5-HT1B Agonists

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A Escalante - One of the best experts on this subject based on the ideXlab platform.

  • role of presynaptic serotonergic receptors on the mechanism of action of 5 ht1a and 5 ht1b Agonists on masculine sexual behaviour physiological and pharmacological implications
    Journal of Neural Transmission, 1991
    Co-Authors: A Fernandezguasti, A Escalante
    Abstract:

    In order to establish whether the 5-HT1A or the 5HT1B Agonists, 8-OH-DPAT or TFMPP, produce their facilitatory or inhibitory actions on masculine sexual behaviour via a mechanism involving: (a) the serotonin synthesis or release; (b) the stimulation of presynaptic receptors, or (c) the stimulation of somatodendritic receptors, three series of experiments were performed. The administration of the serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA, 300mg/kg×3 days), facilitated sexual behaviour but does not interfere neither with the inhibitory nor with the facilitatory effects of TFMPP (0.5mg/kg) or 8-OH-DPAT (0.5 mg/kg), respectively. The icv or the intraraphe administration of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), slightly stimulated masculine sexual behaviour and produced a decrease in serotonin and its metabolite levels. In lesioned animals TFMPP (0.5 mg/kg) resulted in an inhibitory effect reflected as a prolongation of the ejaculation latency. The inhibitory effect of this drug on mounting behaviour was not observed in 5,7-DHT treated rats. In lesioned animals 8-OH-DPAT (0.5 mg/kg) produced the same facilitatory effect. Present data indicate that serotonergic postsynaptic receptors mediate both the inhibitory and the facilitatory actions of TFMPP or 8-OH-DPAT in copulation. All data further support the idea that endogenous serotonin acts via the stimulation of 5-HT1B receptors to induce its inhibitory effects on masculine sexual behaviour.

A Fernandezguasti - One of the best experts on this subject based on the ideXlab platform.

  • role of presynaptic serotonergic receptors on the mechanism of action of 5 ht1a and 5 ht1b Agonists on masculine sexual behaviour physiological and pharmacological implications
    Journal of Neural Transmission, 1991
    Co-Authors: A Fernandezguasti, A Escalante
    Abstract:

    In order to establish whether the 5-HT1A or the 5HT1B Agonists, 8-OH-DPAT or TFMPP, produce their facilitatory or inhibitory actions on masculine sexual behaviour via a mechanism involving: (a) the serotonin synthesis or release; (b) the stimulation of presynaptic receptors, or (c) the stimulation of somatodendritic receptors, three series of experiments were performed. The administration of the serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA, 300mg/kg×3 days), facilitated sexual behaviour but does not interfere neither with the inhibitory nor with the facilitatory effects of TFMPP (0.5mg/kg) or 8-OH-DPAT (0.5 mg/kg), respectively. The icv or the intraraphe administration of the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), slightly stimulated masculine sexual behaviour and produced a decrease in serotonin and its metabolite levels. In lesioned animals TFMPP (0.5 mg/kg) resulted in an inhibitory effect reflected as a prolongation of the ejaculation latency. The inhibitory effect of this drug on mounting behaviour was not observed in 5,7-DHT treated rats. In lesioned animals 8-OH-DPAT (0.5 mg/kg) produced the same facilitatory effect. Present data indicate that serotonergic postsynaptic receptors mediate both the inhibitory and the facilitatory actions of TFMPP or 8-OH-DPAT in copulation. All data further support the idea that endogenous serotonin acts via the stimulation of 5-HT1B receptors to induce its inhibitory effects on masculine sexual behaviour.

G. Curzon - One of the best experts on this subject based on the ideXlab platform.

  • The 5-HT1A Agonists 8-OH-DPAT, buspirone and ipsapirone attenuate stress-induced anorexia in rats
    2016
    Co-Authors: C. T. Dourish, G. A. Kennett, G. Curzon
    Abstract:

    tricyclic antidepressants on restraint stress-induced anorexia in rats were examined. The selective 5-HT1A Agonists 8-hydroxy-2-(di--propylamino)tetralin (8-OH-DPAT), buspirone and ipsapirone, when injected 2 h after the termination of stress, attenuated stress-induced anor-exia and body weight loss. The effects of 8-OH-DPAT on stress-induced anorexia were blocked by the 5-HT1Aantagonist spiperone but not by the 5-HT2antagonist ketanserin. The preferential 5-HT1B Agonists RU-24969 and quipazine induced anorexia in unstressed rats and tended to supplement the anorectic effects of stress. The benzodiazepines chlordiazepoxide and diazepam and the 5-HT antagonist cyproheptadine had no effect on stress-induced anorexia, when given (like the 5-HT1A Agonists) 2 h after the stress. Similarly, daily injection for 2 weeks of the tricyclic antidepressants desipramine and sertraline had no beneficial effect. The data suggest that 8-OH-DPAT, buspirone and ipsapirone attenuate stress-induced anorexia in rodents by a hyperphagic action on 5-HT1A receptors

