Further evidence that brain histamine H2 receptors are stimulatory in the control of prolactin in the rat

1988 ◽  
Vol 119 (4) ◽  
pp. 488-492 ◽  
Author(s):  
Carmela Netti ◽  
Valeria Sibilia ◽  
Francesca Guidobono ◽  
Isabella Villa ◽  
Paola Franco ◽  
...  

Abstract. The effects of administration into the brain ventricle of H2 receptor agonists (4-methylhistamine, 0.8 μmol/rat; dimaprit, 0.4–0.8 μmol/rat), H2 antagonists (cimetidine, 0.8 μmol/rat; ranitidine, 0.4–0.8 μmol/rat; famotidine, 0.03 μmol/rat) and of the dimaprit chemical analogue SK&F 91487 (0.4 μmol/rat) on unstimulated and histamine-stimulated prolactin secretion in normal male rats were studied. The H2 agonist 4-methylhistamine caused a significant increase in unstimulated blood PRL, whereas dimaprit, SK&F 91487, and the H2 antagonists tested did not change PRL levels. 4-Methylhistamine significantly enhanced the stimulatory effects of histamine on prolactin, whereas all the H2 antagonists inhibited histamine-induced prolactin release. The inhibition of histamine-induced prolactin secretion by the H2 agonist dimaprit is nonspecific, since its chemical analogue SK&F 91487, which has no H2 agonist activity, also inhibits it. These results indicate that stimulation of the H2 receptors in the central nervous system is facilitatory for PRL secretion, suggesting that the activation of H2 receptors may contribute to the PRL-releasing effects of histamine.

2000 ◽  
pp. 637-641 ◽  
Author(s):  
E Willems ◽  
U Knigge ◽  
H Jorgensen ◽  
A Kjaer ◽  
J Warberg

The effect of inhibition of the neuronal histaminergic system by blockade of postsynaptic H1 or H2 receptors or activation of presynaptic H3 autoreceptors on the ACTH and prolactin responses to the catecholamines epinephrine and norepinephrine was investigated in conscious male rats. Intracerebroventricular infusion of epinephrine and norepinephrine stimulated ACTH and prolactin secretion. Prior intracerebroventricular infusion of the H1 receptor antagonist, mepyramine, or the H2 receptor antagonist, cimetidine, had no effect on the ACTH response to epinephrine or norepinephrine, while these responses were inhibited by pretreatment with the H3 receptor agonist, imetit. The prolactin response to norepinephrine was significantly inhibited by pretreatment with mepyramine, cimetidine or imetit whereas the three histaminergic compounds had no effect on the prolactin response to epinephrine. The findings suggest that the histaminergic system exerts a mediating or permissive action on the norepinephrine-induced stimulation of prolactin secretion, whereas an intact histaminergic system may not be required for catecholamines to stimulate ACTH secretion. The inhibitory effect of imetit on catecholamine-induced release of ACTH may be due to an activation of H3 receptors located presynaptically on non-histaminergic neurons, e.g. aminergic neurons. The study further indicates an important role of histamine in the neuroendocrine regulation of prolactin secretion.


1996 ◽  
Vol 134 (2) ◽  
pp. 209-214 ◽  
Author(s):  
Raimo K Tuominen ◽  
Leena Tuomisto ◽  
Pekka T Männistö

