Effects of intrahippocampal injection of chemicals on the levels of plasma corticosterone in rats

Kawa, A.; Mizuguchi, Katsumi; Maeda, Yoshio; Taniguchi, Yoshiyasu; Ryu, Seiichiro; Yamashita, S; Ariyama, T.; Kamisaki, Takeshi; Kanehisa, Takuya

doi:10.1016/0024-3205(79)90560-5

Cited by 1 publication

(1 citation statement)

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“…Results of direct intracerebral applications of se rotonin in intact rats have not given similar results. Kawa et al [32] found that direct injection of serotonin into the dor sal hippocampus had no effect on plasma corticosterone in rats. Earlier Vermes and Telegdy [70] had reported that in traventricular injection of serotonin did not change the ba sal corticosterone levels but prevented or diminished the stress-induced elevation of plasma corticosterone in rats; they concluded from these and other findings that seroton ergic neurons may inhibit pituitary-adrenocortical function physiologically.…”

Section: Local Application Of Serotonin To Brain Regionsmentioning

confidence: 99%

Serotonergic Stimulation of Pituitary-Adrenocortical Function in Rats

Fuller¹

1981

Neuroendocrinology

189

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Various pharmacologic studies have supported a stimulatory role of brain serotonin neurons in the hypothalamic regulation of pituitary-adrenocortical function in rats. The serotonin precursor L-5-hydroxytryptophan (L-5HTP), serotonin uptake inhibitors, serotonin releasers, and direct-acting serotonin agonists all elevate serum corticosterone levels in rats. The elevation of serum corticosterone by L-5HTP is stereospecific and is potentiated by monoamine oxidase inhibition or by inhibition of serotonin uptake. Elevation of serum corticosterone by direct-acting receptor agonists is not altered by uptake inhibition or by depletion of serotonin stores. The elevation of serum corticosterone by p-chloroamphetamine, a serotonin-releasing drug, is antagonized by prevention of its uptake into serotonin neurons or by prior depletion of serotonin stores. The elevation of serum corticosterone by fluoxetine (an uptake inhibitor), by 1-m-trifluoromethylphenyl)piperazine (a direct agonist), and by p-chloroamphetamine (a serotonin releaser) does not occur with close structural analogs of those compounds lacking their specific effects on serotonin neurons. Pretreatment of rats with fluoxetine potentiates the elevation of corticosterone by L-5HTP, antagonizes the elevation of corticosterone by p-chloroamphetamine (which requires active transport into the serotonin neuron in order to release serotonin) and does not alter elevation of corticosterone by quipazine or 1-m-trifluoromethylphenyl)piperazine (direct-acting serotonin agonists) or by swim stress or insulin-induced hypoglycemia. Serotonin depletion in some cases leads to enhanced responsiveness to direct-acting drugs not requiring serotonin stores. Some serotonin receptor antagonists prevent corticosterone elevation by agents that enhance serotonergic function, but the differences among antagonists with regard to their ability to block the actions of particular agonists suggests that subpopulations of serotonin receptors may be involved. Thus most in vivo studies support the postulate developed from in vitro studies that serotonin neurons stimulate the release of corticotrophin-releasing factor from the hypothalamus, leading to enhanced secretion of adrenocorticotrophin from the pituitary gland and corticosterone from the adrenal glands. The physiological role of this postulated stimulatory serotonergic pathway is unknown, but some evidence suggests it may play a part in the diurnal rhythmicity of adrenocortical function.

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Section: Local Application Of Serotonin To Brain Regionsmentioning

confidence: 99%