C. T. Dourish - One of the best experts on this subject based on the ideXlab platform.

  • The 5-HT1A Agonists 8-OH-DPAT, buspirone and ipsapirone attenuate stress-induced anorexia in rats
    2016
    Co-Authors: C. T. Dourish, G. A. Kennett, G. Curzon
    Abstract:

    tricyclic antidepressants on restraint stress-induced anorexia in rats were examined. The selective 5-HT1A Agonists 8-hydroxy-2-(di--propylamino)tetralin (8-OH-DPAT), buspirone and ipsapirone, when injected 2 h after the termination of stress, attenuated stress-induced anor-exia and body weight loss. The effects of 8-OH-DPAT on stress-induced anorexia were blocked by the 5-HT1Aantagonist spiperone but not by the 5-HT2antagonist ketanserin. The preferential 5-HT1B Agonists RU-24969 and quipazine induced anorexia in unstressed rats and tended to supplement the anorectic effects of stress. The benzodiazepines chlordiazepoxide and diazepam and the 5-HT antagonist cyproheptadine had no effect on stress-induced anorexia, when given (like the 5-HT1A Agonists) 2 h after the stress. Similarly, daily injection for 2 weeks of the tricyclic antidepressants desipramine and sertraline had no beneficial effect. The data suggest that 8-OH-DPAT, buspirone and ipsapirone attenuate stress-induced anorexia in rodents by a hyperphagic action on 5-HT1A receptors

Alfredo Meneses - One of the best experts on this subject based on the ideXlab platform.

  • could the 5 ht1b receptor inverse agonism affect learning consolidation
    Neuroscience & Biobehavioral Reviews, 2001
    Co-Authors: Alfredo Meneses
    Abstract:

    Abstract Diverse evidence indicates that, the 5-HT system might play a role in learning and memory, since it occurs in brain areas mediating such processes and 5-HT drugs modulate them. Hence in this work, in order to explore further 5-HT involvement on learning and memory 5-HT1B receptors' role is investigated. Evidence indicates that SB-224289 (a 5-HT1B receptor inverse agonist) post-training injection facilitated learning consolidation in an associative autoshaping learning task, this effect was partially reversed by GR 127935 (a 5-HT1B/1D receptor antagonist), but unaffected by MDL 100907 (a 5-HT2A receptor antagonist) or ketanserin (a 5-HT1D/2A/7 receptor antagonist) at low doses. Moreover, SB-224289 antagonized the learning deficit produced by TFMPP (a 5-HT1A/1B/1D/2A/2C receptor agonist), GR 46611 (a 5-HT1A/1B/1D receptor agonist), mCPP (a 5-HT2A/2C/3/7 receptor agonist/antagonist) or GR 127935 (at low dose). SB-224289 did not alter the 8-OH-DPAT (a 5-HT1A/7 receptor agonist) learning facilitatory effect. SB-224289 eliminated the deficit learning produced by the anticholinergic muscarinic scopolamine or the glutamatergic antagonist dizocilpine. Administration of both, GR 127935 (5 mg/kg) plus ketanserin (0.01 mg/kg) did not modify learning consolidation; nevertheless, when ketanserin dose was increased (0.1–1.0 mg/kg) and SB-224289 dose was maintained constant, a learning facilitation effect was observed. Notably, SB-224289 at 1.0 mg/kg potentiated a subeffective dose of the 5-HT1B/1D receptor agonist/antagonist mixed GR 127935, which facilitated learning consolidation and this effect was abolished by ketanserin at a higher dose. Collectively, the data confirm and extend the earlier findings with GR 127935 and the effects of non-selective 5-HT1B receptor Agonists. Clearly 5-HT1B Agonists induced a learning deficit which can be reversed with SB-224289. Perhaps more importantly, SB-224289 enhances learning consolidation when given alone and can reverse the deficits induced by both cholinergic and glutamatergic antagonist. Hence, 5-HT1B receptor inverse Agonists or antAgonists could represent drugs for the treatment of learning and memory dysfunctions.