Tuominen RK, Tuomisto L, Männistö PT. Effect of modified brain histamine contents on prolactin and thyrotropin secretion in male rats. Eur J Endocrinol 1996;134:209–14. ISSN 0804–4643 Effects of modified brain histamine contents on thyrotropin and prolactin secretion were studied in male rats. Under basal conditions the histamine content in the hypothalamus was approximately 8–10-fold higher than that in the striatum and the rest of the brain. l-Histidine (1000 mg/kg, ip), a histamine precursor, and metoprine (20 mg/kg, ip), an inhibitor of histamine methyltransferase, elevated histamine content in the brain by 65% and 167%, respectively. When the treatments were given together an additive effect (119–250% increase) on brain histamine was observed. Metoprine significantly decreased serum prolactin levels, while l-histidine had no effect. This effect of metoprine was not modified by treatment with l-histidine. Thus, metoprine has an inhibitory effect on prolactin secretion that is not related to elevated brain histamine contents. The increased brain histamine content after l-histidine treatment had no effect on prolactin secretion. Basal levels of serum thyrotropin were decreased by both l-histidine and metoprine, l-histidine being more potent. In rats treated with α-fluoromethylhistidine, an inhibitor of l-histidine decarboxylase, the cold-induced (rats kept for 60 min at +4°C) thyrotropin secretion was increased while the stress-induced prolactin secretion was decreased. In these rats, metoprine did not affect thyrotropin release but blunted the prolactin response. In conclusion, endogenous histamine inhibits thyrotropin secretion but does not affect prolactin release. Owing to its other effects, metoprine is not suitable as a tool to elevate endogenous histamine contents in the brain, at least when the regulation of anterior pituitary hormone release is being studied. Raimo K Tuominen, Institute of Biomedicine, Department of Pharmacology and Toxicology, PO Box 8, FIN-00014 University of Helsinki, Finland


1962 ◽  
Vol 39 (3) ◽  
pp. 423-430
Author(s):  
H. L. Krüskemper ◽  
F. J. Kessler ◽  
E. Steinkrüger

ABSTRACT 1. Reserpine does not inhibit the tissue respiration of liver in normal male rats (in vitro). 2. The decrease of tissue respiration of the liver with simultaneous morphological stimulation of the thyroid gland after long administration of reserpine is due to a minute inhibition of the hormone synthesis in the thyroid gland. 3. The morphological alterations of the thyroid in experimental hypothyroidism due to perchlorate can not be prevented with reserpine.


2022 ◽  
Author(s):  
Domênika Rubert Rossato ◽  
Higor Zuchetto Rosa ◽  
Jéssica Leandra Oliveira Rosa ◽  
Laura Hautrive Milanesi ◽  
Vinícia Garzella Metz ◽  
...  

Abstract Amphetamine (AMPH) is a psychostimulant drug frequently related to addiction, which is characterized by functional and molecular changes in the brain reward system, favoring relapse development and pharmacotherapies have shown low effectiveness. Considering the beneficial influences of tactile stimulation (TS) in different diseases that affect the central nervous system (CNS), here we evaluated if TS applied in adult rats could prevent or minimize the AMPH-relapse behavior also accessing molecular neuroadaptations in the Nucleus accumbens (NAc). Following AMPH conditioning in the conditioned place preference (CPP) paradigm, male rats were submitted to TS (15-min session, 3 times a day, for 8 days) during the drug abstinence period, which were re-exposed to the drug in the CPP paradigm for additional 3 days for relapse observation and molecular assessment. Our findings showed that besides AMPH relapse; TS prevented the dopamine transporter (DAT), dopamine 1 receptor (D1R), tyrosine hydroxylase (TH), mu opioid receptor (MOR) increase and AMPH-induced delta FosB (ΔFosB). Based on these outcomes, we propose TS as a useful tool to treat psychostimulant addiction, which subsequent to clinical studies; it could be included in detoxification programs together with pharmacotherapies and psychological treatments already conventionally established.


1977 ◽  
Vol 74 (2) ◽  
pp. 315-NP ◽  
Author(s):  
A. DANGUY ◽  
J. L. PASTEELS ◽  
F. ECTORS

A single injection of 1 mg of a complex of testosterone esters on day 5 of life was used to prepare constantly oestrous rats. Such androgenized female rats were then ovariectomized and submitted to stereotaxical implantation of 1 μg oestradiol benzoate, 5 μg testosterone isobutyrate or, as a control, 10 μg cholesterol in the anterior hypothalamic areas. The effects of the steroids on plasma and pituitary FSH and LH were assessed by radioimmunoassay. As reported previously by us in normal female and male rats, the preoptic–suprachiasmatic area (POA) was able to control synthesis and secretion of both gonadotrophins and did not lose its sensitivity to oestradiol and testosterone in androgenized rats. Evidence for enhanced prolactin secretion in androgenized rats was derived from immunofluorescence studies of the pituitary gland and from histology of the mammary glands. In this respect the condition of the androgenized females was opposite to that of the males. The present work demonstrated that stimulation of prolactin secretion in androgenized female rats resulted from oestrogen action due to permanent oestrus rather than from impairment of hypothalamo-hypophysial relationships. Indeed, prolactin stimulation was suppressed when the androgenized rats were ovariectomized and restored when they were subsequently implanted with oestradiol in the POA.


