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731.
Abstract: The present study addressed the possibility that disinhibition of serotonin (5-HT) autoreceptor-mediated negative feedback might potentiate the elevation of nerve terminal 5-HT output induced by selective 5-HT reuptake blockade. To this end, rats were given citalopram and the 5-HT autoreceptor-blocking agents ( S )-UH-301 (5-HT1A) and (−)-penbutolol (5-HT1A/1B), and the effect on extracellular 5-HT in the ventral hippocampus was monitored by means of in vivo microdialysis. Citalopram (5 mg/kg, s.c.) approximately doubled the 5-HT output, a response that was markedly augmented by ( S )-UH-301 (3 mg/kg, s.c.) and (−)-penbutolol (8 mg/kg, s.c.) and by combined treatment with ( S )-UH-301 (3 mg/kg, s.c.) plus (−)-penbutolol (1 μ M ; via the dialysis perfusion medium), but not by (−)-penbutolol (1 μ M ) alone. These findings provide evidence that 5-HT, in particular 5-HT1A, autoreceptor-mediated negative feedback mechanisms are pivotal in determining the nerve terminal 5-HT output level after 5-HT reuptake inhibition. These findings have important implications for the interplay between different processes controlling 5-HT transmission in vivo and might possibly offer a lead toward novel, therapeutically exploitable principles.  相似文献   
732.
We used single-family crosses to confirm the Mendelian interpretation of allozyme variation and to examine linkage relationships at five polymorphic loci in freshwater and anadromous threespine sticklebacks (Gasterosteus aculeatus) from the Little Campbell River, British Columbia. The electrophoretic pattern of a sixth locus, mitochondrial NADP-dependent isocitrate dehydrogenase (IDH), was found to be sexually dimorphic but otherwise invariant in sticklebacks. This raised the possibility of a sex-linked Idh locus. No differences in IDH quantity or substrate affinities (apparent Km values) were detected between male and female sticklebacks. The electrophoretic pattern of IDH expression was not changed in sticklebacks in which sexual development was altered by hormonal treatment.  相似文献   
733.
734.
Objective: To determine whether meal size is related to body mass index (BMI) in obese subjects with binge-eating disorder (BED). Research Methods and Procedures: Five groups of subjects each consumed two laboratory-test meals on nonconsecutive days. Forty-two women, categorized by BMI and BED diagnosis, were instructed to “binge” during one meal and to eat “normally” during another. Eighteen women had BMI values >38 kg/m2 (more-obese) and 17 had BMI values between 28 to 32 kg/m2 (less-obese). Twelve of the more-obese and nine of the less-obese individuals met Diagnostic and Statistical Manual (DSM)-IV criteria for BED. Seven normal-weight women also participated as controls. Results: Subjects with BED ate significantly more in both meals than subjects without BED. Binge meals were significantly larger than normal meals only among subjects with BED. The more-obese subjects with BED ate significantly more than the less-obese subjects with BED, but only when they were asked to binge. Intake of the binge meal was significantly, positively correlated with BMI among subjects with BED. Subjects with BED reported significantly higher satiety ratings after the binge than after the normal meal, but subjects without BED reported similar ratings after both meals. Regardless of instructions and diagnosis, obese subjects consumed a significantly higher percentage of energy from fat (38.5%) than did normal-weight subjects (30.8%). Discussion: During binge meals, the energy intake of subjects with BED is greater than that of individuals of similar body weight without BED and is positively correlated with BMI.  相似文献   
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