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Methods and Findings
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Methods Find Exp Clin Pharmacol 2010, 32(10): 721
ISSN 0379-0355
Copyright 2010 Clarivate Analytics
CCC: 0379-0355
DOI: 10.1358/mf.2010.32.10.1545783
 
 
Regulation of a2-adrenoceptor gene expression by chronic lithium treatment in rat brain
Cuffi, M.L., Artells, R., Navarro, A., Ciruela, F., Carbonell, L.
 
 
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 α₂D-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.


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