Abstract
Hypoxic–ischemic encephalopathy (HIE) is a devastating neonatal brain condition caused by lack of oxygen and limited blood flow. Environmental enrichment (EE) is a classic paradigm with a complex stimulation of physical, cognitive, and social components. EE can exert neuroplasticity and neuroprotective effects in immature brains. However, the exact mechanism of EE on the chronic condition of HIE remains unclear. HIE was induced by a permanent ligation of the right carotid artery, followed by an 8% O2 hypoxic condition for 1 h. At 6 weeks of age, HIE mice were randomly assigned to either standard cages or EE cages. In the behavioral assessments, EE mice showed significantly improved motor performances in rotarod tests, ladder walking tests, and hanging wire tests, compared with HIE control mice. EE mice also significantly enhanced cognitive performances in Y-maze tests. Particularly, EE mice showed a significant increase in Cav 2.1 (P/Q type) and presynaptic proteins by molecular assessments, and a significant increase of Cav 2.1 in histological assessments of the cerebral cortex and hippocampus. These results indicate that EE can upregulate the expression of the Cav 2.1 channel and presynaptic proteins related to the synaptic vesicle cycle and neurotransmitter release, which may be responsible for motor and cognitive improvements in HIE.
Highlights
Hypoxic–ischemic encephalopathy (HIE) is a brain condition that is caused by a lack of oxygen and limited blood flow in infants [1]
The representative Western blot (WB) images of the synaptic protein are shown in Figure analysis, EE mice showed a significant increase in the protein expression of Mu
The molecular and histohistological analysis revealed that EE upregulates Cav 2.1 expression and the presynlogical analysis revealed that EE upregulates Cav 2.1 expression and the presynaptic aptic related proteins in various brain regions, such as the cerebral cortex and hippocamrelated proteins in various brain regions, such as the cerebral cortex and hippocampus pus in HI mice
Summary
Hypoxic–ischemic encephalopathy (HIE) is a brain condition that is caused by a lack of oxygen and limited blood flow in infants [1]. Munc18-syntaxin complex, resulting in the synthesis of the tetramer of Munc, Munc, syntaxin, VAMP2 [34,35], and, with the arrival of SNAP25, the full SNARE complex is assembled as Munc is released [36] From this view, it can be inferred that Munc participates in short-term presynaptic plasticity [37], and Munc contributes to the improvement of synaptic function probability and plasticity [38,39]. We asked whether functional improvements and changes induced by EE are accompanied with changes of presynaptic proteins, related to the synaptic vesicle cycle and neurotransmitter release, in various brain regions after HI brain injury
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