Site-Dependent Action of Intracerebroventricular 5-Hydroxytryptamine on the Cold-Stimulated Thyrotropin Secretion in Male Rats

Toivonen, Markku; Rauhala, Pekka; Männistö, Pekka T.

doi:10.1159/000125314

Cited by 9 publications

(11 citation statements)

References 26 publications

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“…:O, 31). Our recent study (13) suggested that icv 5-HT has a dual ;:nd site-dependent effect on the cold-stimulated TSH secretion. 5-liT infusion (9 pg) into the anterior third ventricle augmented T H levels, whereas the same dose into the posterior third \ mtricle attenuated the cold response.…”

Section: Methodological Discussionmentioning

confidence: 95%

“…For the central &ministration of drugs to conscious animals, stainless steel cannulae (length 18 mm) made from 23 gauge injection needles were implanted stereotaxically during the same session either into the anterior or the posterior third ventricle as described previously (13). For saline and CSH pretreatments, the cannulae were either placed into the anterior or into both the anterior and the posterior third ventricle under chloral hydrate (300 mg/kg ip) anaesthesia.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…The location of the infusion targets and the extent of the PeVN lesions were controlled in each rat in two preliminary experiments and 15% to 25% of the animals in each of the experiments by an infusion of 1% methylene blue solution through the guide cannulae after decapitation as described previously (13). For histological control of the lesions, formalintreated brains were cut in frontal sections of 200 to 250 prn with a Lancer vibratome and examined unstained under the light microscope.…”

Section: Experimental Protocolmentioning

confidence: 99%

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Effects of Cysteamine Pretreatment and Hypothalamic Periventricular Nucleus Lesion on the Cold‐Stimulated Thyrotropin Responses to Intracerebroventricular 5‐Hydroxytryptamine in Male Rats

Toivonent

Tuomainen

Rauhala

et al. 1990

J Neuroendocrinology

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Abstract?he hypothalamic somatostatinergic system was devitalized in male rats by intracerebroventricular (icv) cysteamine (CSH) pretreatment (250 pglratlday into the third ventricle) on 4 consecutive days or by a limited lesion of the hypothalamic periventricular nucleus (PeVNx). The acute effect of icv serotonin (5-HT) on the cold-stimulated thyrotropin (TSH) and prolactin responses were studied in these animals. The experiments were performed 24 h after the last saline or CSH infusions and 7 days after the sham-or PeVN-lesions. CSH and PeVNx decreased the hypothalamic somatostatin content by 44% to 57% and 19% to Z8%, respectively. PeVNx did not affect hypothalamic thyrotropin-releasing hormone content. 5-HT infusion (9 pglrat icv) into the anterior third ventricle elevated, although not significantly, TSH levels in both saline-or CSH-pretreated rats. 5-HT infusion into the anterior third ventricle did not affect TSH in sham-operated rats. However, 5-HT augmented the cold-stimulated TSH levels after PeVNx compared to shamlesion. Inversely, 5-HT infusion (9 pglrat) into the posterior third ventricle inhibited TSH secretion irrespective of the pretreatment or lesion. The inhibitory action of 5-HT on TSH was significantly suppressed by CSH. 5-HT infusions elevated serum prolactin levels irrespective of the infusion site, pretreatment or lesion. 5-HT infusion into both the anterior and the posterior third ventricle decreased rectal temperature in saline-pretreated, sham-and PeVN-lesioned rats. The hypothermic effect of 5-HT was weakened by CSH. The hypothalamic levels of noradrenaline, dopamine and their metabolites were not significantly affected by CSH and PeVNx. 5-HT infusion into the anterior third ventricle decreased hypothalamic dopamine content in both saline-and CSH-pretreated rats. However, such an effect was not seen in sham-or PeVN-lesioned animals. Although CSH is an inhibitor of dopamine-13-hydroxylase, this activity was not reflected in serum TSH or prolactin levels. The results support our hypothesis of the site-dependent action of icv 5-HT or TSH secretion. The elevation of TSH levels may arise from the inhibition of somatostatin release from rostra1 anterior hypothalamus. The inhibition of TSH secretion may result from the inhibition of thyrotropin-releasing hormone release from more caudal periventricular structures of the hypothalamus.Tliyrotropin (TSH) secretion is stimulated by thyrotropin-releasing hormone (TRH) derived from the hypothalamic paraventricular (PVN) and periventricular (PeVN) nuclei (1, 2). Lesion of the PVN results in a profound decrease in serum TSH levels (3-5). Sornatostatin (SRIF), which is abundant in the preoptic-anterior hypothalamus and PeVN (6), inhibits basal, TRH-and coldStimulated TSH release (7-10). Since both treatments with SRIF anilserum (7) and PeVN lesions (8) increase TSH levels in blood, SRIF may be a physiological regulator of TSH secretion. SRlF inhibits the release of most peptide hormones, e.g. growth hormone, TRH and prolactin (1 1).The stimulatory eff...

