Overexpression of Neuropeptide Y in the Central Nucleus of the Amygdala Decreases Ethanol Self‐administration in “Anxious” Rats

Primeaux, Stefany D.; Wilson, Steven P.; Bray, George A.; York, David A.; Wilson, Marlene A.

doi:10.1111/j.1530-0277.2006.00092.x

Cited by 67 publications

(70 citation statements)

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“…These involve reward, pleasure, or choice and can override the hypothalamic homeostatic control pathways. Indeed, the intake of specific nutrients, including carbohydrates, fats, and alcohol can be affected by neuropeptide activity within the amygdala (3,4,36,47,48,55). The amygdala system is also well connected to other areas of the brain through numerous projections from and toward the cortex, other areas of the limbic system, areas of the hypothalamus or the brain stem (39).…”

Section: Discussionmentioning

confidence: 99%

High-fat diets induce a rapid loss of the insulin anorectic response in the amygdala

Boghossian

Lemmon

Park

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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(FI). The central bed nucleus of the amygdala (CeA), as other regions of the brain regulating feeding behavior, expresses insulin receptors. Our objectives were to show an insulin anorectic response in the amygdala, study the effect of high-fat diets on this response, and map the neural network activated by CeA insulin using c-Fos immunohistochemistry. Sprague-Dawley (SD) rats fitted with unilateral CeA cannulas were adapted to a low-fat (LFD) diet before they were fed a high-fat diet (HFD). Their feeding response to CeA saline or insulin (8 mU) was tested after 24 h, 72 h, or 7 days of being on a HFD. In a second experiment, SD rats were fed the HFD for 3, 7, or 49 days and were then refed with the LFD. They were tested for their insulin response before and after an HFD and every 3 days for the following weeks. Insulin tolerance tests were performed in a parallel group of rats. The CeA insulin stimulation c-Fos expression was studied to identify the distribution of activated neuronal populations. Feeding an HFD for 72 h or more induced a CeA, but not peripheral, insulin resistance, which was slowly reversed by LFD refeeding. The duration of HFD feeding determined the time frame for reversal of the insulin resistance. CeA insulin increased c-Fos in multiple brain regions, including the arcuate nucleus/paraventricular nucleus region of the hypothalamus. We conclude that the amygdala may be an important site for insulin regulation of food intake and may have a significant role in determining susceptibility to HFD-induced obesity. rat; food intake; central insulin sensitivity; limbic system THE INCREASING INCIDENCE OF obesity and type 2 diabetes presents a major health challenge, as well as a huge economic burden upon health care systems. Understanding the etiology of this "diabesity pandemic" (45), insulin resistance (23), and associated pathologies of the metabolic syndrome is essential if this epidemic is to be reversed. Environmental factors, such as the lack of exercise or the excessive consumption of food, associated with modern life styles, have been linked to the development of insulin resistance.Food intake regulation and energy balance are achieved through a complex coordination of peripheral signals and central regulatory circuitry (8,25). These processes determine the initiation, termination, size, composition and frequency of meals, and the long-term regulation of food intake in relation to body energy requirements. The hypothalamus has a central role in the regulation of feeding and of energy expenditure (52). It receives a variety of endocrine, neural, or metabolic information, relating the current status of body energy stores and feeding activity and integrates this information to help regulate the efferent pathways and match energy intake to energy expenditure. Central to these control mechanisms are the arcuate nuclei, the paraventricular nucleus (PVN), and the lateral hypothalamus, which are particularly important for the control of food intake (8, 25, 32, 52). However, many other regions of the...

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Section: Discussionmentioning

confidence: 99%

High-fat diets induce a rapid loss of the insulin anorectic response in the amygdala

Boghossian

Lemmon

Park

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Also, increases in amygdalar NPY expression suppress excessive drinking associated with repeated cycles of ethanol liquiddiet access and periods of abstinence in Wistar rats (Thorsell et al, 2007). Injection into the CeA of a viral vector encoding prepro-NPY selectively reduces ethanol drinking by Long Evans rats determined to be "anxious" based on behavior in an elevated plus maze (Primeaux et al 2006). Finally, Pandey and coworkers (2005) showed that infusion of NPY (100 pmol) into the CeA reduced ethanol drinking in P rats with continuous access to ethanol solution.…”

Section: Discussionmentioning

confidence: 99%

“…Viral vector-induced increases in amygdalar NPY expression blunt excessive drinking associated with repeated cycles of ethanol liquid-diet access and periods of abstinence in Wistar rats (Thorsell et al, 2007). Injection into the CeA of a viral vector encoding prepro-NPY reduces continuous access-ethanol drinking by "anxious," but not "nonanxious" Long Evans rats, divided based on behavior in an elevated plus maze (Primeaux et al 2006). Finally, P rats with a brief history of ethanol selfadministration consume less ethanol following NPY infusion into the CeA, and also following increases in NPY activity in the CeA produced via alterations in cAMP-responsive elementbinding protein (CREB) function (Pandey et al 2005).…”

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confidence: 99%

Neuropeptide Y administration into the amygdala suppresses ethanol drinking in alcohol-preferring (P) rats following multiple deprivations

