Modulation of haloperidol-induced patterns of the transcription factor Nur77 and Nor-1 expression by serotonergic and adrenergic drugs in the mouse brain
Authors: Maheux, J., Vuillier, L., Mahfouz, M., Rouillard, C. and Lévesque, D.
Journal: International Journal of Neuropsychopharmacology
Volume: 15
Issue: 4
Pages: 509-521
eISSN: 1469-5111
ISSN: 1461-1457
DOI: 10.1017/S1461145711000630
Abstract:Different patterns of expression of the transcription factors of Nur77 and Nor-1 are induced following acute administration of typical and atypical antipsychotic drugs. The pharmacological profile of atypical antipsychotics suggests that serotonergic and/or adrenergic receptors might contribute to these reported differences. In order to test this possibility, we examined the abilities of serotonin 5-HT 1A and 5-HT 2A/2C, and α 1-and α 2-adrenergic receptor drugs to modify the pattern of Nur77 (NR4A1) and Nor-1 (NR4A3) mRNA expression induced by haloperidol. Various groups of mice were treated with either saline, DOI, a 5-HT 2A/2C agonist, MDL11939, a 5-HT2A antagonist, 8-OH-DPAT, a 5-HT 1A agonist, prazosin, an 1-adrenergic antagonist and idazoxan, an 2-adrenergic antagonist, alone or in combination with haloperidol. The 5-HT 2A/2C agonist DOI alone significantly increased Nur77 expression in the medial striatum and nucleus accumbens. DOI reduced Nor-1 expression, while MDL11939 increased the expression of this transcript in the cortex. Prazosin reduced Nur77 expression in the dorsal striatum and nucleus accumbens. Interestingly, 8-OH-DPAT and MDL11939 partially prevented haloperidol-induced Nur77 up-regulation, while MDL11939 completely abolished Nor-1 expression in the striatum. In addition, MDL11939 decreased haloperidol-induced Nur77 and Nor-1 mRNA levels in the ventral tegmental area. On the contrary, idazoxan (2 antagonist) consistently potentiated haloperidol-induced Nur77, but not Nor-1 mRNA levels in the striatum, whereas prazosin (1 antagonist) remained without effect. Taken together, these results show the ability of a 5-HT 1A agonist or a 5-HT2A antagonist to reduce haloperidol-induced Nur77 and Nor-1 striatal expression, suggesting that these serotonin receptor subtypes participate in the differential pattern of gene expression induced by typical and atypical antipsychotic drugs. © 2011 CINP.
Source: Scopus
Modulation of haloperidol-induced patterns of the transcription factor Nur77 and Nor-1 expression by serotonergic and adrenergic drugs in the mouse brain.
Authors: Maheux, J., Vuillier, L., Mahfouz, M., Rouillard, C. and Lévesque, D.
Journal: Int J Neuropsychopharmacol
Volume: 15
Issue: 4
Pages: 509-521
eISSN: 1469-5111
DOI: 10.1017/S1461145711000630
Abstract:Different patterns of expression of the transcription factors of Nur77 and Nor-1 are induced following acute administration of typical and atypical antipsychotic drugs. The pharmacological profile of atypical antipsychotics suggests that serotonergic and/or adrenergic receptors might contribute to these reported differences. In order to test this possibility, we examined the abilities of serotonin 5-HT(1A) and 5-HT(2A/2C), and α₁- and α₂-adrenergic receptor drugs to modify the pattern of Nur77 (NR4A1) and Nor-1 (NR4A3) mRNA expression induced by haloperidol. Various groups of mice were treated with either saline, DOI, a 5-HT(2A/2C) agonist, MDL11939, a 5-HT(2A) antagonist, 8-OH-DPAT, a 5-HT(1A) agonist, prazosin, an α₁-adrenergic antagonist and idazoxan, an α₂-adrenergic antagonist, alone or in combination with haloperidol. The 5-HT(2A/2C) agonist DOI alone significantly increased Nur77 expression in the medial striatum and nucleus accumbens. DOI reduced Nor-1 expression, while MDL11939 increased the expression of this transcript in the cortex. Prazosin reduced Nur77 expression in the dorsal striatum and nucleus accumbens. Interestingly, 8-OH-DPAT and MDL11939 partially prevented haloperidol-induced Nur77 up-regulation, while MDL11939 completely abolished Nor-1 expression in the striatum. In addition, MDL11939 decreased haloperidol-induced Nur77 and Nor-1 mRNA levels in the ventral tegmental area. On the contrary, idazoxan (α₂ antagonist) consistently potentiated haloperidol-induced Nur77, but not Nor-1 mRNA levels in the striatum, whereas prazosin (α₁ antagonist) remained without effect. Taken together, these results show the ability of a 5-HT(1A) agonist or a 5-HT(2A) antagonist to reduce haloperidol-induced Nur77 and Nor-1 striatal expression, suggesting that these serotonin receptor subtypes participate in the differential pattern of gene expression induced by typical and atypical antipsychotic drugs.
Source: PubMed
Modulation of haloperidol-induced patterns of the transcription factor <i>Nur77</i> and <i>Nor</i>-<i>1</i> expression by serotonergic and adrenergic drugs in the mouse brain
Authors: Maheux, J., Vuillier, L., Mahfouz, M., Rouillard, C. and Levesque, D.
