Modulation Of 5-hydroxytryptamine Release Research Articles

Receptors involved in the modulation of 5-hydroxytryptamine release in bovine cerebral arteries.

The uptake of [3H]5-hydroxytryptamine (5-HT) in bovine cerebral arteries was reduced by cocaine (1 microM), ouabain (100 microM), pretreatment with 6-hydroxydopamine (6-OHDA) (1.46 mM, 10 min) and metitepine (1 microM). Electrically-stimulated tritium release was decreased by tetrodotoxin (0.8 microM), Ca-free medium, denervation with 6-OHDA (1.46 mM, 10 min), 5-HT (10 microM), noradrenaline (1 microM) and the agonist of alpha 2-adrenoceptors B-HT 920 (0.1 and 1 microM), enhanced by metitepine (1 microM, antagonists of presynaptic 5-HT1 receptors) and rauwolscine (1 microM, antagonist at alpha 2-adrenoceptors, and also of 5-HT1D receptors) and not affected by ketanserin (1 microM, antagonist of 5-HT2 receptors), methysergide (0.1 microM, antagonist of 5-HT1 and 5-HT2 receptors) and phentolamine (1 and 3 microM antagonist of alpha-adrenoceptors and less potent of 5-HT1 receptors). The inhibitory action of 10 microM 5-HT was partially reversed by phentolamine (3 microM) and cocaine (1 microM) and completely reversed by both metitepine (1 microM) and rauwolscine (1 microM). Ketanserin (1 microM), methysergide (0.1 microM) or phentolamine (1 microM) had no effect. Rauwolscine (1 microM) antagonized the inhibition induced by both noradrenaline (1 microM) and B-HT 920 (0.1 and 1 microM). 5-HT induced tritium release which was inhibited by cocaine (an antagonist of 5-HT3 receptors) and denervation with 6-OHDA.(ABSTRACT TRUNCATED AT 250 WORDS)

Modulation of 5-hydroxytryptamine release in hippocampal slices of rats: Effects of fimbria-fornix lesions on 5-HT 1b-autoreceptor and α 2-heteroreceptor function

Fimbria-fornix lesions disrupt important parts of serotonergic and noradrenergic hippocampal afferents and elicit sprouting of sympathetic fibers from the superior cervical ganglion. Since 5-hydroxytryptamine (5-HT) release in the hippocampus is modulated by 5-HT 1B auto- and α 2-heteroreceptors, we investigated whether such lesions may alter these presynaptic mechanisms. Hippocampal slices of sham-operated (SHAM) and fimbria-fornix–lesioned (LES) rats (14 months after surgery) were preincubated with [ 3H]5-HT, superfused continuously, and stimulated electrically using two stimulation conditions: either (a) 360 pulses 3 Hz, or (b) 20 pulses 100 Hz (2 ms, 28 mA, 4 V/chamber). The amount of [ 3H]5-HT taken up by slices from LES rats was significantly reduced, whereas the evoked 5-HT release (in percent of tissue- 3H) was unchanged compared to that of SHAM rats. The 5-HT 1B agonist CP 93,129 or the α 2-agonist UK 14,304 reduced the evoked 5-HT release more potently in slices from LES rats, but only using stimulation condition (a), which permits inhibition by endogenously released transmitters. In LES rats, the facilitatory effect of the 5-HT antagonist metitepine was weaker, whereas that of the α 2-antagonist idazoxane was more pronounced than in SHAM rats. In LES rats, hippocampal 5-HT content was reduced to about 45% of SHAM levels, whereas that of noradrenaline was increased by about 30% (high-performance liquid chromatography). We conclude: (1) despite LES-induced changes in tissue levels of endogenous ligands, there is no down- or upregulation of 5-HT 1B-autoreceptors or α 2-heteroreceptors on serotonergic neurons in the denervated rat hippocampus. (2) The reduced endogenous autoinhibition (by 5-HT) seems to be compensated for by an increased heteroinhibition (by noradrenaline).

5-Hydroxytryptamine release in dorsal hippocampus of freely moving rats: Modulation by pindolol

Bosker, Fokko J., Martin G. Donker, Andre A Klompmakers, Kouichi Kurata and Herman G.M. Westenberg: 5-Hydroxytryptamine Release in Dorsal Hippocampus of Freely Moving Rats: Modulation by Pindolol. Prog. Neuro-Psychopharmacol. & Biol. Psychiat. 1994, 18 : 3 765–778. 1. The aim of the present study was to investigate the origin and modulation of 5-hydroxytryptamine release in dorsal hippocampus of freely moving rats using brain microdialysis. 2. Basal release of 5-hydroxytryptamine and 5-hydroxyindole-acetic acid was 3.0 ± 0.2 pg/15 min and 519 ± 18 pg/15 min, respectively. Stimulation by 60 mM K + increased 5-hydroxytryptamine release by 66%. Inclusion of 10 μM tetrodotoxin in the perfusion medium reduced 5-hydroxytryptamine release to approximately 5% of basal levels. 3. In addition, release could be modulated by the 5-hydroxytryptamine receptor agonist 8-hydroxy-2-(di-N-propylamino)-tetralin (50 % decrease) and this effect was completely blocked by the 5-hydroxytryptamine-1 receptor antagonist pindolol. 4. These data are in concordance with results from the ventral hippocampus and indicate that release of 5-hydroxytryptamine is predominantly of neuronal origin. In contrast with other studies, the authors found the non-selective 5-hydroxytryptamine-l antagonist, pindolol, to increase 5-hydroxytryptamine release by 65% following systemic admininistration. This may hint at a different autoreceptor control in serotonergic fibers ascending from the median raphe as compared to the dorsal raphe nucleus.

