Antipsychotic-Like Actions of the Satiety Peptide, Amylin, in Ventral Striatal Regions Marked by Overlapping Calcitonin Receptor and RAMP-1 Gene Expression

Baisley, Sarah K.; Bremer, Quentin; Bakshi, Vaishali P.; Baldo, Brian A.

doi:10.1523/jneurosci.2260-13.2014

Cited by 11 publications

(8 citation statements)

References 49 publications

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“…Recently, antipsychotic-like actions of amylin were demonstrated after central injections (Baisley et al, 2014). Amylin infusion into the accumbens shell, but not the dorsal striatum, reversed amphetamineinduced prepulse inhibition without affecting baseline startle.…”

Section: E Antipsychotic-like Actions Of Amylinmentioning

confidence: 99%

Amylin: Pharmacology, Physiology, and Clinical Potential

Hay¹,

Chen²,

Lutz³

et al. 2015

Pharmacol Rev

289

297

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Section: E Antipsychotic-like Actions Of Amylinmentioning

confidence: 99%

Amylin: Pharmacology, Physiology, and Clinical Potential

Hay¹,

Chen²,

Lutz³

et al. 2015

Pharmacol Rev

289

297

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“…It has been shown that m-OR stimulation outside the Acb, in select dorsal striatal regions, increases feeding (Bakshi and Kelley, 1993a;DiFeliceantonio et al, 2012). However, these striatal territories possess neither AMY-R binding nor expression of AMY-R-component genes (Sexton et al, 1994;van Rossum et al, 1994;Baisley et al, 2014). Therefore, our results indicate that DAMGO-induced hyperphagia is only reduced when amylin is infused into striatal regions rich in AMY-R receptors, suggesting that targeting this receptor may represent a mechanism for modulating opioid effects in the ventral striatum specifically.…”

Section: Discussionmentioning

confidence: 99%

“…The 0.25 mg/ 0.5 ml/side dose of DAMGO was chosen because it has been shown to elicit robust feeding in satiated rats (eg, Perry et al, 2009). The dose of the AMY-R antagonist AC187 (Hay et al, 2005) was chosen because in our laboratory it altered prepulse inhibition upon intra-AcbSh infusion (Baisley et al, 2014). In other literature, an AC187 dose of 30 mg but not 10 mg delivered into lower levels of the CNS increased food intake in rats (Lutz et al, 1997;Mollet et al, 2004).…”

Section: Drugs and Microinfusionsmentioning

confidence: 99%

“…Less is known about feeding-modulatory effects of amylin in the telencephalon, despite the fact that one of the densest concentrations of high-affinity amylin-binding sites, and expression of component genes encoding the high-affinity AMY-R (Poyner et al, 2002) is found in the medial nucleus accumbens shell (AcbSh) (Sexton et al, 1994;van Rossum et al, 1994;Baisley et al, 2014). This zone of intense AMY-R binding conforms remarkably well with the circumscribed medial AcbSh area from which intense feeding responses are elicited by GABA or m-opioid receptor (m-OR) stimulation (Bakshi and Kelley, 1993;Stratford and Kelley, 1997;Zhang and Kelley, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Amylin Receptor Signaling in the Nucleus Accumbens Negatively Modulates μ-opioid-Driven Feeding

Baisley

Baldo

2014

Neuropsychopharmacol

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Amylin is a peptide co-secreted with insulin that penetrates into the brain, and produces satiation-like effects via actions in the brainstem, hypothalamus, and mesencephalon. Little is known, however, about the effects of amylin in the nucleus accumbens shell (AcbSh), where a circumscribed zone of intense amylin receptor (AMY-R) binding overlaps reported mappings of a 'hotspot' for m-opioid receptor (m-OR) amplification of food reward. Here, the ability of intra-AcbSh AMY-R signaling to modulate m-OR-driven feeding was explored. Amylin (1-30 ng) was administered with the m-OR agonist, D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) (0.25 mg), directly into the AcbSh of ad libitum-maintained rats. Amylin dose-dependently reversed DAMGO-induced hyperphagia; 3 ng of amylin reduced DAMGO-mediated feeding by nearly 50%. This dose was, however, completely ineffective at altering DAMGO-induced feeding in the anterior dorsal striatum. Intra-AcbSh amylin alone (3-30 ng) modestly suppressed 10% sucrose intake in ad libitum-maintained rats, and chow in food-deprived rats, but only at the 30-ng dose. This result indicates that reversal of AcbSh DAMGO-induced feeding at a 10-fold lower dose was neither due to malaise nor motoric impairment. Finally, intra-AcbSh infusion of the AMY-R antagonist, AC187 (20 mg), significantly attenuated the ability of prefeeding to suppress DAMGO-induced food intake, with no effects in non-prefed rats. Hence, AMY-R signaling negatively modulates m-OR-mediated appetitive responses at the level of the AcbSh. The results with AC187 indicate that endogenous AMY-R transmission in the AcbSh curtails opioid function in the postprandial period, suggesting a novel pathway for peripheral-central integration in the control of appetitive motivation and opioid reward.

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“…Recent research has brought to light a putative novel role for amylin in processes related to cognition, including possible ameliorative effects on neurodegenerative and psychotic disorders [33, 34]. Although this area of research is still relatively new, the notion that amylin-based pharmacotherapies could be used for treatment of such disorders is already being considered [35].…”

Section: Introductionmentioning

confidence: 99%

Amylin-mediated control of glycemia, energy balance, and cognition

Mietlicki‐Baase

2016

Physiology & Behavior

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Amylin, a peptide hormone produced in the pancreas and in the brain, has well-established physiological roles in glycemic regulation and energy balance control. It improves postprandial blood glucose levels by suppressing gastric emptying and glucagon secretion; these beneficial effects have led to the FDA-approved use of the amylin analog pramlintide in the treatment of diabetes mellitus. Amylin also acts centrally as a satiation signal, reducing food intake and body weight. The ability of amylin to promote negative energy balance, along with its unique capacity to cooperatively facilitate or enhance the intake- and body weight-suppressive effects of other neuroendocrine signals like leptin, have made amylin a leading target for the development of novel pharmacotherapies for the treatment of obesity. In addition to these more widely studied effects, a growing body of literature suggests that amylin may play a role in processes related to cognition, including the neurodegeneration and cognitive deficits associated with Alzheimer's disease (AD). Although the function of amylin in AD is still unclear, intriguing recent reports indicate that amylin may improve cognitive ability and reduce hallmarks of neurodegeneration in the brain. The frequent comorbidity of diabetes mellitus and obesity, as well as the increased risk for and occurrence of AD associated with these metabolic diseases, suggests that amylin-based pharmaceutical strategies may provide multiple therapeutic benefits. This review will discuss the known effects of amylin on glycemic regulation, energy balance control, and cognitive/motivational processes. Particular focus will be devoted to the current and/or potential future clinical use of amylin pharmacotherapies for the treatment of diseases in each of these realms.

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Antipsychotic-Like Actions of the Satiety Peptide, Amylin, in Ventral Striatal Regions Marked by Overlapping Calcitonin Receptor and RAMP-1 Gene Expression

Cited by 11 publications

References 49 publications

Amylin: Pharmacology, Physiology, and Clinical Potential

Amylin: Pharmacology, Physiology, and Clinical Potential

Amylin Receptor Signaling in the Nucleus Accumbens Negatively Modulates μ-opioid-Driven Feeding

Amylin-mediated control of glycemia, energy balance, and cognition

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