Neuropeptide Y administration into the third ventricle does not increase sucrose or ethanol self-administration but does affect the cortical EEG and increases food intake

Katner, Simon N.; Slawecki, Craig J.; Ehlers, Cindy L.

doi:10.1007/s00213-001-0950-9

Cited by 38 publications

(1 citation statement)

References 58 publications

(92 reference statements)

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“…Following initial studies in transgenic mice that seemed to suggest an inverse relationship between NPY and alcohol intake (Thiele et al, 1998), subsequent studies evaluated the ability of NPY to attenuate ethanol intake when administered intracerebroventricularly (ICV; Badia-Elder et al, 2001, 2003; Bertholomey et al, 2011; Gilpin et al, 2003, 2005, 2011; Katner et al, 2002b, Slawecki et al, 2000; Thorsell et al, 2005a,b). Results from these studies hinted that the ability of NPY to attenuate ethanol reinforcement might be modulated by the anxiolytic effects of NPY.…”

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y (NPY) in the central nucleus of the amygdala (CeA) does not affect ethanol-reinforced responding in binge-drinking, nondependent rats

Henderson

Czachowski

2012

Pharmacology Biochemistry and Behavior

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The central nucleus of the amygdala (CeA) has been implicated as having a significant role in mediating alcohol-drinking behavior. Neuropeptide Y (NPY) has been investigated as a potential pharmacotherapeutic due to its ability to attenuate ethanol intake, particularly when administered into the CeA. Previous research suggests, though the evidence is somewhat conflicting, that the efficacy of NPY is contingent upon genetic background and/or prior history of ethanol dependence in rats. However, studies looking at the effects of NPY in nonselected animals lacking a history of ethanol dependence have two factors that could impact the interpretation of the results: ethanol history/selection AND relatively low baseline ethanol intakes as compared to ethanol-dependent and/or genetically selected controls. The purpose of the present study was to generate higher baseline ethanol intakes upon which to examine the effects of NPY on ethanol and sucrose drinking in nonselected rats using a binge drinking model. Long Evans rats were trained to complete a single response requirement resulting in access to either 2% sucrose (Sucrose Group) or 2% sucrose/10% ethanol (Ethanol Group) for a 20-min drinking session. On treatment days, rats were bilaterally microinjected into the CeA with aCSF or one of three doses of NPY (0.25ug, 0.50ug, or 1.00ug/.5uL). Subjects in the Ethanol Group were consuming an average of 1.2 g/kg of ethanol (yielding BELs of ~90mg%) during the 20 minute access period following aCSF treatments. The results revealed that NPY had no effect on either sucrose or ethanol consumption or on appetitive responding (latency to respond). Overall, the findings indicate that even a history of binge-like ethanol consumption is not sufficient to recruit CeA NPY activity, and are consistent with previous studies showing that the role of NPY in regulating ethanol reinforcement in the CeA may be contingent upon a prior history of ethanol dependence.

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