Electroconvulsive stimulations prevent chronic stress-induced increases in L-type calcium channel mRNAs in the hippocampus and basolateral amygdala
Research output: Contribution to journal › Journal article › Research › peer-review
Although affective disorders have high prevalence, morbidity and mortality, we do not fully understand disease etiopathology, nor have we determined the exact mechanisms by which treatment works. Recent research indicates that intracellular calcium ion dysfunction might be involved. Here we use the chronic restraint stress model of affective disorder (6 h restraint per day for 21 days) in combination with electroconvulsive stimulations to examine the effects of stress and an effective antidepressive treatment modality on L-type voltage gated calcium channel subunit mRNA expression patterns in the brain. We find that stress tended to upregulate Ca(v)1.2 and Ca(v)1.3 channels in a brain region specific manner, while ECS tended to normalise this effect. This was more pronounced for Ca(v)1.2 channels, where stress clearly increased expression in both the basolateral amygdala, dentate gyrus and CA3, while stress only upregulated Ca(v)1.3 channel expression significantly in the dentate gyrus. ECS effects on Ca(v)1.2 channel expression were generally specific to stressed animals. Our findings are consistent with and extent previous studies on the involvement of intracellular calcium ion dysfunction in affective disorders. Selective modulation of neuronal L-type voltage gated calcium channels appears to be a promising target for the development of novel antidepressive treatment modalities.
|Number of pages
|Published - 2012
- Amygdala, Animals, Calcium Channels, L-Type, Chronic Disease, Electroconvulsive Therapy, Hippocampus, Male, RNA, Messenger, Rats, Rats, Sprague-Dawley, Stress, Psychological, Tissue Distribution, Treatment Outcome, Up-Regulation