Gilpin

Stewart

Badia-Elder

2008

Pharmacology Biochemistry and Behavior

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The present experiment examines the effects of NPY administered into the amygdala on ethanol drinking by alcohol-preferring P rats following long-term continuous ethanol access, with and without multiple periods of imposed ethanol abstinence. P rats had access to 15% (v/v) ethanol and water for 11 weeks followed by 2 weeks of ethanol abstinence, re-exposure to ethanol for 2 weeks, 2 more weeks of ethanol abstinence, and a final ethanol re-exposure. Immediately prior to the second ethanol re-exposure, 4 groups of rats received bilateral infusions NPY (0.25, 0.5, 1.0 μg) or artificial cerebrospinal fluid (aCSF) into the amygdala. Two additional groups were given uninterrupted ethanol access and were infused with a single NPY dose (1.0 μg) or aCSF. The highest NPY dose (1.0 μg) suppressed ethanol intake for 24 hrs in rats with a history of ethanol abstinence (i.e. deprivation) periods, but had no effect in rats with a history of continuous ethanol access. Water and food intakes were not altered. These results suggest that the amygdala mediates the suppressive effects of centrally administered NPY on ethanol drinking, and that NPY may block relapse-like drinking by opposing the anxiogenic effects of ethanol abstinence. KeywordsAlcohol-preferring rats; neuropeptide Y; abstinence; deprivation; anxiety; amygdala; allostasis Dysregulation of brain neuropeptide Y (NPY) systems involved in emotionality may mediate both the negative affective state that defines ethanol abstinence and the negative reinforcing effects of ethanol during relapse drinking (Valdez & Koob, 2004). NPY decreases anxiety-like behavior in rats in multiple behavioral assays (Heilig et al., 1989;1992;Broqua et al., 1995;Britton et al., 1997;Sajdyk et al., 1999Sajdyk et al., , 2008. The anxiolytic effects of NPY appear to be mediated by the central nucleus of the amygdala (CeA; Heilig et al., 1993), although a role has also been suggested for the basolateral nucleus of the amygdala (Sajdyk et al., 1999(Sajdyk et al., , 2008. Since there is a body of evidence suggesting that the CeA is involved in the regulation of both Corresponding Author: Nancy E. Badia-Elder, Department of Psychology, IUPUI, 402 N. Blackford Street, LD 124, Indianapolis, IN 46202, Phone:317-278-1815, Fax:317-274-6756, Email: nbadiael@iupui.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Davis, 1992) and ethanol drinking (McBride, 2002), the focus of this investigation was to examine the effects of NPY infusions into the CeA on ethanol intake. NIH Public AccessThe alcohol-preferring (P) and high alcohol drinking (HAD1) lines of r...

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“…NPY microinjection into the CeA suppresses alcohol consumption in alcohol-dependent and abstinent P rats (Gilpin et al 2008a,b), and also in rats showing innately high anxietylike behavior (Primeaux et al 2006 (Sajdyk et al 2002) in anxiety-like behavior. Mouse studies indicate that Y 1 Rs mediate the suppressive effects of NPY on alcohol drinking (Thiele et al 2002;Sparta et al 2004;Eva et al 2006).…”

Section: Neuropeptide Y (Npy) and Alcohol-related Behaviormentioning

confidence: 99%

The Central Amygdala and Alcohol: Role of -Aminobutyric Acid, Glutamate, and Neuropeptides

Roberto

Gilpin

Siggins

2012

Cold Spring Harbor Perspectives in Medicine

122

107

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Alcohol dependence is a chronically relapsing disorder characterized by compulsive drug seeking and drug taking, loss of control in limiting intake, and the emergence of a withdrawal syndrome in the absence of the drug. Accumulating evidence suggests an important role for synaptic transmission in the central amygdala (CeA) in mediating alcohol-related behaviors and neuroadaptative mechanisms associated with alcohol dependence. Acute alcohol facilitates g-aminobutyric acid-ergic (GABAergic) transmission in CeA via both pre-and postsynaptic mechanisms, and chronic alcohol increases baseline GABAergic transmission. Acute alcohol inhibits glutamatergic transmission via effects at N-methyl-D-aspartate (NMDA) and AMPA receptors in CeA, whereas chronic alcohol up-regulates N-methyl-D-aspartate receptor (NMDAR)-mediated transmission. Pro-(e.g., corticotropin-releasing factor [CRF]) and anti-stress (e.g., NPY, nociceptin) neuropeptides affect alcohol-and anxiety-related behaviors, and also alter the alcohol-induced effects on CeA neurotransmission. Alcohol dependence produces plasticity in these neuropeptide systems, reflecting a recruitment of those systems during the transition to alcohol dependence.

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Overexpression of Neuropeptide Y in the Central Nucleus of the Amygdala Decreases Ethanol Self‐administration in “Anxious” Rats

Abstract: These results suggest that virally mediated alterations in NPY levels in the CeA differentially affect ethanol consumption in rats with low and high basal levels of anxiety.

Cited by 67 publications

References 53 publications

High-fat diets induce a rapid loss of the insulin anorectic response in the amygdala

High-fat diets induce a rapid loss of the insulin anorectic response in the amygdala

Neuropeptide Y administration into the amygdala suppresses ethanol drinking in alcohol-preferring (P) rats following multiple deprivations

The Central Amygdala and Alcohol: Role of -Aminobutyric Acid, Glutamate, and Neuropeptides

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