Modulation of 5-hydroxytryptamine release by presynaptic inhibitory ?2-adrenoceptors in the human cerebral cortex

Slices and synaptosomes from human cerebral cortex (which had to be removed to reach deeply located tumours) and, for comparison, synaptosomes from guinea-pig and rat cerebral cortex were preincubated with [3H]5-hydroxytryptamine and superfused with physiological salt solution containing an inhibitor of 5-hydroxytryptamine uptake. The effects of alpha-adrenoceptor agonists and antagonists on the electrically (slices) or potassium-evoked (synaptosomes) tritium overflow were studied. In human cerebral cortical slices, the electrically-evoked [3H] overflow was inhibited by noradrenaline (pIC25 value: 6.35); the non-selective alpha-adrenoceptor antagonist phentolamine, at a concentration of 0.32 mumol/l, strongly antagonized the inhibitory effect of noradrenaline (apparent pA2 value: 8.19) but did not affect the evoked overflow by itself. In synaptosomes from humans, guinea-pigs and rats, noradrenaline also inhibited the K(+)-evoked [3H] overflow in a concentration dependent manner; the alpha 2-adrenoceptor clonidine (1 mumol/l), but not the alpha 1-adrenoceptor agonist methoxamine (1 mumol/l), mimicked the effects of noradrenaline; the effect of noradrenaline (0.3 mumol/l) was abolished by the alpha 2-adrenoceptor antagonist idazoxan (0.5 mumol/l), but not by the alpha 1-adrenoceptor antagonist prazosin (1 mumol/l). It is concluded that release-inhibiting adrenoceptors of the alpha 2-subtype exist on 5-hydroxytryptamine terminals innervating the cerebral cortex in human and guinea-pig brain.

Modulation of 5-hydroxytryptamine release by opiates

Modulation of 5-hydroxytryptamine release by opiates

Alpha-adrenoceptor-mediated modulation of 5-hydroxytryptamine release from rat brain cortex slices.

Slices of rat brain cortex preincubated with 3H-5-hydroxytryptamine were superfused with physiological salt solution and stimulated electrically, or they were superfused with Ca2+-free solution containing 25 mM K+ and stimulated by introduction of 1.3 mM CaCl2 for 2 min. 1. The electrically evoked 3H overflow was decreased by noradrenaline and increased by phentolamine in a concentration-dependent manner. 2. Phentolamine caused a parallel shift to the right of the concentration-response curve of noradrenaline for its inhibitory effect on impulse-evoked 3H overflow; by contrast, it left the inhibitory effect of unlabelled 5-hydroxytryptamine on the electrically evoked 3H overflow unaffected. 3. Propranolol did not alter the inhibitory effect of noradrenaline on impulse-induced 3H overflow. 4. The increasing effect of phentolamine on the electrically evoked 3H overflow was not modified by paroxetine. 5. Cocaine (at a concentration which almost completely blocks the uptake of 3H-noradrenaline but only partially that of 3H-5-hydroxytryptamine into cortex slices) decreased impulse-evoked 3H overflow. This effect was abolished by phentolamine. 6. In the presence of tetrodotoxin throughout superfusion, the Ca2+-evoked 3H-overflow from slices superfused with Ca2+-free solution was inhibited by noradrenaline and increased by phentolamine. These findings suggest that the terminal serotoninergic fibers of rat brain cortex possess alpha-adrenoceptors, activation of which by exogenous or endogenous noradrenaline leads to inhibition of the release of 5-hydroxytryptamine.

Modification of vascular response to serotonin by drugs.

ArticleModification of Vascular Response to Serotonin by DrugsIrvine H. Page, and J. W. McCubbinIrvine H. PageFrom the Research Division of the Cleveland Clinic Foundation and The Frank E. Bunts Educational Institute, Cleveland, Ohio, and J. W. McCubbinFrom the Research Division of the Cleveland Clinic Foundation and The Frank E. Bunts Educational Institute, Cleveland, OhioPublished Online:01 Sep 1953https://doi.org/10.1152/ajplegacy.1953.174.3.436MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe role of serotonin receptors in the control of cardiovascular functionOh, the places you'll go! My many colored serotonin (apologies to Dr. Seuss)Stephanie W. 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