PubMed HealthSearch

PubMed · 34116

Role of putative neurotransmitters in prolactin, GH and LH response to acute immobilization stress in male rats.

Abstract

Immobilization for 30 min induced a significant rise of prolactin (Prl), a significant reduction of growth hormone (GH), and no modification of plasma luteinizing hormone (LH) values in male rats. Depletion of brain catecholamine stores increased Prl and decreased LH levels while GH secretion was not affected. Blockade of beta-adrenergic receptors reduced GH and increased LH values. Plasma GH levels were also drastically reduced by depletion of brain serotonin (SER) levels and by atropine, and were increased by blockade of the H1 histamine (HIS) receptor. The anti-gamma-aminobutyric acid (GABA) agent picrotoxin significantly reduced Prl and GH plasma levels. Depletion of brain catecholamine stores or blockade of beta-adrenergic receptors antagonized the restraint-induced rise of plasma Prl values, while the decrease of GH elicited by stress was not modified by any pharmacological manipulation. These results indicate that although several putative neurotransmitters (PN) of the central nervous system (CNS) are implicated in the modulation of baseline levels of Prl, GH and LH, only the stress-induced activation of Prl secretion appears to be mediated by a PN, namely through a noradrenergic, beta-adrenergic route.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R Collu, P Du Rusisseau, Y Taché. 1979. Role of putative neurotransmitters in prolactin, GH and LH response to acute immobilization stress in male rats.. https://doi.org/10.1159/000122860

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Correlation between the increase in tyrosine hydroxylase activity and the decrease in serotonin content in the rat locus coeruleus after 5,6-dihydroxytryptamine.

A correlation is demonstrated between the increase in tyrosine hydroxylase activity and the decrease in serotonin concentration in the rat locus coeruleus after various doses of 5,6-dihydroxytryptamine and gradual protection of serotonin neurons by pretreatment with two serotonin uptake inhibitors: fluoxetine or citalopram.

5,6-Dihydroxytryptamine

Effects of parachlorophenylalanine and 5, 6-dihydroxytryptamine on the free-running rhythms of locomotor activity and plasma corticosterone in the rat exposed to continuous light.

Parachlorophenylalanine (PCPA) and 5,6-dihydroxytryptamine (5,6-DHT), depletors of brain serotonin, were administered to the rat and circadian rhythms of locomotor activity and plasma corticosterone were determined simultaneously in individual rats in light-dark cycles (LD) and in 200 lux continuous light (LL). Free-running periods and acrophases on the 12th day in LL (LL12) were calculated by a least squares spectrum method. In PCPA-treated rats which showed 70% depletion of brain serotonin, circadian rhythms of locomotor activity in LL and of plasma corticosterone and ACTH in LD disappeared for several days after the drug injection. Circadian rhythms of locomotor activity reappeared after the LL7 day and free-ran with a phase shift. Free-running periods of these rats did not differ significantly from that of control rats. However, the acrophase of PCPA-treated group on the LL11 day was 5 h advanced as compared to that of control. Circadian rhythm of plasma corticosterone in the PCPA-treated rats was detected on the LL12 day but their peak times were distributed around 24:00 h instead 08:00 h observed rats. The 5,6-DHT-treated rats which showed only 40% depletion of brain serotonin exhibited normal free-running rhythms in both locomotor activity and plasma corticosterone in LL and no difference in the acrophases of these functions on the LL12 day as compared to controls. These results suggest that PCPA affects the circadian clock (or clocks) itself in such a way that it blocks the clock to free-run or at least it effectively shortens the free-running periods of locomotor activity and plasma corticosterone in the rat.

5,6-Dihydroxytryptamine

Mediation of central prostaglandin effects by serotoninergic neurons.

Ten days after administration of 5,6-dihydroxytryptamine, which causes degeneration of central serotoninergic neurons, the depressive behavioral effects of PGF2 alpha and PGE2 were evidently inhibited. Central chemical serotoninectomy abolished the hyperthermic and hypertensive effects of PGF2 alpha, but only slightly affected those of PGE2. It is concluded that serotoninergic neurons mediate the depressive behavioral action of both PGF2 alpha and PGE2. They also mediate the hyperthermic and hypertensive action of PGF2 alpha but not of PGE2. This suggests that these prostaglandins have different central modes of action.

5,6-Dihydroxytryptamine