No description available.

No description available.

Excitatory M5 muscarinic acetylcholine receptors are expressed at the highest level in the brain, in the ventromedial hypothalamus (VMH). M5 knockout (KO) mice emit fewer ultrasonic vocalizations (USVs) during mating, and show 40-50% lesser morphine-induced locomotion as compared to wild-type (WT) mice. Following viral transfection of M5 muscarinic receptors in the ventral tegmentum (VTA), KO mice depict restored mating-induced USVs and enhanced morphine-induced locomotion. The VMH is important for motivational processes, such as, feeding and producing USVs in rats. With a Herpes simplex virus (HSV), the M5 receptor gene was transfected into the VMH of WT mice. M5 transfection into neurons of the VMH increased locomotion in mice injected with 10mg/kg morphine. When a D2-selective dopamine blocker was injected into the same mice, locomotion was drastically reduced. There were no significant differences in amount of USVs produced. VMH may exert its effects on morphine through a DA dependent VTA pathway.

Excitatory M5 muscarinic acetylcholine receptors are expressed at the highest level in the brain, in the ventromedial hypothalamus (VMH). M5 knockout (KO) mice emit fewer ultrasonic vocalizations (USVs) during mating, and show 40-50% lesser morphine-induced locomotion as compared to wild-type (WT) mice. Following viral transfection of M5 muscarinic receptors in the ventral tegmentum (VTA), KO mice depict restored mating-induced USVs and enhanced morphine-induced locomotion. The VMH is important for motivational processes, such as, feeding and producing USVs in rats. With a Herpes simplex virus (HSV), the M5 receptor gene was transfected into the VMH of WT mice. M5 transfection into neurons of the VMH increased locomotion in mice injected with 10mg/kg morphine. When a D2-selective dopamine blocker was injected into the same mice, locomotion was drastically reduced. There were no significant differences in amount of USVs produced. VMH may exert its effects on morphine through a DA dependent VTA pathway.

No description available.

The objectives of the present study were to examine the effects of dietary fat type and level of energy intake on hypothalamic leptin binding affinity and membrane fatty acid composition, circulating leptin levels, and body weight homeostasis in rats. Animals were fed diets containing tallow, safflower oil, or menhaden oil (20% wt/wt) for 10 wks, ad libitum or at 60% of ad libitum intakes. Specific leptin binding could not be detected in hypothalamic membrane homogenates; hypothalamic leptin levels were unaffected by diet or energy intake. Levels of tracer exceeding assay reference values were found in homogenates, suggesting intra-membrane binding. Excess tracer levels were weakly associated (p < 0.07) with the sum of hypothalamic phospholipid monounsaturates. Restriction lowered weight gain and food intakes (p < 0.0001 for both). In hypothalamic phospholipids, energy restriction lowered levels of 18:3(n-3) and increased levels of 20:1(n-9), 20:4(n-6), and 22:4(n-6) (p < 0.05, p < 0.02, p < 0.05, and p < 0.04, respectively). Fat type and energy level interactively affected hypothalamic levels of 20:4(n-6), 22:5(n-3) and 22:6(n-3) (p < 0.05, p < 0.006, and p < 0.05, respectively). Restriction lowered circulating leptin levels (p < 0.0001); overall plasma leptin levels were marginally associated (p < 0.07) with hypothalamic 16:0 concentrations. The results of the study support previous findings suggesting that leptin binding at the level of the hypothalamic membrane may not be detectable. The results also support the lack of a dietary fat effect on plasma leptin levels and levels of certain hypothalamic fatty acids, such as 20:4(n-6), 22:4(n-6), and 22:5(n-3), with energy restriction. The findings of the study suggest a link between increased membrane fluidity, increased binding affinity, and lower circulating leptin levels, promoting the possibility that the biological actions of leptin can be controlled through dietary effects on

Freie Universiẗat, Diss., 2006--Berlin. / Dateiformat: zip, Dateien im PDF-Format.

Dissertation (Ph.D.).--University of Texas Graduate School of Biomedical Sciences at San Antonio, 2007. / Vita. Includes bibliographical references.

Ulm, Univ., Diss., 2008.

Freie Univ., Diss.--Berlin, 1997.