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Biomedical subjects

E M Stricker

Publications and source records attributed to E M Stricker.

At least 163 records · Page 9Linked to original sources
PubMed1976

The renin-angiotensin system and thirst: a reevaluation.

Systemic injections of renin that stimulate substantial amounts of drinking in nephrectomized rats can produce plasma renin activities that fall well above the physiological range. Furthermore, increases in plasma renin activities that occur in rats with intact kidneys during experimental hypotension appear to be too low to provide the basis for the observed elevations in water intake. These findings question the contribution of the renin-angiotensin system to thirst under normal physiological conditions.

Angiotensin II↗
PubMed1976

Hyperphagia and increased growth in rats after intraventricular injection of 5,7-dihydroxytryptamine.

Juvenile male rats given intracerebroventricular injections of 5,7-dihydroxytryptamine, following treatment with desmethylimipramine, maintained body weight gains of 5 to 6 grams per day into adulthood and grew much larger than control rats. Biochemical analyses of brain tissue obtained 50 to 140 days after the injections revealed 60 to 86% depletions of telencephalic 5-hydroxytryptamine, with catecholamine levels unchanged. Hyperphagia did not develop despite comparable losses of 5-hydroxytryptamine when the pretreatment was withheld, perhaps because substantial depletions of norepinephrine occurred as well.

Animals↗
PubMed1976

Drinking by rats after lateral hypothalamic lesions: a new look at the lateral hypothalamic syndrome.

Rats that have recovered from aphagia and adipsia following lateral hypothalamic lesions are believed to be incapable of experiencing thirst and to drink water simply to facilitate the consumption of dry food. However, the present results indicate that these animals will drink in response to dehydration of the intracellular or intravascular fluid compartments and to hyperangiotensinemia, if testing continues beyond a few hours. Comparable effects also were obtained in rats with mesencephalic brain damage, which appeared to destroy portions of the substantia nigra and the ascending nigrostriatal dopaminergic projections. These findings, when placed in the context of a recent neurochemical model for recovery of function, provide the basis for a new interpretation of the lateral hypothalamic syndrome.

Angiotensin II↗
PubMed1976

Activation-induced restoration of sensorimotor functions in rats with dopamine-depleting brain lesions.

Bilateral electrolytic lesions of the lateral hypothalamus or intraventricular 6-hydroxydopamine injections produced substantial depletions of striatal dopamine in rates. All animals with brain damage showed marked sensorimotor impairments. However, they began to move and respond appropriately to environmental stimuli when placed in a sink of water, in a shallow ice bath, or among a colony of cats or rats. A reversal of the sensorimotor dysfunctions was still apparent shortly after the animals were removed from each activating situation. However, the terapeutic effects dissipated rapidly, and by 4 hr after an exposure the rats responded as poorly as they had prior to activation. These findings are strikingly similar to the "paradoxical kinesia" seen in parkinsonism, a clinical disorder attributed to degeneration of central dopamine-containing neurons. Collectively, they suggest the importance of activation in maintaining responsiveness to senory stimuli in rats following dopamine-depleting brain lesions.

Animals↗
PubMed1976

Thermal homeostasis in rats after intrahypothalamic injections of 6-hyroxydopamine.

Specific destruction of at least 90% of the noradrenergic neurons in the preoptic/anterior hypothalamic region (PO/AH) by local injection of 9-hyroxydopamine (6-HDA) did not disrupt thermoregulation by rats either in the heat or the cold. Examination of the multiple effector mechanisms suggested that thermal balance was maintained in a normal fashion, and that compensatory adjustments did not conceal individual dysfunctions. In contrast with the ineffectual 6-HDA lesions of the PO/AH were the outstanding impairments seen in rats following electrolytic lesions of this area. All the latter animals became severely hyperthermic during the 1st h of exposure to an ambient temperature of 40 degrees C, and half of them were additionally unable to maintain body temperatures when exposed to an ambient temperature of 6 degrees C. The electrolytic lesions reduced norepinephrine levels in the PO/AH, but the 50-70% depletions were substantially smaller than those found in 6-HDA-treated rats. These results raise new doubts about whether central noradrenergic fibers have an important role in the regulation of body temperature by rats.

Animals↗
PubMed1975

Glucoregulatory feeding by rats after intraventricular 6-hydroxydopamine or lateral hypothalamic lesions.

Rats given intravenricular injections of 6-hydroxydopamine or bilateral electrolytic lesions of the lateral hypothalamus do not show the normal increase in food intake in response to large decreases in glucose utilization or exposure to severe cold stress. However, they will eat more during chronic glucoprivation that is less intense, or during exposure to more moderate cold stress. Thus, the feeding deficits of these lesioned rats may not reflect an inability to respond to certain qualitatively different stimuli, but rather an inability to respond to quantitatively different intensities of the same stimulus.

Animals↗
PubMed1973

Recovery of feeding and drinking by rats after intraventricular 6-hydroxydopamine or lateral hypothalamic lesions.

Rats given intraventricular injections of 6-hydroxydopamine after pretreatment with pargyline become aphagic and adipsic, and show severe loss of brain catecholamines. Like rats with lateral hypothalamic lesions, these animals gradually recover ingestive behaviors, although catecholamine depletions are permanent. Both groups decrease food and water intakes markedly after the administration of alpha-methyltyrosine, at doses that do not affect the ingestive behaviors of control rats. Thus, both the loss and recovery of feeding and drinking behaviors may involve central catecholamine-containing neurons.

Animals↗
PubMed1972

Deficits in feeding behavior after intraventricular injection of 6-hydroxydopamine in rats.

Intraventricular injections of 6-hydroxydopamine produced 95 percent depletion of telencephalic norepinephrine and 62 percent depletion of striatal dopamine in rats. Treated rats maintained body weight at subnormal levels and failed to increase food intake in response to a short-term decrease in glucose utilization. After treatment with the monoamine oxidase inhibitor pargyline, 6-hydroxydopamine produced no further norepinephrine depletion but increased the dopamnine depletion to 95 percent and produced complete aphagia. These effects are comparable to events that follow bilateral electrolytic lesions of the lateral hypothalanmus.

Animals↗