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Modulation of behavioral responses and CA1 neuronal death by nitric oxide in the neonatal rat's hypoxia model
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Modulation of behavioral responses and CA1 neuronal death by nitric oxide in the neonatal rat's hypoxia model
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Journal Article
Modulation of behavioral responses and CA1 neuronal death by nitric oxide in the neonatal rat's hypoxia model
2020
Overview
Introduction Neonatal hypoxia leads to cognitive and movement impairments that might persist throughout life. Hypoxia impairs hippocampal blood circulation and metabolism. The exact mechanisms underlying hypoxia‐induced memory impairment are not fully understood. Nitric oxide (NO) is a key neuromodulator that regulates cerebral blood flow. In this study, we aimed to evaluate the possible role of NO on behavioral and histomorphometric changes in the hippocampus following hypoxia in neonate rats. Material and methods Neonate male rats (n = 28) were randomly divided into 4 groups: control, hypoxia, hypoxia plus L‐NAME (20 mg/kg), and hypoxia plus L‐arginine (200 mg/kg). Drugs were injected intraperitoneally for seven consecutive days. Hypoxia was induced by keeping rats in a hypoxic chamber (7% oxygen and 93% nitrogen intensity). Ten to 14 days after hypoxia, behavioral changes were measured using a shuttle box, a rotarod, and an open field test. The histological changes in the hippocampus were measured using H&E and Nissl staining methods. Results Findings showed that hypoxia caused significant atrophy in the hippocampus. Furthermore, the administration of L‐NAME decreased the atrophy of the hippocampus in comparison with the hypoxic group. Behavioral results showed that hypoxia impaired memory performance and motor activity responses. Additionally, the administration of L‐NAME improved behavioral performance in a significant manner compared with the hypoxic group. Conclusions Hypoxia damaged the neurons of hippocampal CA1 region and induced memory impairment. The NOS inhibitor, L‐NAME, significantly attenuated the negative effects of hypoxia on behavior and observed changes in the hippocampus. Because there are many conflicting reports on the role of NO in learning and memory processes following brain injury, in this work, we induced hypoxia model in neonate rats as a sensitive period of synaptic plasticity formation on memory, and after exposing neonate rats to hypoxia, to evaluate the neuromodulatory effect of NO, we tested memory and histomorphometric changes in adult rat offspring in the presence of NO agonist and antagonist. Our main research findings were memory impairment and hippocampus cell atrophy in hypoxia rat, whereas the NOS inhibitor, L‐NAME, significantly attenuated the negative effects of hypoxia on behavior and observed changes in the hippocampus.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc,Wiley
Subject
