Electroconvulsive stimulations prevent chronic stress-induced increases in L-type calcium channel mRNAs in the hippocampus and basolateral amygdala

TY - JOUR

T1 - Electroconvulsive stimulations prevent chronic stress-induced increases in L-type calcium channel mRNAs in the hippocampus and basolateral amygdala

AU - Maigaard, Katrine

AU - Pedersen, Ida Hageman

AU - Jørgensen, Anders

AU - Jørgensen, Martin B

AU - Wörtwein, Gitta

N1 - Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

PY - 2012/5/10

Y1 - 2012/5/10

N2 - 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.

AB - 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.

KW - Amygdala

KW - Animals

KW - Calcium Channels, L-Type

KW - Chronic Disease

KW - Electroconvulsive Therapy

KW - Hippocampus

KW - Male

KW - RNA, Messenger

KW - Rats

KW - Rats, Sprague-Dawley

KW - Stress, Psychological

KW - Tissue Distribution

KW - Treatment Outcome

KW - Up-Regulation

U2 - 10.1016/j.neulet.2012.03.043

DO - 10.1016/j.neulet.2012.03.043

M3 - Journal article

C2 - 22465249

SN - 0167-6253

VL - 516

SP - 24

EP - 28

JO - Neuroscience letters. Supplement

JF - Neuroscience letters. Supplement

IS - 1

ER -