ArticleMolecular pain
Chronic myocardial infarction changed the excitatory-inhibitory synaptic balance in the medial prefrontal cortex of rat.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Long-term social isolation during adolescence exacerbated cardiac dysfunction after myocardial infarction.Translational psychiatry · 2026Article
- Changes in Rats' Gut Microbiota Composition Caused by Induced Chronic Myocardial Infarction Lead to Depression-Like Behavior.Frontiers in microbiology · 2021Article
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Abstract
The medial prefrontal cortex is a key area for the regulation of pain and emotion. However, the functional involvement of the medial prefrontal cortex for visceral nociception, at the neuronal or synaptic level, is obscure yet. In the present study, the properties of excitatory and inhibitory synaptic transmission within the layer II/III of rat medial prefrontal cortex after chronic myocardial infarction were studied. It is found that the excitation-inhibition ratio of the medial prefrontal cortex was greatly changed, with enhanced excitation and decreased inhibition inputs to the pyramidal cells of the medial prefrontal cortex, which largely due to decreased spike firing in gamma-aminobutyric acid-ergic neurons. Behaviorally, inhibition of gamma-aminobutyric acid-ergic synaptic transmission alleviated the visceral pain and anxiety. It is thus for the first time showing that the excitation-inhibition ratio is increased in the medial prefrontal cortex after chronic myocardial infarction, which may come from the reduced intrinsic activity of gamma-aminobutyric acid-ergic neurons and is important for regulating the angina pectoris and anxiety induced by chronic myocardial infarction.
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