Linhua Xiang,
Rong Wu,
Kangling Liu,
Jing Wang
Department of Pediatrics, Wuhan Fifth Hospital, Wuhan 430050, Hubei Province, China;
For correspondence:- Jing Wang
Email: spxfg4@163.com
Accepted: 16 August 2021
Published: 30 September 2021
Citation:
Xiang L, Wu R, Liu K, Wang J.
Oxytocin protects neurons from hypoxic-ischemic brain injury by enhancing inhibitory neurotransmission in neonatal rats. Trop J Pharm Res 2021; 20(9):1909-1914
doi:
10.4314/tjpr.v20i9.18
© 2021 The authors.
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Abstract
Purpose: To study the protective effect of oxytocin on hypoxic-ischemic brain neuron injury in neonatal rats, and the mechanism of action involved.
Methods: Hippocampal slices from neonatal SD rats were cultured in oxygen/glucose-deprived (OGD) solution, leading to establishment of hypoxic-ischemic model of hippocampal slices in vitro. The slices were assigned to 3 groups: control (ACSF solution), model (OGD solution), and oxytocin (OGD solution + 1 μM oxytocin). The effect of oxytocin on vertebral neurons in hippocampal CA1 region of HIBD rats was determined using TOPRO-3 staining, while the effects of oxytocin on hypoxic depolarization (AD) and inhibitory postsynaptic currents (iPSCs) were measured by cell patch clamp technique.
Results: The fluorescence intensity of vertebral lamina in hippocampal CA1 area of model group was significantly higher than that of control group, while the corresponding value for oxytocin group was significantly lower than that of model group (p < 0.05). The time lapse before occurrence of AD in hippocampal CA1 area was significantly longer in oxytocin group than in model group, while the time lapse before neuronal AD in oxytocin receptor antagonist group was lower than that in oxytocin group. The frequency and amplitude of iPSCs in oxytocin group were markedly higher than the corresponding control values.
Conclusion: Oxytocin exerts protective effect against hypoxic-ischemic brain neuronal damage in neonatal rats by regulating the activation of oxytocin receptor and GABA receptor, and inhibiting nerve transmission. These findings may be of benefit in the development of a suitable therapy for HIBD.
Keywords: Oxytocin receptor, Neurotransmission; Hypoxic-ischemic brain neuron damage, Vertebral lamina, Hippocampal