Temperature effects of reserpine injected into the cerebral ventricles of rabbits and cats

Abstract

SUMMARY1. In unanaesthetized rabbits and cats reserpine was injected through a chronically implanted cannula in the left lateral cerebral ventricle, and rectal temperature was recorded.2. In rabbits the reserpine (0-5-0.6 mg) caused a rise in temperature, frequent defaecation and sedation. On repeating the intraventricular injections at 24 hr intervals the rise in temperature was not obtained with the second or third injection, but defaecation and sedation still occurred. When the hyperthermic response to intraventricular reserpine had disappeared the anterior hypothalamus still responded to intraventricular noradrenaline which produced a rise in temperature.3. In cats the reserpine (0.5-0.75 mg) caused a biphasic change in temperature, i.e. an initial fall followed by a rise, frequent defaecation, and catalepsy. On repeating the intraventricular injections at 24 hr intervals the initial hypothermic phase of the temperature response was not obtained with the second or third injection, but the late rise, defaecation and catalepsy were still produced. When the hypothermic phase had disappeared the hypothalamus still responded to intraventricular noradrenaline or adrenaline which produced a fall, and to intraventricular 5-hydroxytryptamine (5-HT) which produced a rise in temperature.4. It is concluded that the rise in temperature in rabbits and the initial fall produced in cats is not due to a direct action of reserpine on the cells of the anterior hypothalamus but to noradrenaline released from adrenergic

The Pharmacology of Rauwolfia Alkaloids

“…After the initial temperature response to reserpine in the cat and rabbit, intraventricular noradrenaline produces a rise in temperature in the rabbit and a fall in the cat (BANERJEE et aI., 1968) which parallels the effects of noradrenaline in untreated rabbits (COOPER et aI., 1965) and cats (FELDBERG and MYERS, 1965). Similarly, injection of serotonin intraventricularly in untreated (FELDBERG andMYERS, 1963, 1964) or reserpine-treated cats (BANERJEE et aI., 1968) produces hyperthermia which is blocked by noradrenaline and adrenaline (FELDBERG andMYERS, 1963, 1964). It has been suggested that the initial temperature effects of reserpine in the rabbit and cat are not due to a direct action but to noradrenaline released from adrenergic nerve endings in hypothalamic temperature-regulating centres (BANERJEE et aI., 1968).…”

Body temperature and 5‐hydroxytryptamine during early postnatal maturation in mice

“…Under conditions in which ambient temperature is cooler than body temperature, both NE and 5-hydroxytryptamine (5-HT) have been reported to decrease body temperature when injected intraventricularly (Brittain di Iiandley, 1967;Feldberg & Lotti, 1967). These monoamines are normally present in high concentrations in the hypothalamus (Page, 1954;Vogt, 1954), and release of endogenous amines following intraventricular administration of reserpine results in temperature changes consistent with the observed effects of individual ailnines for a particular species (Banerjee, Burks, Feldberg, & Goodrich, 1968). Finally, Myers and his coworkers have demonstrated the release of amines under conditions of thermal stress and suggested a more detailed scheme of neurons and neurotransmitters for physiologic thernioregdation (Myers & Yaksh, 1969).…”

Possible association of schizophrenia with a disturbance in prostaglandin metabolism: a physiological hypothesis

“…These regions would be reached from the cisterna interpeduncularis as the morphine spreads in the subarachnoid space rostrally along the ventral surface of the brain stem. Some of these regions are also reached from the third ventricle, so that on injection into the cerebral ventricle they may be reached both from the inner and outer surface of the brain (Banerjee et al 1968).…”