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Section: Methodological Discussionmentioning

confidence: 95%

Section: Surgical Proceduresmentioning

confidence: 99%

Section: Experimental Protocolmentioning

confidence: 99%

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Effects of Cysteamine Pretreatment and Hypothalamic Periventricular Nucleus Lesion on the Cold‐Stimulated Thyrotropin Responses to Intracerebroventricular 5‐Hydroxytryptamine in Male Rats

Toivonent

Tuomainen

Rauhala

et al. 1990

J Neuroendocrinology

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“…The stimulating effect of the brain serotonergic system on growth hormone secretion can be initiated by either growth hormone-releasing hormone release from the arcuate nucleus (Vijayan et al, 1978;Murakami et al, 1986; or the suppression of somatostatin release from the paraventricular nucleus (Mota et al, 1995;Valverde et al, 2000). A majority of data indicate a complex mechanism of the serotoninregulated thyroid-stimulating hormone (TSH) secretion which may occur at the level of the hypothalamus (inhibition of thyrotropinreleasing hormone release or somatostatin secretion) or pituitary gland (stimulation of TSH secretion) (Abrahamson et al, 1987;Toivonen et al, 1990;Masalova and Sapronov, 2009).…”

Section: Introductionmentioning

confidence: 99%

Damage to the Brain Serotonergic System Increases the Expression of Liver Cytochrome P450

Rysz

Bromek

Haduch

et al. 2015

Drug Metabolism and Disposition

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Genes coding for cytochrome P450 are regulated by endogenous hormones such as the growth hormone, corticosteroids, thyroid, and sex hormones. Secretion of these hormones is regulated by the respective hypothalamus-pituitary-secretory organ axes. Since the brain sends its serotonergic projections from the raphe nuclei to the hypothalamus, we have assumed that damage to these nuclei may affect the neuroendocrine regulation of cytochrome P450 expression in the liver. Thereby, 5,7-dihydroxytryptamine (5,7-DHT), a serotonergic neurotoxin, was injected into the dorsal and median raphe nuclei of male Wistar rats. Ten days after the neurotoxin injections, the brain concentrations of neurotransmitters, serum hormone, and cytokine levels, as well as the expression of cytochrome P450 in the liver were measured. Injection of 5,7-DHT decreased serotonin concentration in the brain followed by a significant rise in the levels of the growth hormone, corticosterone, and testosterone, and a drop in triiodothyronine concentration in the serum. No changes in interleukin (IL) levels (IL-2 and IL-6) were observed. Simultaneously, the activity and protein level of liver CYP1A, CYP3A1, and CYP2C11 rose (the activity of CYP2A/2B/2C6/2D was not significantly changed). Similarly, the mRNA levels of CYP1A1, CYP1A2, CYP2C11, and CYP3A1 were elevated. This is the first report demonstrating the effect of intracerebral administration of serotonergic neurotoxin on liver cytochrome P450. The obtained results indicate involvement of the brain serotonergic system in the neuroendocrine regulation of liver cytochrome P450 expression. The physiologic and pharmacological significance of the findings is discussed.

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“…compounds which activate 5-HT receptors through their 5-HT-releasing properties) has indicated that serotonergic systems exert both an inhibitory and a stimulatory influence on the HPT axis [6][7][8][9][10]. The recent availability of 5-HT receptor ligands has indicated that stimulation of 5-HTk and/or 5-HT: receptors inhibits cold-induced TSH release [8].…”

mentioning

confidence: 99%

Are 5-HT<sub>1A</sub> Autoreceptors Involved in the Inhibitory Effect of Ipsapirone on Cold-Elicited Thyrotropin Secretion?

Broqua

Laude²,

Bluet‐Pajot³

et al. 1993

Neuroendocrinology

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Administration of the serotonin (5-HT)_1a receptor agonist ipsapirone has been shown to decrease cold-elicited thyrotropin (TSH) secretion. We have analyzed (1) the influence of 5-HT_1a receptors and ipsapirone metabolism into 1-(2-pyrimidinyl)-piperazine (1-PP, an α₂-adrenoceptor antagonist) on the effect of ipsapirone on TSH release, and (2) the interaction between the corticosterone-releasing effect of ipsapirone and its inhibitory influence on TSH release. Pretreatment with proadifen (50 mg/kg, 5 h before ipsapirone), i.e. an inhibitor of ipsapirone metabolism into 1-PP, did not affect ipsapirone-induced inhibition of cold-elicited TSH secretion. Pretreatment (15 min before ipsapirone) with the 5-HT₁/5-HT₂ receptor antagonist metergoline 2 mg/kg) or with the 5-HT_1A receptor blocker (–)-pindolol (5 mg/kg) increased baseline and cold-elicited TSH release but the inhibitory influence of ipsapirone on cold-elicited TSH release was alleviated by (–)-pindolol pretreatment only. Cold exposure increased corticosterone release, an effect which was insensitive to (–)-pindolol pretreatment. Lastly, pretreatment with the 5-HT synthesis inhibitor p-chlorophenylalanine prevented the immediate inhibitory effect of the selective 5-HT_1a receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) upon cold-induced TSH release, but it amplified the late release of TSH in cold-exposed 8-OH-DPAT-injected rats. These results suggest that presynaptic 5-HT_1a receptors mediate ipsapirone-induced inhibition of cold-elicited TSH release, an effect which may be partially opposed by postsynaptic 5-HT_1a receptor stimulation.

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Site-Dependent Action of Intracerebroventricular 5-Hydroxytryptamine on the Cold-Stimulated Thyrotropin Secretion in Male Rats

Cited by 9 publications

References 26 publications

Effects of Cysteamine Pretreatment and Hypothalamic Periventricular Nucleus Lesion on the Cold‐Stimulated Thyrotropin Responses to Intracerebroventricular 5‐Hydroxytryptamine in Male Rats

Effects of Cysteamine Pretreatment and Hypothalamic Periventricular Nucleus Lesion on the Cold‐Stimulated Thyrotropin Responses to Intracerebroventricular 5‐Hydroxytryptamine in Male Rats

Damage to the Brain Serotonergic System Increases the Expression of Liver Cytochrome P450

Are 5-HT<sub>1A</sub> Autoreceptors Involved in the Inhibitory Effect of Ipsapirone on Cold-Elicited Thyrotropin Secretion?

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