Activation of the 5-HT1A receptor subtype increases rat plasma ACTH concentration

Gilbert, François; Brazell, Celia; Tricklebank, Mark D.; Stahl, Stephen M.

doi:10.1016/0014-2999(88)90178-1

Cited by 167 publications

(43 citation statements)

References 24 publications

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“…Buspirone has been found to increase serum ACTH and cortisol and to decrease temperature in rats and humans (Cowen et al 1990;Koenig et al 1988). These effects are similar to the effects of 8-0H-DPAT (the prototypical 5-HT 1a receptor agonist) in rats (Gilbert et al 1988;Aulakh et al 1988). Buspirone also increases serum prolactin in both laboratory animals and man (Meltzer et al 1982(Meltzer et al , 1983Cowen et al 1990), similar to the 5-HT -releasing agent fenfluramine (Serri et al 1987;Coccaro et al 1988;Siever et al 1984;Quattrone et al 1983), and the 5-HT precursors L-tryptophan and 5-HTP (Lamberts et al (1978;MacIndoe et al 1973).…”

Section: Resultssupporting

confidence: 56%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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We administered the serotonin-1a agonist buspirone (0.4 mglkg orally) as a neuroendocrine challenge agent to a group of male patients with DSM-III -R major depressive disorder (MOD) (n = 13) and a group of male healthy controls (n = 10). The primary hypothesis of the study was that the prolactin response to buspirone would be blunted in the depressed patients. The prolactin response was significantly lower in depressed patients than in controls. There was no significant relationship between KEY WORDS: Depressive disorder; Serotonin; Buspirone; Prolactin 655 Avenue of the Americas, New York, NY 10010 placebo corrected-peak prolactin level and severity of depression or suicidality. There was a nonsignificant trend for the melancholic (n = 5) depressed patients to have a lower placebo corrected-peak prolactin level than nonmelancholic depressed patients (n = B).Our findings support a role for the serotonin-1a receptor in the etiology of MOD, specifically at the postsynaptic site. and 5-HT -releasing agents (Siever et al. 1984; Coccaro et al. 1989;Mitchell and Smythe 1990;Lichtenberg et al. 1992;Shapira et al. 1992aShapira et al. , 1992b.There has been a relatively consistent ii.nding of de creased prolactin response to various serotonergic agents in subjects with major depressive disorder (MOD) using nonspecific 5-HT challenge agents; thus, recent research has focused on the role of specific subtypes

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Section: Resultssupporting

confidence: 56%

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Moeller

Steinberg

Fulton

et al. 1994

Neuropsychopharmacol

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“…Intra-amygdala (and in some cases systemic) administration of 5-HT1A-R agonists can attenuate both the behavioral and neuroendocrine responses to various stressors, including restraint, forced swim and conditioned fear stimuli (Krysiak et al, 2000;Li et al, 2006;Rittenhouse et al, 1992). Conversely, although mRNA for the receptor is not abundant in the paraventricular nucleus of the hypothalamus (Heisler et al, 2007b), 5-HT1A-R agonists such as 8-OH-DPAT injected directly into this structure stimulates the HPA-axis (Calogero et al, 1990(Calogero et al, , 1993Gilbert et al, 1988;Pan and Gilbert, 1992). A pro-HPA-axis action of 5-HT1A-Rs would be consistent with the observation that systemic administration of the 5-HT1A-R agonist flesinoxan increased cFos expression in corticotropin-releasing hormone (CRH)-labeled cells in the PVN of the hypothalamus (as well as the central nucleus of the amygdala) (Compaan et al, 1996(Compaan et al, , 1997.…”

Section: Role Of 5-ht1a Receptorsmentioning

confidence: 99%

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

Holmes

2008

Neuroscience & Biobehavioral Reviews

249

166

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The serotonin system is strongly implicated in the pathophysiology and therapeutic alleviation of stress-related disorders such as anxiety and depression. Serotonergic modulation of the acute response to stress and the adaptation to chronic stress is mediated by a myriad of molecules controlling serotonin neuron development (Pet-1), synthesis (tryptophan hydroxylase 1 and 2 isozymes), packaging (vesicular monoamine transporter 2), actions at presynaptic and postsynaptic receptors (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3A, 5-HT4, 5-HT5A, 5-HT6, 5-HT7), reuptake (serotonin transporter), and degradation (monoamine oxidase A). A growing body of evidence from preclinical rodents models, and especially genetically modified mice and inbred mouse strains, has provided significant insight into how genetic variation in these molecules can affect the development and function of a key neural circuit between the dorsal raphe nucleus, medial prefrontal cortex and amygdala. By extension, such variation is hypothesized to have a major influence on individual differences in the stress response and risk for stress-related disease in humans. The current article provides an update on this rapidly evolving field of research.

