Low-Level Inhibition of GABAergic Synapses Enhances Gene Expressions Crucial for Neuronal Plasticity in the Hippocampus After Ischemic Stroke.


Journal article


M. Okamura, Takahiro Inoue, Y. Takamatsu, H. Maejima
Journal of Stroke & Cerebrovascular Diseases, 2020

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APA   Click to copy
Okamura, M., Inoue, T., Takamatsu, Y., & Maejima, H. (2020). Low-Level Inhibition of GABAergic Synapses Enhances Gene Expressions Crucial for Neuronal Plasticity in the Hippocampus After Ischemic Stroke. Journal of Stroke &Amp; Cerebrovascular Diseases.


Chicago/Turabian   Click to copy
Okamura, M., Takahiro Inoue, Y. Takamatsu, and H. Maejima. “Low-Level Inhibition of GABAergic Synapses Enhances Gene Expressions Crucial for Neuronal Plasticity in the Hippocampus After Ischemic Stroke.” Journal of Stroke & Cerebrovascular Diseases (2020).


MLA   Click to copy
Okamura, M., et al. “Low-Level Inhibition of GABAergic Synapses Enhances Gene Expressions Crucial for Neuronal Plasticity in the Hippocampus After Ischemic Stroke.” Journal of Stroke &Amp; Cerebrovascular Diseases, 2020.


BibTeX   Click to copy

@article{m2020a,
  title = {Low-Level Inhibition of GABAergic Synapses Enhances Gene Expressions Crucial for Neuronal Plasticity in the Hippocampus After Ischemic Stroke.},
  year = {2020},
  journal = {Journal of Stroke & Cerebrovascular Diseases},
  author = {Okamura, M. and Inoue, Takahiro and Takamatsu, Y. and Maejima, H.}
}

Abstract

OBJECTIVE Pharmacological inhibition of GABAergic synapses could represent a potent neuromodulation strategy to activate hippocampal neurons and increase neurotrophic factor gene expression, thus exerting a beneficial effect on post-stroke cognitive impairment (PSCI). The objective of this study was to assess the effects of low-level inhibition of GABAergic synapses on hippocampal gene expressions related to neuroplasticity using the middle cerebral artery occlusion surgery (MCAO) ischemic stroke rat model.

METHODS The animals were randomly assigned to three experimental groups-(1) a sham operated group (SHAM), (2) a control group (CON), and (3) a bicuculline group (BIC). MCAO was performed in the CON and BIC groups. A non-epileptic dose of bicuculline (0.25 mg/kg) was intraperitoneally administered every day for two weeks, starting three days after surgery, to the rats in the BIC group. The mRNA expression of brain-derived neurotrophic factor (BDNF), tropomyosin-related kinase B (TrkB), in relation to neurotrophic intracellular signal, p75, in relation to apoptosis, and synaptophysin (SYP) and PSD-95, synaptic markers, were assessed in the hippocampus ipsilateral to the ischemic site.

RESULTS MCAO increased the gene expression of TrkB. Furthermore, MCAO plus bicuculline administration increased the expression ratio of TrkB to p75 and SYP gene expression.

CONCLUSION Therefore, this study showed that administration of bicuculline after stroke beneficially modulated the expression of crucial genes for neuroplasticity, including BDNF receptors and SYP, in the ipsilateral hippocampus, suggesting that low-level inhibition of GABAergic synapses could lead to beneficial neuromodulation in the hippocampus after stroke.


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