An electrophysiological preparation of Ascaris suum pharyngeal muscle suitable for recording changes of input conductance using a 2-microelectrode current clamp and pharmacological study is described. The preparation is shown to contain a glutamate-gated Cl (ion sensitive) channel sensitive to the avermectin analogue, milbemycin D. The application of glutamate produces a dose-dependent increase in Cl conductance and the effect of glutamate is potentiated by milbemycin D. Milbemycin D also produced a dose-dependent increase in input conductance.

Activity-based anorexia is characterized by suppressed food intake and excessive physical activity. These behaviors are typical of persons with anorexia nervosa. Activity of the hypothalamic-pituitary-adrenal axis is known to be elevated in anorexia nervosa. We investigated the status of this axis in activity-based anorexia. Meal fed-control (MFC) and meal fed-wheel running (MFWR) rats were given access to food for 90 min daily; MFWR animals were allowed access to an activity wheel the remainder of the day. The experiment terminated when MFWR animals reached 75% of preexperimental body weight (males 3.9 +/- 0.3 d; females 4.2 +/- 0.2 d). Male and female MFWR rats consumed less food than MFC animals, while maintaining a high level of wheel running. Corticosterone concentrations were significantly elevated in MFWR animals. Corticotropin-releasing hormone mRNA concentrations in the paraventricular nucleus were not different. Relative adrenal gland weights were greater and thymus gland weights were lower in MFWR animals. Changes in food intake could not be explained by differences in insulin, glucose, beta-hydroxybutyrate or norepinephrine concentrations. Our results suggest increased activity of the hypothalamic-pituitary-adrenal axis in activity-based anorexia.

A study of diurnal patterns of serum hormone levels was made in genetically lean and obese Zucker rats. Serum glucose and insulin were elevated in the obese through the 24-hour period; immunoreactive insulin being 12 times higher in the obese rat. A similar pattern of serum hormone levels in lean and obese rats was found for triiodothyronine, thyroid stimulating hormone and prolactin. At peak levels, prolactin was 2.5 times higher in lean than obese rats (P is less than .01). Thyroxine levels tended to be lower in the obese rats throughout the sampling periods when compared to lean rats. Growth hormone levels were severely depressed in the obese rat with the largest differences between lean and obese rats being observed during the light periods of the cycle. These differences in growth hormone secretion may be responsible for the impaired nitrogen retention in the obese rat. Serum levels of corticosterone were highest at the beginning of the dark cycle and decreased drastically thereafter in the lean rats. The obese rat did not exhibit a distinct pattern of corticosterone secretion and tended to be elevated throughout the periods tested.

Growth hormone and thyroid hormones have been implicated as important serum factors for adipocyte development in cell culture. Fetal decapitation removes these factors from serum of the growing fetal pig and results in development of fewer adipocytes than in intact fetuses. These experiments examined the effects of growth hormone or thyroxine supplementation to decapitated fetal pig sera upon pre-adipocyte proliferation and differentiation. Hormones were supplemented to concentrations present in sera from intact pig littermates (reference). Sera +/- hormones were analyzed for their effects upon pre-adipocyte proliferation as determined by [3H]-thymidine incorporation; enzyme expression as determined by sn-glycerol-3-phosphate dehydrogenase activity; and induction of complete differentiation into lipid filled adipocytes as based upon a pre-adipocyte proliferation and enzyme expression than reference sera. Growth hormone had no effect in decap sera upon these parameters. Decap sera permitted detection of 54% more lipid-accumulating, newly formed adipocytes on percol gradients than reference sera, but growth hormone reduced detection to 29% of reference sera. Thyroxine specifically stimulated pre-adipocyte proliferation more than decap sera, but not to the level of reference sera. Complete differentiation, a formation of lipid-accumulating adipocytes was promoted also by thyroxine in comparison to basal decap sera. The results of these experiments indicate thyroid hormones are an important component of fetal sera for regulation of adipocyte development, whereas growth hormone may only affect cellular metabolism and not promote pre-adipocyte growth and development.

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