ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2013
A sequential impairment of cortical astrocytes and GABAergic neurons during ischemia is improved by mGluR₁,₅ activation.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 7 citations in OpenAlex.
- Metabotropic glutamate receptors-guardians and gatekeepers in neonatal hypoxic-ischemic brain injury.Pharmacological reports : PR · 2024Review
- Article
- Ginseng Rb fraction protects glia, neurons and cognitive function in a rat model of neurodegeneration.PloS one · 2014Article
- Inhibition of microRNA-181 reduces forebrain ischemia-induced neuronal loss.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2013Article
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6 authors at 2 institutions in 1 country.
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Abstract
Ischemic brain cell death is presumably caused by excitotoxicity. In addition to an increase of glutamate release during ischemia, the deficiency of astrocytic glutamate-reuptake may cause glutamate accumulation, which results in GABAergic neurons being vulnerable to ischemia. To confirm this hypothesis, we studied the pathophysiological changes of cortical astrocytes and GABAergic neurons during ischemia as well as the prevention of their injuries. Ischemia led to the sequential impairments of astrocytic glutamate-transporter currents and GABAergic neuronal excitability. The changes were partially reversed by 3,5-DHPG, an agonist of type-I/V metabotropic glutamate receptors (mGluR). Thus, mGluR₁,₅ activation may be useful against the sequential impairment of cortical astrocytes and GABAergic neurons in an early stage of ischemia.
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