system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Anti-Ulcer Agents, Apoptosis, Brain, Carbenoxolone, Caspase 3, Caspases, Cell Communication, Connexins, DNA, Disease Models, Animal, Electrophysiology, Female, Gap Junctions, Glucose, Hippocampus, Hypoxia, Hypoxia-Ischemia, Brain, Ischemia, Male, Mice, Mice, Inbred C57BL, Microscopy, Fluorescence, Nerve Degeneration, Neurons, Neuroprotective Agents, Nucleosomes, Oxygen, Polymerase Chain Reaction, Propidium, RNA, Messenger, Rats, Rats, Sprague-Dawley, Time Factors.
user
Does blockade of gap junctions in vivo provide neuroprotection after perinatal global ischemia? Context: We investigated the contribution of gap junctions to brain damage and delayed neuronal death produced by oxygen-glucose deprivation (OGD). Histopathology, molecular biology, and electrophysiological and fluorescence cell death assays in slice cultures after OGD and in developing rats after intrauterine hypoxia-ischemia (HI). OGD persistently increased gap junction coupling and strongly activated the apoptosis marker caspase-3 in slice cultures. The gap junction blocker carbenoxolone applied to hippocampal slice cultures before, during, or 60 minutes after OGD markedly reduced delayed neuronal death. Administration of carbenoxolone to ischemic pups immediately after intrauterine HI prevented caspase-3 activation and dramatically reduced long-term neuronal damage.
assistant
Gap junction blockade may be a useful therapeutic tool to minimize brain damage produced by perinatal and early postnatal HI. Final Decision: yes