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PubMed1967

The mechanism of body temperature changes induced by intraventricular injections of adrenaline, noradrenaline and 5-hydroxytryptamine in the ox (Bos taurus).

1. Adrenaline, noradrenaline and 5-hydroxytryptamine (5-HT) were injected into the lateral ventricle of the ox. The effect of these drugs was measured on the respiratory rate, tidal volume, heat production, skin temperature of the ear, evaporative loss from the skin and the rectal temperature at 20 and 10 degrees C ambient temperature.2. Neither adrenaline (3 mg) nor noradrenaline (3 mg) had any effect on the temperature regulating mechanisms of the ox, except to produce vasoconstriction if vasodilatation was already present due to high ambient temperature or previous injection of 5-HT.3. Injection of 5-HT (5 mg) caused a rise in respiratory rate, a fall in tidal volume and heat production, elevation of ear skin temperature and skin evaporative loss and a decrease in rectal temperature. Sedation of the animals occurred.4. In its reaction to these monoamines the ox is similar to the goat, sheep and rabbit, but is unlike the cat and dog.5. It was concluded that neither adrenaline nor noradrenaline has a role in the central control of temperature regulation in the ox, but that 5-HT may be involved in the control of heat dissipation mechanisms.

Animals↗
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↗
PubMed1966

Periventricular cerebral impedance after intraventricular injection of calcium.

Injection of small volumes of calcium solution into the lateral ventricle of the cat wa followed by large electrical-impedance changes in gray matter bounding the ventricle, including the caudate nucleus and hippocampus. These changes lasted more than 24 hours and were accompanied by epileptiform electroencephalographic activity. Biweekly injections led to status epilepticus. Injections of similar amounts of magnesium ions were without comparable effects. Possible interactions between calcium ions and intercellular macromolecular material are discussed as a basis for certain impedance shifts in cerebral tissue.

Animals↗
PubMed1971

Morphine tolerance and dependence induced by intraventricular injection.

Injection of small quantities of morphine into the cerebral ventricular system of awake, relatively unrestrained, monkeys depressed or abolished operant food-reinforced lever pressing. After repeated injections progressively higher doses of morphine were needed to depress responding. Also, dependence could be demonstrated in these animals by precipitating specific abstinence signs with an antagonist.

Animals↗
PubMed1980

Compensatory increase in tyrosine hydroxylase activity in rat brain after intraventricular injections of 6-hydroxydopamine.

The neurotoxin 6-hydroxydopamine produced a permanent loss of endogenous norepinephrine and of 3H-labeled norepinephrine uptake sites in the hippocampus within 5 days. These losses were initially accompanied by parallel decreases in tyrosine hydroxylase activity and synaptosomal norepinephrine synthesis. Within 21 days, however, hippocampal tyrosine hydroxylase activity and norepinephrine synthesis rate increased three- to fivefold. These data suggest a novel form of plasticity in brain-damaged animals characterized by an increase in the capacity for transmitter biosynthesis in residual neurons.

Animals↗