ArticleBiomedicines2022
Hypoxia Depresses Synaptic Transmission in the Primary Motor Cortex of the Infant Rat-Role of Adenosine A
Article in Biomedicines, 2022. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Brain Injury and Neurodegeneration: Molecular, Functional, and Translational Approach 2.0.Biomedicines · 2024Article
- Neonatal Resuscitation Online Registry in Shenzhen: protocol for a prospective, multicentre, open, observational cohort study.BMJ open · 2024Observational
- Hypothermia improves neuronal network recovery in a human-derived in vitro model of oxygen-deprivation.PloS one · 2024Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The acute and long-term consequences of perinatal asphyxia have been extensively investigated, but only a few studies have focused on postnatal asphyxia. In particular, electrophysiological changes induced in the motor cortex by postnatal asphyxia have not been examined so far, despite the critical involvement of this cortical area in epilepsy. In this study, we exposed primary motor cortex slices obtained from infant rats in an age window (16-18 day-old) characterized by high incidence of hypoxia-induced seizures associated with epileptiform motor behavior to 10 min of hypoxia. Extracellular field potentials evoked by horizontal pathway stimulation were recorded in layers II/III of the primary motor cortex before, during, and after the hypoxic event. The results show that hypoxia reversibly depressed glutamatergic synaptic transmission and neuronal excitability. Data obtained in the presence of specific blockers suggest that synaptic depression was mediated by adenosine acting on pre-synaptic A
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