Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock: A stereology-based study
Shozo Jinno, Toshio Kosaka
There is an increasing body of evidence suggesting that GABAergic dysfunction is involved in various psychiatric disorders. The goal of our study was to investigate the influences of electroconvulsive therapy (ECT), one of the most effective treatments for depression, on the GABAergic system in the hippocampus. In this stereology-based study, we identified GABAergic neurons by immunostaining for two isoforms of glutamic acid decarboxylase (GAD), GAD65, and GAD67 and estimated the expression changes induced by single or repeated electroconvulsive shock (ECS; an animal model of ECT). The numerical density (ND) of entire population of GABAergic neurons (expressing GAD65 and/or GAD67) was seldom altered by the administration of ECS. GAD67-positive (GAD671) neurons were also rarely affected by ECS. On the other hand, the ND of GAD651 neurons was changed in a layer-specific manner. In the CA1 region, the ND of GAD651 neurons was increased in the strata radiatum/ lacunosum-moleculare (SR/SLM) by repeated ECS. In the CA3 region, the ND of GAD651 neurons was decreased in the stratum oriens and SR/SLM after single ECS. The expression ratio of GAD65 in GABAergic neurons was increased specifically in layers receiving afferents from the entorhinal cortex (EC), i.e., SR/SLM of the CA1 region and molecular layer of the dentate gyrus (DG), after repeated ECS administration, whereas the expression ratio of GAD67 in GABAergic neurons was decreased in several layers by the same treatment. These results indicate that the ECSinduced changes in ND of GAD651 or GAD671 neurons were most likely due to alterations in GAD expression rather than actual increases or decreases in cell numbers. Altogether, the neuronal circuit-dependent alterations in GABA-mediated signaling may play a contributory role in the depression treatment process introduced by ECT.
https://doi.org/10.1002/hipo.20576
出版済み - 11 1 2009
認知神経科学
10.1002/hipo.20576
「Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock: A stereology-based study」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。
Electroshock Medicine & Life Sciences 100%
Glutamate Decarboxylase Medicine & Life Sciences 93%
GABAergic Neurons Medicine & Life Sciences 74%
Protein Isoforms Medicine & Life Sciences 60%
Hippocampus Medicine & Life Sciences 60%
Electroconvulsive Therapy Medicine & Life Sciences 56%
Jinno, S., & Kosaka, T. (2009). Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock: A stereology-based study. Hippocampus, 19(11), 1130-1141. https://doi.org/10.1002/hipo.20576
Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock : A stereology-based study. / Jinno, Shozo; Kosaka, Toshio.
In: Hippocampus, Vol. 19, No. 11, 01.11.2009, p. 1130-1141.
Jinno, S & Kosaka, T 2009, 'Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock: A stereology-based study', Hippocampus, vol. 19, no. 11, pp. 1130-1141. https://doi.org/10.1002/hipo.20576
Jinno S, Kosaka T. Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock: A stereology-based study. Hippocampus. 2009 11 1;19(11):1130-1141. https://doi.org/10.1002/hipo.20576
Jinno, Shozo ; Kosaka, Toshio. / Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock : A stereology-based study. In: Hippocampus. 2009 ; Vol. 19, No. 11. pp. 1130-1141.
