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Fluoxetine-induced desensitization of somatodendritic 5-HT1A autoreceptors is independent of glucocorticoid(s).
Synapse 1997; 27(4):303-12S

Abstract

Previous in vitro studies showed that glucocorticoid receptor activation (notably by corticosterone) could induce a functional desensitization of somatodendritic 5-HT1A autoreceptors in the dorsal raphe nucleus [Laaris et al. (1995) Neuropharmacology 34:1201-1210], similar to that due to in vivo subchronic treatment with a 5-HT reuptake inhibitor, such as fluoxetine, in rats. In the present study, we investigated whether a link might exist between these effects, i.e., whether glucocorticoid receptor activation could be responsible for the fluoxetine-induced desensitization of 5-HT1A autoreceptors. In vitro recording in the dorsal raphe nucleus of brain-stem slices showed that subchronic treatment with fluoxetine (5 mg/kg intraperitoneally (i.p.), daily for 3-7 days) significantly reduced the potency of the 5-HT1A receptor agonist ipsapirone to inhibit the firing rate of serotoninergic neurons. Parallel experiments in adrenalectomized and sham-operated rats indicated that subchronic fluoxetine treatment produced a similar shift to the right of the ipsapirone inhibition curve in both groups of animals. Furthermore, the subchronic blockade of glucocorticoid receptors by RU 38486 (25 mg/kg subcutaneously (s.c.), daily) in intact rats treated with fluoxetine (5 mg/kg i.p., daily for 3 days) did not affect the ability of the latter treatment to reduce the potency of ipsapirone to inhibit the firing of serotoninergic neurons. These data suggest that glucocorticoid receptors (and their possible activation by corticosterone) are not involved in the functional desensitization of somatodendritic 5-HT1A autoreceptors, which occurs during long-term treatment with a serotonin reuptake inhibitor such as fluoxetine.

Authors+Show Affiliations

NeuroPsychoPharmacologie, INSERM U.288, CHU Pitié-Salpêtrière, Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9372553

Citation

Le Poul, E, et al. "Fluoxetine-induced Desensitization of Somatodendritic 5-HT1A Autoreceptors Is Independent of Glucocorticoid(s)." Synapse (New York, N.Y.), vol. 27, no. 4, 1997, pp. 303-12.
Le Poul E, Laaris N, Hamon M, et al. Fluoxetine-induced desensitization of somatodendritic 5-HT1A autoreceptors is independent of glucocorticoid(s). Synapse. 1997;27(4):303-12.
Le Poul, E., Laaris, N., Hamon, M., & Lanfumey, L. (1997). Fluoxetine-induced desensitization of somatodendritic 5-HT1A autoreceptors is independent of glucocorticoid(s). Synapse (New York, N.Y.), 27(4), pp. 303-12.
Le Poul E, et al. Fluoxetine-induced Desensitization of Somatodendritic 5-HT1A Autoreceptors Is Independent of Glucocorticoid(s). Synapse. 1997;27(4):303-12. PubMed PMID: 9372553.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fluoxetine-induced desensitization of somatodendritic 5-HT1A autoreceptors is independent of glucocorticoid(s). AU - Le Poul,E, AU - Laaris,N, AU - Hamon,M, AU - Lanfumey,L, PY - 1998/2/12/pubmed PY - 2000/6/20/medline PY - 1998/2/12/entrez SP - 303 EP - 12 JF - Synapse (New York, N.Y.) JO - Synapse VL - 27 IS - 4 N2 - Previous in vitro studies showed that glucocorticoid receptor activation (notably by corticosterone) could induce a functional desensitization of somatodendritic 5-HT1A autoreceptors in the dorsal raphe nucleus [Laaris et al. (1995) Neuropharmacology 34:1201-1210], similar to that due to in vivo subchronic treatment with a 5-HT reuptake inhibitor, such as fluoxetine, in rats. In the present study, we investigated whether a link might exist between these effects, i.e., whether glucocorticoid receptor activation could be responsible for the fluoxetine-induced desensitization of 5-HT1A autoreceptors. In vitro recording in the dorsal raphe nucleus of brain-stem slices showed that subchronic treatment with fluoxetine (5 mg/kg intraperitoneally (i.p.), daily for 3-7 days) significantly reduced the potency of the 5-HT1A receptor agonist ipsapirone to inhibit the firing rate of serotoninergic neurons. Parallel experiments in adrenalectomized and sham-operated rats indicated that subchronic fluoxetine treatment produced a similar shift to the right of the ipsapirone inhibition curve in both groups of animals. Furthermore, the subchronic blockade of glucocorticoid receptors by RU 38486 (25 mg/kg subcutaneously (s.c.), daily) in intact rats treated with fluoxetine (5 mg/kg i.p., daily for 3 days) did not affect the ability of the latter treatment to reduce the potency of ipsapirone to inhibit the firing of serotoninergic neurons. These data suggest that glucocorticoid receptors (and their possible activation by corticosterone) are not involved in the functional desensitization of somatodendritic 5-HT1A autoreceptors, which occurs during long-term treatment with a serotonin reuptake inhibitor such as fluoxetine. SN - 0887-4476 UR - https://www.unboundmedicine.com/medline/citation/9372553/Fluoxetine_induced_desensitization_of_somatodendritic_5_HT1A_autoreceptors_is_independent_of_glucocorticoid_s__ L2 - https://doi.org/10.1002/(SICI)1098-2396(199712)27:4<303::AID-SYN4>3.0.CO;2-G DB - PRIME DP - Unbound Medicine ER -