Acute methylphenidate treatments reduce sucrose intake in restricted-fed bingeing rats.
Recent evidence suggests that methylphenidate HCl may be effective at limiting the frequency and the amount of binge eating. The present study investigated if daily treatments with methylphenidate reduced the bingeing-like behavior observed in restricted-fed adult male rats. Three groups (n = 6) received peripheral injections of methylphenidate in doses of 1.5 or 0.75 mg/kg/day, or saline, 3 days prior and 7 days during a previously characterized intermittent feeding regimen that results in a gradual increase of sucrose and food intake. The higher, but not the lower, dose of methylphenidate reduced sucrose intake to an asymptotic level starting after 3 days of the feeding protocol and concurrently led to an increase in the intake of chow. The high dose methylphenidate group also had two-fold lower plasma insulin levels compared with the saline-treated animals at the time of sacrifice on the last day of the feeding regimen. Further histological assays revealed that the methylphenidate treatments, irrespective of the dose used, resulted in selectively higher dopamine transporter and D2-like receptor labeled bindings in the shell region of the nucleus accumbens. These results suggest that relatively low-dose methylphenidate treatments may be effective for the management of binge eating by reducing the intake of palatable foods and may not interfere with short-term regulation of energy balance. These findings further support the notion that the mesoaccumbens dopamine system plays an important role in restricted access-induced sucrose bingeing in this rat model.
Bello
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NT
Department of Neural and Behavioral Sciences, The Pennsylvania State University, College of Medicine, 500 University Drive, H181, Hershey, PA 17033, USA. ntbello@psu.edu
Hajnal
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A
D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002032:Bulimia / Q000188:drug therapy* / Q000209:etiology; D000697:Central Nervous System Stimulants / Q000627:therapeutic use*; D003042:Cocaine / Q000031:analogs & derivatives / Q000493:pharmacokinetics; D004305:Dose-Response Relationship, Drug; D004326:Drinking / Q000187:drug effects; D004347:Drug Interactions; D004435:Eating / Q000187:drug effects*; D002149:Energy Intake / Q000187:drug effects; D005508:Food Deprivation; D007328:Insulin / Q000097:blood; D008297:Male; D008774:Methylphenidate / Q000627:therapeutic use*; D011485:Protein Binding / Q000187:drug effects; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D013395:Sucrose; D013469:Sulpiride / Q000031:analogs & derivatives / Q000493:pharmacokinetics
D000697:Central Nervous System Stimulants; D007328:Insulin; D019275:Radiopharmaceuticals; C045105:iodosulpride; D008774:Methylphenidate; C069723:2beta-carbomethoxy-3beta-(4-iodophenyl)tropane; D013395:Sucrose; D013469:Sulpiride; D003042:Cocaine