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title = "Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock: A stereology-based study",
abstract = "There is an increasing body of evidence suggesting that GABAergic dysfunction is involved in various psychiatric disorders. The goal of our study was to investigate the influences of electroconvulsive therapy (ECT), one of the most effective treatments for depression, on the GABAergic system in the hippocampus. In this stereology-based study, we identified GABAergic neurons by immunostaining for two isoforms of glutamic acid decarboxylase (GAD), GAD65, and GAD67 and estimated the expression changes induced by single or repeated electroconvulsive shock (ECS; an animal model of ECT). The numerical density (ND) of entire population of GABAergic neurons (expressing GAD65 and/or GAD67) was seldom altered by the administration of ECS. GAD67-positive (GAD671) neurons were also rarely affected by ECS. On the other hand, the ND of GAD651 neurons was changed in a layer-specific manner. In the CA1 region, the ND of GAD651 neurons was increased in the strata radiatum/ lacunosum-moleculare (SR/SLM) by repeated ECS. In the CA3 region, the ND of GAD651 neurons was decreased in the stratum oriens and SR/SLM after single ECS. The expression ratio of GAD65 in GABAergic neurons was increased specifically in layers receiving afferents from the entorhinal cortex (EC), i.e., SR/SLM of the CA1 region and molecular layer of the dentate gyrus (DG), after repeated ECS administration, whereas the expression ratio of GAD67 in GABAergic neurons was decreased in several layers by the same treatment. These results indicate that the ECSinduced changes in ND of GAD651 or GAD671 neurons were most likely due to alterations in GAD expression rather than actual increases or decreases in cell numbers. Altogether, the neuronal circuit-dependent alterations in GABA-mediated signaling may play a contributory role in the depression treatment process introduced by ECT.",
author = "Shozo Jinno and Toshio Kosaka",
doi = "10.1002/hipo.20576",
journal = "Hippocampus",
T1 - Neuronal circuit-dependent alterations in expression of two isoforms of glutamic acid decarboxylase in the hippocampus following electroconvulsive shock
T2 - A stereology-based study
AU - Jinno, Shozo
AU - Kosaka, Toshio
N2 - There is an increasing body of evidence suggesting that GABAergic dysfunction is involved in various psychiatric disorders. The goal of our study was to investigate the influences of electroconvulsive therapy (ECT), one of the most effective treatments for depression, on the GABAergic system in the hippocampus. In this stereology-based study, we identified GABAergic neurons by immunostaining for two isoforms of glutamic acid decarboxylase (GAD), GAD65, and GAD67 and estimated the expression changes induced by single or repeated electroconvulsive shock (ECS; an animal model of ECT). The numerical density (ND) of entire population of GABAergic neurons (expressing GAD65 and/or GAD67) was seldom altered by the administration of ECS. GAD67-positive (GAD671) neurons were also rarely affected by ECS. On the other hand, the ND of GAD651 neurons was changed in a layer-specific manner. In the CA1 region, the ND of GAD651 neurons was increased in the strata radiatum/ lacunosum-moleculare (SR/SLM) by repeated ECS. In the CA3 region, the ND of GAD651 neurons was decreased in the stratum oriens and SR/SLM after single ECS. The expression ratio of GAD65 in GABAergic neurons was increased specifically in layers receiving afferents from the entorhinal cortex (EC), i.e., SR/SLM of the CA1 region and molecular layer of the dentate gyrus (DG), after repeated ECS administration, whereas the expression ratio of GAD67 in GABAergic neurons was decreased in several layers by the same treatment. These results indicate that the ECSinduced changes in ND of GAD651 or GAD671 neurons were most likely due to alterations in GAD expression rather than actual increases or decreases in cell numbers. Altogether, the neuronal circuit-dependent alterations in GABA-mediated signaling may play a contributory role in the depression treatment process introduced by ECT.
AB - There is an increasing body of evidence suggesting that GABAergic dysfunction is involved in various psychiatric disorders. The goal of our study was to investigate the influences of electroconvulsive therapy (ECT), one of the most effective treatments for depression, on the GABAergic system in the hippocampus. In this stereology-based study, we identified GABAergic neurons by immunostaining for two isoforms of glutamic acid decarboxylase (GAD), GAD65, and GAD67 and estimated the expression changes induced by single or repeated electroconvulsive shock (ECS; an animal model of ECT). The numerical density (ND) of entire population of GABAergic neurons (expressing GAD65 and/or GAD67) was seldom altered by the administration of ECS. GAD67-positive (GAD671) neurons were also rarely affected by ECS. On the other hand, the ND of GAD651 neurons was changed in a layer-specific manner. In the CA1 region, the ND of GAD651 neurons was increased in the strata radiatum/ lacunosum-moleculare (SR/SLM) by repeated ECS. In the CA3 region, the ND of GAD651 neurons was decreased in the stratum oriens and SR/SLM after single ECS. The expression ratio of GAD65 in GABAergic neurons was increased specifically in layers receiving afferents from the entorhinal cortex (EC), i.e., SR/SLM of the CA1 region and molecular layer of the dentate gyrus (DG), after repeated ECS administration, whereas the expression ratio of GAD67 in GABAergic neurons was decreased in several layers by the same treatment. These results indicate that the ECSinduced changes in ND of GAD651 or GAD671 neurons were most likely due to alterations in GAD expression rather than actual increases or decreases in cell numbers. Altogether, the neuronal circuit-dependent alterations in GABA-mediated signaling may play a contributory role in the depression treatment process introduced by ECT.
U2 - 10.1002/hipo.20576
DO - 10.1002/hipo.20576
JO - Hippocampus
JF - Hippocampus