Neural adaptation in response to chronic imipramine and electroconvulsive shock: evidence for separate mechanisms

Abstract

The effects of chronic imipramine and electroconvulsive shock alone or combined were assessed on rat brain β-adrenoceptors and serotonin 2 (5-HT 2) receptors and on dynorphin and thyrotropin releasing hormone (TRH) levels. These treatments resulted in regionally discrete and treatment-specific patterns of change in β-adrenoceptor and 5-HT 2 receptor density and in TRH and dynorphin levels. Electroconvulsive shock eliminated the serotonergic component of hippocampal DHA binding, suggesting an effect of this treatment on 5-HT 1 receptors. The effects of combined electroconvulsive shock and imipramine treatments on cortical 5-HT 2 and β-adrenoceptor density appeared to be the additive sum of the individual treatment effects. No treatment interaction was observed on hippocampal 5-HT 2 and β-adrenoceptors, except after day 2. No treatment interaction on peptide content was observed at any time. These results demonstrate independent anatomical specificity for the effects of electroconvul- sive shock and imipramine and provide evidence that the mechanisms responsible for their antidepressant actions differ.