Inhibition of glucose sham drinking by water in rats: Sequential satiety signals?

Inhibition of glucose sham drinking by water in rats: Sequential satiety signals?

226 ABSTRACTS Inhibition of Glucose Sham Drinking by Water in Rats: Satiety Signals? DOUGLAS S. MOOK. Department of Psychology, Virginia, Sequentia...

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226

ABSTRACTS

Inhibition of Glucose Sham Drinking by Water in Rats: Satiety Signals? DOUGLAS S. MOOK. Department of Psychology, Virginia,

Sequential University

of

VA, U.S.A.

Intragastric water infusion along with rats’ sham-drinking reduces sham intake, though intake is still higher than normal. Therefore, intragastric water acts as an inhibitor for sham drinking. Decrementing the water load increases the size of the sham-feeding bout (as expected); incrementing the load decreases bout size at low glucose concentrations (as expected), but fails to do so at high concentrations (not as expected). These data are intelligible if we assume that (a) there are multiple oral and systemic criteria for bout termination; (b) the rat checks its state against various criteria sequentially; and(c) the sequence itselfchanges as gustatory input varies. Neuropeptides Sepulveda, U.S.A.

and Control

CA 91343,

of Foodlntake.

U.S.A. and UCLA School

J. E. MORLEY. VA Medical Center, of Medicine, Los Angeles, CA 90024,

Numerous peptides have been shown to modulate food ingestion; these include opioid peptides, neuropeptide Y (NPY), galanin, and growth hormone-releasing hormone. Of these peptides, the most potent is NPY, which produces a specific increase in carbohydrate intake and which may play a role in the pathophysiology of bulimia. Endogenous opioids have been thought to be involved in stress-induced eating. Corticotropin-releasing factor appears to play a role in the pathophysiology of anorexia nervosa. Of the peripherally active peptides that produce satiety, recent studies have shown that a potent cholecystokinin (CCK) antagonist can enhance feeding. In addition, it appears that CCK is involved in the memory enhancement associated with feeding. The regulation of feeding appears to involve the interaction of monoamines and peptides both within the central nervous system and the gastrointestinal tract. Satiety Dorsal

Function of Neurons Parabrachial Nucleus.

Containing

CCK-like

Substance

in the

K. NAGAI, H. INO, A. TAKAGI, S. INAGAKI, M. TOHYAMA, N. YANAI HARA and H. NAKAGAWA. Institute for Protein Research, Osaka University, Suita, Osaka 565, Japan.

Since neurons containing CCK-like substance in the lateral part of the dorsal parabrachial nucleus (LPBD) project to the ventromedial hypothalamus (VMH), effects of LPBD-lesions and injection of CCK-8 and glutaryl-CCK-8 (Glt-CCK-8) on food intake were examined in male Wistar rats. The following things were observed: (1) electrical lesions of bilateral LPBD caused hyperphagia and obesity, (2) an injection of Glt-CCK-8 but not of CCK-8 into bilateral VMH elicited the satiety action in 24-h fasted rats, but Glt-CCK-8 into peritoneal cavity did not, and (3) preinjection of a large dose of CCK-8 into bilateral VMH inhibited the satiety action of GltCCK-8. These findings suggest that neurons containing CCK-like substance in the LPBD have satiety function. Involvement of Dopaminergic and Aversive Conditioning

and Cholinergic Systems in Appetitive in the Rat Lateral Hypothalamus. K.

NAKAMURA, T. ONO, M. FUKUDA and E. TABUCHI. Department of Physiology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Sugitani, Toyama, Japan.

Unit activity in the rat lateral hypothalamus was recorded during discrimination of cue tones (CTS) that predicted juice or ICSS as reward, or electric shock or tail pinch as aversion, and during electrophoretic application of dopamine (DA), ACh and their antagonists. Of 224 neurons tested, 73 were inhibited and 79 excited during fluid intake. Of these, 113 acquired similar responses to CTS predicting juice (50 inhibited, 63 excited). Learned CTS responses to fluid intake mimicked the effects of DA, and were blocked by spiperone. Learned CTS responses to aversive stimuli mimicked the effects of ACh and were blocked by atropine.