ArticleExperimental neurology2027
Therapeutic hypothermia does not prevent dysmaturity of medial ganglionic eminence-derived interneurons in the dorsal hippocampus after neonatal hypoxia-ischemia.
Article in Experimental neurology, 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionNeonatal hypoxic-ischemic (HI) brain injury results in a persistent deficit of hippocampal parvalbumin (PV)
methodsFollowing HI at P10, mice were randomized to normothermia (36 °C, NT) or hypothermia (31 °C, TH) with anesthesia-exposed littermates as shams. Hippocampus was evaluated at P11, P18, and P40 for PV, SST, SAtb1, GFAP, Kv3.1b, and Kv3.2 (IF-IHC), electrical phenotyping and mIPSC (patch clamping), and RNA (real time RT PCR) and protein (western blot). Y-maze task and open field were performed for the P40 cohort.
resultsThe number of SAtb1
conclusionsNeonatal HI brain injury leads to dysmature GE-derived INs in the hippocampus, which persists to adulthood and not prevented by TH. Surviving GE-derived SAtb1
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