Journal: INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
Volume: 15
Issue: 4
Pages: 509-521
ISSN: 1461-1457
DOI: 10.1017/S1461145711000630
Source: Web of Science (Lite)
Modulation of haloperidol-induced patterns of the transcription factor Nur77 and Nor-1 expression by serotoninergic and adrenergic drugs in the mouse brain
Authors: Maheux, J., Vuillier, L., Mahfouz, M., Rouillard, C. and Levesque, D.
Journal: International Journal of Neuropsychopharmacology
Volume: 15
Issue: 4
Pages: 509-521
Publisher: Oxford University Press (OUP): Policy C - Option B
ISSN: 1469-5111
DOI: 10.1017/S1461145711000630
Abstract:Different patterns of expression of the transcription factors of Nur77 and Nor-1 are induced following acute administration of typical and atypical antipsychotic drugs. The pharmacological profile of atypical antipsychotics suggests that serotonergic and/or adrenergic receptors might contribute to these reported differences. In order to test this possibility, we examined the abilities of serotonin 5-HT1A and 5-HT2A/2C, and α1- and α2-adrenergic receptor drugs to modify the pattern of Nur77 (NR4A1) and Nor-1 (NR4A3) mRNA expression induced by haloperidol.
Various groups of mice were treated with either saline, DOI, a 5-HT2A/2C agonist, MDL11939, a 5-HT2A antagonist, 8-OH-DPAT, a 5-HT1A agonist, prazosin, an α1-adrenergic antagonist and idazoxan, an α2-adrenergic antagonist, alone or in combination with haloperidol. The 5-HT2A/2C agonist DOI alone significantly increased Nur77 expression in the medial striatum and nucleus accumbens. DOI reduced Nor-1 expression, while MDL11939 increased the expression of this transcript in the cortex. Prazosin reduced Nur77 expression in the dorsal striatum and nucleus accumbens. Interestingly, 8-OH-DPAT and MDL11939 partially prevented haloperidol-induced Nur77 up-regulation, while MDL11939 completely abolished Nor-1 expression in the striatum. In addition, MDL11939 decreased haloperidol-induced Nur77 and Nor-1 mRNA levels in the ventral tegmental area. On the contrary, idazoxan (α2 antagonist) consistently potentiated haloperidolinduced Nur77, but not Nor-1 mRNA levels in the striatum, whereas prazosin (α1 antagonist) remained without effect. Taken together, these results show the ability of a 5-HT1A agonist or a 5- HT2A antagonist to reduce haloperidol-induced Nur77 and Nor-1 striatal expression, suggesting that these serotonin receptor subtypes participate in the differential pattern of gene expression induced by typical and atypical antipsychotic drugs.
Source: Manual
Modulation of haloperidol-induced patterns of the transcription factor Nur77 and Nor-1 expression by serotonergic and adrenergic drugs in the mouse brain.
Authors: Maheux, J., Vuillier, L., Mahfouz, M., Rouillard, C. and Lévesque, D.
Journal: The international journal of neuropsychopharmacology
Volume: 15
Issue: 4
Pages: 509-521
eISSN: 1469-5111
ISSN: 1461-1457
DOI: 10.1017/s1461145711000630
Abstract:Different patterns of expression of the transcription factors of Nur77 and Nor-1 are induced following acute administration of typical and atypical antipsychotic drugs. The pharmacological profile of atypical antipsychotics suggests that serotonergic and/or adrenergic receptors might contribute to these reported differences. In order to test this possibility, we examined the abilities of serotonin 5-HT(1A) and 5-HT(2A/2C), and α₁- and α₂-adrenergic receptor drugs to modify the pattern of Nur77 (NR4A1) and Nor-1 (NR4A3) mRNA expression induced by haloperidol. Various groups of mice were treated with either saline, DOI, a 5-HT(2A/2C) agonist, MDL11939, a 5-HT(2A) antagonist, 8-OH-DPAT, a 5-HT(1A) agonist, prazosin, an α₁-adrenergic antagonist and idazoxan, an α₂-adrenergic antagonist, alone or in combination with haloperidol. The 5-HT(2A/2C) agonist DOI alone significantly increased Nur77 expression in the medial striatum and nucleus accumbens. DOI reduced Nor-1 expression, while MDL11939 increased the expression of this transcript in the cortex. Prazosin reduced Nur77 expression in the dorsal striatum and nucleus accumbens. Interestingly, 8-OH-DPAT and MDL11939 partially prevented haloperidol-induced Nur77 up-regulation, while MDL11939 completely abolished Nor-1 expression in the striatum. In addition, MDL11939 decreased haloperidol-induced Nur77 and Nor-1 mRNA levels in the ventral tegmental area. On the contrary, idazoxan (α₂ antagonist) consistently potentiated haloperidol-induced Nur77, but not Nor-1 mRNA levels in the striatum, whereas prazosin (α₁ antagonist) remained without effect. Taken together, these results show the ability of a 5-HT(1A) agonist or a 5-HT(2A) antagonist to reduce haloperidol-induced Nur77 and Nor-1 striatal expression, suggesting that these serotonin receptor subtypes participate in the differential pattern of gene expression induced by typical and atypical antipsychotic drugs.
Source: Europe PubMed Central