Stimulation of food intake following opiate agonists in rats but not hamsters

The diencephalic area most sensitive to microinjections of noradrenaline lay outside the area of the lateral hypothalamus in which feeding can be produced by electrical stimulation. Injection of either area, including injections that caused increased feeding, failed to have any effect on hoarding activity. Since hoarding can be elicited both by food deprivation and by electrical stimulation of the lateral hypothalamus, these findings indicate biochemical, anatomical and motivational differences between the central feeding mechanism sensitive to adrenergic stimulation, and that responding to electrical stimulation or nutritional depletion. The former mechanism may be disinhibitory; the latter, excitatory.

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Is mammary output capacity limiting to lactational performance in mice?

Journal of Experimental Biology ◽

10.1242/jeb.199.2.337 ◽

1996 ◽

Vol 199 (2) ◽

pp. 337-349 ◽

Cited By ~ 25

Author(s):

K A Hammond ◽

K C Lloyd ◽

J Diamond

Keyword(s):

Food Intake ◽

Litter Size ◽

Mammary Glands ◽

High Food ◽

Uptake Capacity ◽

Start Up ◽

Lactational Performance ◽

Teat Number ◽

Size Controlled ◽

Stimulation Of

Using lactation in mice as a model, we sought to determine whether ceilings on sustained energy expenditure reside in the capacities of energy-acquiring and input organs (such as the intestine) or of energy-expending and output organs (such as the mammary glands). To distinguish between these possibilities experimentally, we surgically varied the teat number of lactating mother mice while simultaneously varying their litter size. The energy burden on each teat (i.e. the pup/teat ratio) could thus be varied independently of the energy burden (i.e. litter size) on the mother herself or on her intestine. At each teat number, pup mass proved to be maximal at intermediate litter sizes. At a given pup/teat ratio, mothers with five teats weaned pups no larger than the pups of normal (10-teat) mothers, even though the total energy burden on the former mothers was only half as large. Mothers with only two teats could not wean any pups. Litter size controlled maternal food intake, which in turn controlled intestinal mass and nutrient uptake capacity. Disproportionately high food intake for the smallest litters appears to reflect capital start-up costs of lactation. Pup mass is evidently limited by inadequate suckling stimulation of mammary glands.

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Brain oxytocin receptors mediate corticotropin-releasing hormone-induced anorexia

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.260.2.r448 ◽

1991 ◽

Vol 260 (2) ◽

pp. R448-R452 ◽

Cited By ~ 13

Author(s):

B. R. Olson ◽

M. D. Drutarosky ◽

E. M. Stricker ◽

J. G. Verbalis

Keyword(s):

Food Intake ◽

Adrenocorticotropic Hormone ◽

Central Administration ◽

Corticotropin Releasing Hormone ◽

Releasing Hormone ◽

Oxytocin Receptors ◽

Artificial Cerebrospinal Fluid ◽

Pituitary Secretion ◽

Inhibit Food Intake ◽

Stimulation Of

Central administration of corticotropin-releasing hormone (CRH) is known to inhibit food intake and stimulate pituitary oxytocin (OT) secretion in rats. These experiments addressed the possibility that the inhibition of food intake that follows central CRH administration is mediated through oxytocinergic pathways. Male food-deprived rats, with stable baseline food intakes after intracerebroventricular (icv) injections of artificial cerebrospinal fluid, received 150 pmol of CRH icv. Food intake was inhibited by 62 +/- 5% during a 90-min test period. Pretreatment with 9 nmol of the OT antagonist [d(CH2)5, Tyr(Me)2, Orn8]vasotocin icv completely eliminated the inhibition of food intake produced by icv CRH. In contrast, pretreatment with the OT-receptor antagonist did not significantly alter pituitary secretion of adrenocorticotropic hormone and OT stimulated by icv CRH. The results of these experiments implicate OT as a possible central mediator of CRH-induced anorexias in rats, particularly those that are accompanied by stimulation of neurohypophysial OT secretion.

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Stimulation of eating by the second messenger cAMP in the perifornical and lateral hypothalamus

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1997.273.1.r107 ◽

1997 ◽

Vol 273 (1) ◽

pp. R107-R112 ◽

Cited By ~ 1

Author(s):

E. R. Gillard ◽

A. M. Khan ◽

A. ul-Haq ◽

R. S. Grewal ◽

B. Mouradi ◽

...

Keyword(s):

Food Intake ◽

Lateral Hypothalamus ◽

Second Messengers ◽

Second Messenger ◽

Cyclic Monophosphate ◽

Camp Analog ◽

Complex Goal ◽

Intracellular Action ◽

Stimulation Of ◽

Goal Oriented Behavior

Despite intense study of neurotransmitters mediating hypothalamic controls of food intake, little is known about which second messengers are critical for these mechanisms. To determine whether adenosine 3',5'-cyclic monophosphate (cAMP) might participate in these mechanisms, we injected the membrane-permeant cAMP analog 8-bromo-cAMP (8-BrcAMP) hypothalamically in satiated rats. Injection of 8-BrcAMP (10-100 nmol) into the perifornical (PFH) and lateral hypothalamus (LH) dose dependently stimulated food intake of up to 15.7 g in 2 h. Significantly smaller responses were obtained with thalamic injections. In contrast to the strong stimulatory effects of PFH and LH 8-BrcAMP, cAMP and 8-bromo-guanosine 3',5'-cyclic monophosphate (100 nmol) were ineffective, suggesting a chemically specific, intracellular action. Consistent with this, combined PFH injection of 7-deacetyl-7-O-(N-methylpiperazino)-tau-butyryl-forskolin dihydrochloride and 3-isobutyl-1-methylxanthine, agents that increase endogeneous cAMP, stimulated eating of up to 9.9 g in 2 h. These results demonstrate that increases in PFH/LH cAMP can elicit complex, goal-oriented behavior, suggesting an important role for cAMP in hypothalamic mechanisms stimulating food intake.

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