Electroconvulsive stimulations prevent chronic stress-induced increases in L-type calcium channel mRNAs in the hippocampus and basolateral amygdala
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Electroconvulsive stimulations prevent chronic stress-induced increases in L-type calcium channel mRNAs in the hippocampus and basolateral amygdala. / Maigaard, Katrine; Pedersen, Ida Hageman; Jørgensen, Anders; Jørgensen, Martin B; Wörtwein, Gitta.
In: Neuroscience Letters, Vol. 516, No. 1, 2012, p. 24-8.Research output: Contribution to journal › Journal article › Research › peer-review
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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
Y1 - 2012
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
VL - 516
SP - 24
EP - 28
JO - Neuroscience letters. Supplement
JF - Neuroscience letters. Supplement
SN - 0167-6253
IS - 1
ER -
ID: 41851788