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Published on: December 18, 2014
Noradrenergic lesion antagonizes desipramine-induced adaptation of NMDA receptors
1Laboratory of Neurobehavioral Pharmacology, Division of Neurobiology and Behavior Research, Department of Psychiatry, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS, USA.
Abstract:
Repeated administration of the tricyclic antidepressant, desipramine, for 28 days to mice effected a decrease in the potency of glycine to displace [3H]5,7-dichlorokynurenic acid (5,7-DCKA) in mouse cortical homogenates. Pre-treatment with the noradrenergic neurotoxin DSP-4, while having no effect alone, attenuated the desipramine-induced effect. The present findings support a norepinephrine-dependent adaptation of the NMDA receptor complex in vivo following chronic desipramine treatment. The inter-relationship of norepinephrine and glutamate transmission may provide insight into the mechanism underlying the action of antidepressant drugs.
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