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Journal ArticleDOI

5-HT1A receptor function in depression : effect of chronic amitriptyline treatment

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TLDR
The results indicate a subsensitive (presynaptic) 5-HT1A receptor and/or a defective post-receptor signalling pathway in depression and are consistent with the hypothesis that 5- HT1A receptors are down-regulted during AMI treatment.
Abstract
Hypothermic responses to 5-HT1A receptor activation by the selective ligand ipsapirone (IPS) were attenuated in depressed patients as compared to controls. Chronic treatment with amitriptyline (AMI) further impaired 5-HT1Amediated hypothermia. The results indicate a subsensitive (presynaptic) 5-HT1A receptor and/or a defective post-receptor signalling pathway in depression and are consistent with the hypothesis that 5-HT1A receptors are down-regulted during AMI treatment.

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Book ChapterDOI

Mechanisms of Psychiatric Comorbidities in Epilepsy.

TL;DR: Lopez et al. as discussed by the authors reviewed the current understanding of the potential mechanisms contributing to these comorbidities, focusing on both basic science and clinical research findings, and raised awareness regarding the scope of the problem as it relates to comorbi psychiatric illnesses and epilepsy.
Journal ArticleDOI

Serotonin receptor-specific mediation of antidepressant treatment effects in depressed patients

TL;DR: Drawing conclusions from examining different 5-HT receptor-specific responses in depressed patients before and after antidepressant therapy are reviewed within the context of what is known about the human serotonin transporter, the5-HTIA receptor, and the 5- HT2 receptor subtypes.
Journal ArticleDOI

Role of Serotonin Type-1A/B (Hydroxytryptamine) Receptors in Depression Revisited

TL;DR: The present review evidence the link between 5- HT 1A/B receptors in the brain and depression, the possible pathways involved and their alterations in depression, and it reviews the preclinical evidences of 5-HT 1a/B receptor modulators as antidepressant agents and their effectiveness.
Book ChapterDOI

92 – The Neuroendocrinology of Mood Disorders

TL;DR: Overactivity of the HPA-axis hyperactivity in depression correlates with familial risk of mood disorder, suicide, nonresponse to placebo or psychotherapy, and clinical relapse following successful pharmacological treatment.
References
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Journal ArticleDOI

5-HT1A receptor-related anxiolytics

TL;DR: The novel anti-anxiety agents buspirone, gepirone and ipsapirone which directly affect the serotonergic system by interacting with the 5- HT 1A subtype of the high affinity 5-HT 1 receptor.
Journal ArticleDOI

Zur serotonin-hypothese der depression

TL;DR: Current theoretical and experimental developments in serotonin research extend from the differentiated description of central cytoarchitectonic structures over the identification and characterization of multiple receptor subtypes by pharmacological and molecular biological methods to the elucidation of neurobiochemical and physiological mechanisms of interneuronal communication and postreceptor signal transduction.
Journal ArticleDOI

5-Hydroxytryptamine receptor subtypes: molecular, biochemical and physiological characterization

TL;DR: A state of equilibrium has been achieved in which most of the 5-HT binding sites have been successfully correlated with multiple physiological, biochemical and behavioral effects of5-HT.
Journal ArticleDOI

Thermoregulatory responses to serotonin (5-HT) receptor stimulation in the rat. Evidence for opposing roles of 5-HT2 and 5-HT1A receptors.

TL;DR: Treatment of rats with ketanserin (3 mg/kg) completely prevented the hyperthermic effects of 5-MeODMT, and, in fact, converted ahyperthermic response to 5- MeODMT into a marked hypothermic response.
Journal ArticleDOI

The pharmacology of the behavioral and hypothermic responses of rats to 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT)

TL;DR: It is concluded that 8-OH-DPAT probably produces its hypothermic effects by actions at 5-HT receptors located presynaptically on5-HT neurones, while the stereotyped components of the serotonin syndrome appear to be mediated by post-synaptic receptors.
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