Regulation of α2-adrenoceptor gene expression by chronic lithium treatment in rat brain.
Methods Find Exp Clin Pharmacol
; 32(10): 721-5, 2010 Dec.
Article
in En
| MEDLINE
| ID: mdl-21225007
ABSTRACT
One of the approaches for the treatment of bipolar disorder involves the coadministration of lithium, a mood stabilizer, with α2-adrenoceptor antagonists possessing an antidepressant effect. Since lithium accelerates the recovery of α2(D)-adrenoceptors following their irreversible inactivation with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ), our aim was to examine if it could be to some changes in Adra2A gene expression which codifies these adrenoceptors. Animals were treated with lithium chloride (120 mg/kg i.p.) or saline once a day for 10 days. A group of lithium- or saline-treated rats was killed 48 h after the last injection. The remaining animals were treated with EEDQ and were killed at 0.25, 4 and 14 days following this administration. Total RNA was extracted from cerebral cortex and Adra2A gene expression was measured by RT-QPCR. The results show that chronic lithium raised the Adra2A gene expression (P < 0.05), and after EEDQ administration this expression decreased to the basal level. No change in Adra2A gene expression was detected in the saline-treated group. However, EEDQ administration produced an insignificant increase in α2-adrenoceptors mRNA levels followed by a progressive decrease until basal levels. Lithium produced an overexpression of the Adra2A gene after chronic treatment that made the neuron ready to produce α2-adrenoceptors to deal with their inactivation.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Gene Expression Regulation
/
Receptors, Adrenergic, alpha-2
/
Lithium Chloride
/
Antimanic Agents
Limits:
Animals
Language:
En
Journal:
Methods Find Exp Clin Pharmacol
Year:
2010
Document type:
Article