neuropeptide-y and Alcoholic-Intoxication

Topics: Alcohol Drinking; Alcoholic Intoxication; Animals; Ethanol; Feeding Behavior; Humans; Mice; Mice, Mutant Strains; Neuropeptide Y; Rats

Multiple episodes of ethanol intoxication and withdrawal result in progressive, irreversible intensification of the withdrawal reaction, a process termed "ethanol withdrawal kindling." Previous studies show that a single episode of chronic ethanol intoxication and withdrawal causes prominent changes in neuropeptide Y (NPY) and its receptors that have been implicated in regulating withdrawal hyperexcitability. This study for the first time examined the NPY system during ethanol withdrawal kindling.. Ethanol withdrawal kindling was studied in rats receiving 16 episodes of 2 days of chronic ethanol intoxication by intragastric intubations followed by 5 days withdrawal. The study included 6 groups: 4 multiple withdrawal episode (MW) groups [peak withdrawal plus (MW+)/minus (MW-) seizures, 3-day (MW3d), and 1-month (MW1mth) withdrawal], a single withdrawal episode group (SW), and an isocalorically fed control group. Gene expression of NPY and its receptors Y1, Y2, and Y5 was studied in the hippocampal dentate gyrus (DG) and CA3/CA1, as well as piriform cortex (PirCx), and neocortex (NeoCx).. MW+/- as well as SW groups showed decreased NPY gene expression in all hippocampal areas compared with controls, but, in the DG and CA3, decreases were significantly smaller in the MW- group compared with the SW group. In the MW+/- and SW groups, Y1, Y2, and Y5 mRNA levels were decreased in most brain areas compared with controls; however, decreases in Y1 and Y5 mRNA were augmented in the MW+/- groups compared with the SW group. The MW+ group differed from the MW- group in the PirCx, where Y2 gene expression was significantly higher.. Multiple withdrawal episodes reversibly decreased NPY and NPY receptor mRNA levels at peak withdrawal, with smaller decreases in NPY mRNA levels and augmented decreases in Y1/Y5 mRNA levels compared with a SW episode. Multiple withdrawal-induced seizures increased the Y2 mRNA levels in PirCx. These complex changes in NPY system gene expression could play a role in the ethanol withdrawal kindling process.

Topics: Alcohol-Induced Disorders, Nervous System; Alcoholic Intoxication; Animals; Central Nervous System Depressants; Cerebral Cortex; Ethanol; Gene Expression Regulation; In Situ Hybridization; Kindling, Neurologic; Male; Neuropeptide Y; Rats; Rats, Wistar; Receptors, Neuropeptide Y

The effects of acute ethanol administration on the ingestion of NaCl and food were assessed in adult rats subjected to 1-hr drinking and feeding tests 30 min after intraperitoneal administration of ethanol. Ethanol pretreatment did not induce spontaneous NaCl ingestion, but significantly potentiated angiotensin II-stimulated salt appetite, but not water intake, in a dose-dependent manner. Similarly, ethanol pretreatment significantly potentiated neuropeptide Y-stimulated food intake in nonfasted rats, but did not, by itself, cause spontaneous food ingestion. Ethanol pretreatment also significantly blunted pituitary secretion of oxytocin in response to multiple excitatory stimuli. Finally, administration of oxytocin intracerebroventricularly prevented the ethanol-induced potentiation of salt appetite elicited by angiotensin II. In view of our previous findings that central oxytocin secretion inhibits both NaCl and food intake, we propose that ethanol potentiates the ingestion of various solutes in rats, in part, by inhibiting brain-projecting oxytocinergic pathways concurrently with its well-known effects to inhibit pituitary oxytocin secretion.

Topics: Alcoholic Intoxication; Animals; Dose-Response Relationship, Drug; Drinking; Eating; Ethanol; Male; Neural Inhibition; Neuropeptide Y; Oxytocin; Pituitary Gland; Rats; Rats, Sprague-Dawley; Renin-Angiotensin System; Water-Electrolyte Balance