1985 ◽  
Vol 5 (3) ◽  
pp. 393-400 ◽  
Author(s):  
Astrid Nehlig ◽  
Linda J. Porrino ◽  
Alison M. Crane ◽  
Louis Sokoloff

The quantitative 2-[14C]deoxyglucose autoradiographic method was used to study the fluctuations of energy metabolism in discrete brain regions of female rats during the estrous cycle. A consistent though statistically nonsignificant cyclic variation in average glucose utilization of the brain as a whole was observed. Highest levels of glucose utilization occurred during proestrus and metestrus, whereas lower rates were found during estrus and diestrus. Statistically significant fluctuations were found specifically in the hypothalamus and in some limbic structures. Rates of glucose utilization in the female rat brain were compared with rates in normal male rats. Statistically significant differences between males and females at any stage of the estrous cycle were confined mainly to hypothalamic areas known to be involved in the control of sexual behavior. Glucose utilization in males and females was not significantly different in most other cerebral structures.


I feel greatly honoured by the invitation to give the Ferrier Lecture. I attended the first Ferrier Lecture, given by Sherrington in 1929, and I learned from Sherrington to value and admire the pioneer contributions of David Ferrier to neurology. In choosing the subject of inhibition for my lecture I was prompted by the peculiar challenge that inhibition has presented to physiologists ever since it was first demonstrated by the Weber brothers in 1846 that stimulation of the vagus nerve could stop the heart and by Setchenov in 1863 that stimulation of areas in the brain could slow or prevent reflex responses of frog limbs. It was Sherrington who greatly extended and organized knowledge of inhibition in the central nervous system; first, by a series of remarkable investigations, and finally by a theoretical paper published by the Royal Society in 1925, in which excitation and inhibition were given equivalent status in the synaptic mechanisms controlling neuronal discharge. His interest in central inhibition continued to the end of his scientific life, and was the subject of his Nobel Lecture in 1932. I might mention that both my first scientific paper and my D.Phil. thesis were concerned with inhibition, and that I have continued to be more interested in the problem of synaptic inhibition than in any other aspect of neurophysiology. In recent years progress has been so rapid that our understanding of the nature of central inhibition is in several respects more complete than that of central excitation. This illumination has followed rather rapidly upon a long period of ingenious theorizing which is now only of historical interest


Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4890-4896 ◽  
Author(s):  
Meghan M. Taylor ◽  
Willis K. Samson

Abstract Adrenomedullin (AM) has been reported to have actions at each level of the hypothalamo-pituitary-adrenal (HPA) axis, suggesting that the peptide plays a role in the organization of the neuroendocrine responses to stress. We examined the mechanism by which AM regulates the central nervous system branch of the HPA axis as well as the possible role of AM in the modulation of the releases of two other hormones, prolactin and GH, whose secretions also are altered by stress. Intracerebroventricular administration of AM led to elevated plasma corticosterone levels in unrestrained, conscious male rats. This effect was abrogated by pretreatment with a CRH antagonist, suggesting that AM activates the HPA axis by causing the release of CRH into hypophyseal portal vessels. In addition, AM given intracerebroventricularly stimulated the release of prolactin but did not alter the secretion of GH. We propose that AM produced in the brain may be an important neuromodulator of the hormonal stress response.


2019 ◽  
Vol 10 (1) ◽  
pp. 63-71
Author(s):  
Aleksandr A. Kalinkin ◽  
Alexey G. Vinokurov ◽  
Olga N. Kalinkina ◽  
Alexander S. Ilinykh ◽  
Andrey A. Bocharov ◽  
...  

The technique of deep brain stimulation is used to treat patients with various diseases of the central nervous system who are not amenable to conservative therapy, while open interventions in them are associated with a high risk of complications. In the review, we evaluate the efficiency of the deep stimulation of different regions of the brain in some pharmacoresistant forms of diseases.


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