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“…Although a presynaptic mechanism has been suggested (Goodwin et al 1985a(Goodwin et al , 1987aHillegaart 1991), the majority of the evidence indicates that the hypothermic effect of 8-OH-DPAT is mediated via postsynaptic 5-HT 1A receptors in the hypothalamus (Hjorth 1985;Hutson et al 1987;O'Connell et al 1992;Millan et al 1993). 5-HT 1A receptor stimulation also evokes ACTH and corticosterone release in rodents, via an effect on corticotrophin releasing factor in the paraventricular nucleus of the hypothalamus (Koenig et al 1987;Gilbert et al 1988;Haleem et al 1989;Bagdy and Makara 1994) and possibly through an action at the level of the pituitary as well (Chaouloff 1993).Ipsapirone, a centrally acting pyrimidinylpiperazine derivative, (Traber and Glaser 1987;Cutler et al 1993), has a radioligand binding profile very similar to that of 8-OH-DPAT (Peroutka 1988). Orally administered ipsapirone (0.3 mg/kg) induces a hypothermic response in normal human subjects (Lesch et al 1990a;Gelfin et al 1995).…”

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confidence: 99%

5-HT1A Receptor Function in Normal Subjects on Clinical Doses of Fluoxetine Blunted Temperature and Hormone Responses to Ipsapirone Challenge

Lerer¹,

Gelfin²,

Gorfine

et al. 1999

Neuropsychopharmacology

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Serotonergic receptors of the 5-HT 1A subtype have been suggested to play a pivotal role in the mechanism of action of antidepressant drugs, including specific serotonin reuptake inhibitors (SSRIs). We examined the effect of clinical doses of the SSRI, fluoxetine, on 5-HTThere is considerable interest in the role of serotonergic (5-HT) receptors of the 5-HT 1A subtype in the therapeutic action of antidepressant drugs. 5-HT 1A receptors are located presynaptically on serotonergic cell bodies in the raphe nuclei where they serve as autoreceptors which inhibit cell firing and reduce 5-HT release by a negative feedback mechanism, and post-synaptically in the hippocampus, cortex and other brain areas, including the hypothalamus. Based on electrophysiological studies in rats, De Montigny and colleagues Mongeau et al. 1997) proposed that each major class of antidepressants increases 5-HT neurotransmission by a distinct mechanism involving either From the Biological Psychiatry Laboratory, Department of Psychiatry, Hadassah-Hebrew University Medical Center (BL, YG, MEN) and the Laboratory of Applied Statistics, Hebrew University (MG), Jerusalem, Israel; the Endocrine Laboratory, Department of Medicine (BA) and Department of Psychiatry (KPL), University of Wuerzburg, Wuerzburg, Germany.Address correspondence to: Prof. Bernard Lerer, Biological Psychiatry Laboratory, Dept. of Psychiatry, Hadassah-Hebrew University Medical Center, Ein Karem, Jerusalem 91120, Israel.Received May 15, 1998; accepted August 25, 1998. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 20 , NO . 6 Ipsapirone Challenge in Normal Subjects on Fluoxetine 629pre-or post-synaptic 5-HT 1A receptors. The selective serotonin re-uptake inhibitors (SSRIs), which raise 5-HT synaptic levels when given acutely, were proposed to increase 5-HT transmission on repeated administration by inducing desensitization of somatodendritic 5-HT 1A autoreceptors in the raphe nuclei and nerve terminal 5-HT 1B autoreceptors, which also mediate feedback inhibition of 5-HT release. These effects would lead to a slow increase in 5-HT levels which corresponds to the delayed clinical effect of the drugs. Evidence for subsensitivity of somatodendritic 5-HT 1A autoreceptors after chronic administration of SSRIs has been provided by microdialysis experiments in which 5-HT levels are measured in vivo in response to a challenge dose of the 5-HT 1A receptor agonist, 8-hydroxy-2 (di-n-propylamino) tetralin (8-OH-DPAT) (Rutter et al. 1994, Kreiss andLucki 1995;Invernizzi et al. 1994). However, other studies using SSRIs (Hjorth and Auerbach 1994; Bosker et al. 1995a,b;Invernizzi et al. 1995Invernizzi et al. , 1996 or clomipramine (Gur et al. 1999) failed to show any change in 5-HT 1A autoreceptor subsensitivity by this method. An increase in basal 5-HT levels after chronic SSRI administration, taken to be due to pre-synaptic 5-HT 1A and 5-HT 1B receptor desensitization, has been observed in cortex (Bel and Artigas 1993), hippocampus (Auerbach and Hjorth 1995) diencephalon (Rutter et al. 1994) an...

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Activation of the 5-HT1A receptor subtype increases rat plasma ACTH concentration

Cited by 167 publications

References 24 publications

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

A Preliminary Neuroendocrine Study with Buspirone in Major Depression

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

5-HT1A Receptor Function in Normal Subjects on Clinical Doses of Fluoxetine Blunted Temperature and Hormone Responses to Ipsapirone Challenge

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