Effect of dopamine-receptor blockade on stimulation-induced feeding

Streather, Angela; Bozarth, Michael A.

doi:10.1016/0091-3057(87)90358-3

Cited by 12 publications

(2 citation statements)

References 17 publications

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“…The boundaries of LH tissue (35) and the refractory periods (36) of corresponding fibers supporting the two behaviors are the same. Because LH stimulation increases dopamine release (10,30), and each behavior is attenuated by dopamine antagonists (20,21,37), it seemed reasonable that this was a common mechanistic element driving both responses. Indeed, early in vivo optogenetic studies have demonstrated convincingly that stimulation of midbrain dopamine neurons is sufficient for reward.…”

Section: Discussionmentioning

confidence: 99%

“…Temporally precise inhibition of VTA dopamine cell firing through optogenetic stimulation of VTA GABA neurons disrupts licking for sucrose solutions in hungry mice (19). Similarly, stimulation-induced eating in sated animals is attenuated by dopamine receptor antagonists at low doses that preserve locomotor function (20,21). Although dopamine is clearly necessary for the initiation of eating, its ability to promote eating in the absence of physiological need is unclear.…”

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confidence: 99%

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Control of food approach and eating by a GABAergic projection from lateral hypothalamus to dorsal pons

Marino

McDevitt

Gantz

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Electrical or optogenetic stimulation of lateral hypothalamic (LH) GABA neurons induces rapid vigorous eating in sated animals. The dopamine system has been implicated in the regulation of feeding. Previous work has suggested that a subset of LH GABA neurons projects to the ventral tegmental area (VTA) and targets GABA neurons, inhibiting them and thereby disinhibiting dopaminergic activity and release. Furthermore, stimulation-induced eating is attenuated by dopamine lesions or receptor antagonists. Here we explored the involvement of dopamine in LH stimulation-induced eating. LH stimulation caused sated mice to pick up pellets of standard chow with latencies that varied based on stimulation intensity; once food was picked up, animals ate for the remainder of the 60-s stimulation period. However, lesion of VTA GABA neurons failed to disrupt this effect. Moreover, direct stimulation of VTA or substantia nigra dopamine cell bodies failed to induce food approach or eating. Looking further, we found that some LH GABA fibers pass through the VTA to more caudal sites, where they synapse onto neurons near the locus coeruleus (LC). Similar eating was induced by stimulation of LH GABA terminals or GABA cell bodies in this peri-LC region. Lesion of peri-LC GABA neurons blocked LH stimulation-induced eating, establishing them as a critical downstream circuit element for LH neurons. Surprisingly, lesions did not alter body weight, suggesting that this system is not involved in the hunger or satiety mechanisms that govern normal feeding. Thus, we present a characterization of brain circuitry that may promote overeating and contribute to obesity.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Control of food approach and eating by a GABAergic projection from lateral hypothalamus to dorsal pons

Marino

McDevitt

Gantz

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Role of dopamine D-1 and D-2 receptor subtypes in mediating dopamine agonist effects on food consumption in rats

Martin‐Iverson

Dourish

1988

Psychopharmacology

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The effects of selective D-2 and D-1 dopamine (DA) receptor agonists on food consumption were investigated in free-feeding rats. A selective D-2 receptor agonist, (+)-4-propyl-9-hydroxynaphthoxazine (PHNO), increased the consumption of standard food pellets in the dose range of 7.5-120 micrograms/kg, while SKF 38393 (5.0 mg/kg), a selective D-1 receptor agonist, decreased food pellet intake. The increase in food pellet intake produced by PHNO was blocked by haloperidol (an antagonist relatively selective for the D-2 receptor at the dose used, 0.05 mg/kg) and SCH 23390 (20 micrograms/kg, a D-1 receptor selective antagonist). Increasing "arousal" by disturbance associated with repeated food weighing also increased food pellet consumption, but did not diminish PHNO-elicited feeding. However, the same range of doses of PHNO (7.5-120 micrograms/kg) which increased food pellet intake decreased consumption of a liquid diet, and had no overall effect on a highly palatable liquid diet. The increase in consumption of solid food induced by PHNO appears to be secondary to enhancement of chewing behaviors. In contrast, the decrease in food intake induced by SKF 39393 may be due to a direct action of the drug on neural feeding mechanisms.

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Norbinaltorphimine blocks the feeding but not the reinforcing effect of lateral hypothalamic electrical stimulation

Papadouka

Wolinsky

1993

Psychopharmacology

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The role of central kappa opioid receptors in the regulation of feeding and reward was evaluated using electrical brain stimulation paradigms in combination with the selective kappa antagonist, norbinaltorphimine (nor-BNI). Lateral ventricular injection of 10.0 and 50.0 nmol doses of nor-BNI increased the lateral hypothalamic stimulation frequency threshold for eliciting feeding behavior but had no effect on threshold for self-stimulation in the absence of food. This result is identical to those previously reported for naloxone and antibodies to dynorphin A and suggests that opioid activity is associated with feeding behavior rather than the eliciting brain stimulation. A further similarity between naloxone, dynorphin antiserum, and nor-BNI is their preferential effect on feeding threshold values obtained later, rather than initially, in a post-injection test session. This pattern of threshold elevation is shown to differ from that of the appetite suppressants, amphetamine and phenylpropanolamine, which elevate threshold uniformly throughout a post-injection test. The signature pattern of threshold elevation produced by opioid antagonism is consistent with the hypothesis that opioid activity is involved in the maintenance rather than the initiation of feeding. Specifically, it is hypothesized that a dynorphin A/kappa receptor mechanism is triggered by food taste and sustains feeding behavior by facilitating incentive reward.

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Effect of dopamine-receptor blockade on stimulation-induced feeding

Cited by 12 publications

References 17 publications

Control of food approach and eating by a GABAergic projection from lateral hypothalamus to dorsal pons

Control of food approach and eating by a GABAergic projection from lateral hypothalamus to dorsal pons

Role of dopamine D-1 and D-2 receptor subtypes in mediating dopamine agonist effects on food consumption in rats

Norbinaltorphimine blocks the feeding but not the reinforcing effect of lateral hypothalamic electrical stimulation

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