (SKF, a dopamine D 1 receptor agonist), plus bromocriptine (BC, a dopamine D 2 receptor agonist) acted synergistically to normalize hyperphagia, body fat, hyperglycaemia and hyperlipidaemia in obaob mice. The present study further investigates the biochemical mechanisms triggered by this drug treatment. DESIGN: Six week old female C57BLa6J obaob mice were divided into three groups and treated for two weeks with either BC and SKF, vehicle (control), or vehicle and pair fed to match the drug-treated group's daily food intake. RESULTS: BCaSKF treatment reduced food consumption by 55%, and treated mice weighed less than either pair fed or ad libitum fed controls after two weeks of treatment. Moreover, oxygen consumption was increased by 2.4-fold and the respiratory quotient (RQ) decreased from 1.23 to 0.96 (indicating a reduction in de novo lipogenesis) by drug treatment relative to ad libitum fed controls, but these parameters were unaffected by pair feeding control mice. The treatment also reduced blood glucose and free fatty acids (FFA) relative to pair fed and ad libitum fed controls. BCaSKF treatment (but not pair feeding) concurrently reduced lipolysis, lipogenic enzyme activities and hepatic gluconeogenic enzyme activities. Treatment also increased hepatic concentrations of glycogen and xylulose-5-phosphate (X-5-P), a key stimulator of glycolysis. Finally, BCaSKF, but not pair feeding, reduced the circulating concentrations of thyroxine and corticosterone, two hormones known to increase lipolysis, lipogenesis and hyperglycaemia. Drug treatment also increased serum dehydroepiandrosterone (DHEA) sulfate concentrations, an inhibitor of body fat store accumulation. CONCLUSION: These ®ndings demonstrate that BCaSKF treatment not only normalizes hyperphagia of obaob mice, but also redirects several metabolic and endocrine activities, independent of its effects on feeding to improve the obese-diabetic syndrome in obaob mice.

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“…Indeed, the perifornical area has been found to be more sensitive to NPY-elicited feeding than the PVN (Stanley et al 1993). The LHA/perifornical area contains neurons expressing melanin-concentrating hormone (MCH) (Marsh et al 2002).…”

Section: Dmhmentioning

confidence: 99%

Appetite control

Wynne¹,

Stanley²,

McGowan³

et al. 2005

Journal of Endocrinology

473

403

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Our understanding of the physiological systems that regulate food intake and body weight has increased immensely over the past decade. Brain centres, including the hypothalamus, brainstem and reward centres, signal via neuropeptides which regulate energy homeostasis. Insulin and hormones synthesized by adipose tissue reflect the long-term nutritional status of the body and are able to influence these circuits. Circulating gut hormones modulate these pathways acutely and result in appetite stimulation or satiety effects. This review discusses central neuronal networks and peripheral signals which contribute energy homeostasis, and how a loss of the homeostatic process may result in obesity. It also considers future therapeutic targets for the treatment of obesity.

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The perifornical area: the major focus of (a) patchily distributed hypothalamic neuropeptide Y-sensitive feeding system(s)

Cited by 237 publications

References 63 publications

Amygdalo-Hypothalamic Circuit Allows Learned Cues to Override Satiety and Promote Eating

Amygdalo-Hypothalamic Circuit Allows Learned Cues to Override Satiety and Promote Eating

Biochemical mechanisms responsible for the attenuation of diabetic and obese conditions in ob/ob mice treated with dopaminergic agonists

Appetite control

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