Guest guest Posted December 8, 2004 Report Share Posted December 8, 2004 Hi All, We have little drug abuse among us, but the below seems of interest in this area. The definition of amphetamine is: " Drug of abuse that acts by increasing extraneuronal dopamine in midbrain. Thought to displace dopamine in synaptic vesicles, leading to increased synaptic levels. " " Leptin, a circulating hormone secreted from adipocytes, is an index of adiposity and is reduced by caloric restriction and weight loss. " http://tinyurl.com/532r9 Yet the pdf not available below states: " Lateral ventricular infusion of leptin, using a regimen that decreases food intake and body weight in ad libitum fed rats (12 mug/day), had no effect on the locomotor response to d-amphetamine in food-restricted rats that were maintained at 80% of prerestriction body weight. " Can this be correct? Physiol Behav. 2004 Dec 15;83(3):377-81. Effects of chronic ICV leptin infusion on motor-activating effects of d-amphetamine in food-restricted and ad libitum fed rats. Hao J, Cabeza de Vaca S, Carr KD. ... endocrine adiposity hormones, such as leptin, may regulate appetitively motivated behavior by modulating brain dopamine function. By extension, it has been hypothesized that the increased behavioral sensitivity of food-restricted, underweight rats to psychostimulant challenge may be triggered by the accompanying hypoleptinemia. The purpose of the present study was to determine whether two weeks of continuous intracerebroventricular (ICV) infusion of leptin alters the motor-activating effect of d-amphetamine (0.75 mg/kg, IP) in food- restricted rats. Lateral ventricular infusion of leptin, using a regimen that decreases food intake and body weight in ad libitum fed rats (12 mug/day), had no effect on the locomotor response to d-amphetamine in food-restricted rats that were maintained at 80% of prerestriction body weight. This result may indicate that hypoleptinemia is not involved in the induction/maintenance of neuroadaptations that mediate enhanced behavioral sensitivity to psychostimulant challenge. Interestingly, ad libitum fed rats treated with leptin displayed an increased locomotor response to d-amphetamine that was most prominent 3-5 days after termination of the infusion. Body weights and d-amphetamine sensitivity of these subjects returned to control values by 8-10 days postinfusion. The enhanced behavioral sensitivity to d-amphetamine in leptin-treated ad libitum fed rats may be a by-product of adipose depletion and, if so, would further support involvement of a peripheral signal other than hypoleptinemia in the modulation of central sensitivity to psychostimulant challenge. PMID: 15581659 [PubMed - in process] Cheers, Alan Pater Quote Link to comment Share on other sites More sharing options...
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