Metabotropic glutamate receptors and neuroadaptation to antidepressants:: imipramine-induced down-regulation of β-adrenergic receptors in mice treated with metabotropic glutamate 2/3 receptor ligands

被引:29
作者
Matrisciano, F
Scaccianoce, S
Del Bianco, P
Panaccione, I
Canudas, AM
Battaglia, G
Riozzi, B
Ngomba, RT
Molinaro, G
Tatarelli, R
Melchiorri, D
Nicoletti, F
机构
[1] Univ Roma La Sapienza, Dept Human Physiol & Pharmacol, I-00185 Rome, Italy
[2] Univ Roma La Sapienza, SantAndrea Hosp, Dept Psychiat & Psychol Med, Rome, Italy
[3] Univ Barcelona, Fac Farm, Unitat Farmacol & Farmacognosia, E-08028 Barcelona, Spain
[4] Ist Neurol Mediterraneo Neuromed, Pozzilli, Italy
关键词
beta-adrenergic receptors; imipramine treatment; LY379268; LY341495; mGlu2/3; receptors; neuroadaptation;
D O I
10.1111/j.1471-4159.2005.03141.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Antidepressant drugs have a clinical latency that correlates with the development of neuroadaptive changes, including down-regulation of beta-adrenergic receptors in different brain regions. The identification of drugs that shorten this latency will have a great impact on the treatment of major depressive disorders. We report that the time required for the antidepressant imipramine to reduce the expression of beta-adrenergic receptors in the hippocampus is reduced by a co-administration with centrally active ligands of type 2/3 metabotropic glutamate (mGlu2/3) receptors. Daily treatment of mice with imipramine alone (10 mg/kg, i.p.) reduced the expression of beta-adrenergic receptors in the hippocampus after 21 days, but not at shorter times, as assessed by western blot analysis of beta(1)-adrenergic receptors and by the amount of specifically bound [H-3]CGP-12177, a selective beta-adrenergic receptor ligand. Down-regulation of beta-adrenergic receptors occurred at shorter times (i.e. after 14 days) when imipramine was combined with low doses (0.5 mg/kg, i.p.) of the selective mGlu2/3 receptor agonist LY379268, or with the preferential mGlu2/3 receptor antagonist LY341495 (1 mg/kg, i.p.). Higher doses of LY379268 (2 mg/kg, i.p.) were inactive. This intriguing finding suggests that neuroadaptation to imipramine - at least as assessed by changes in the expression of beta(1)-adrenergic receptors - is influenced by drugs that interact with mGlu2/3 receptors and stimulates further research aimed at establishing whether any of these drugs can shorten the clinical latency of classical antidepressants.
引用
收藏
页码:1345 / 1352
页数:8
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