Environmental Enrichment Enhances Cav 2.1 Channel-Mediated Presynaptic Plasticity in Hypoxic–Ischemic Encephalopathy

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 neuroprotect...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-03, Vol.22 (7), p.3414
Main Authors: Song, Suk-Young, Pyo, Soonil, Choi, Sungchul, Oh, Hee Sang, Seo, Jung Hwa, Yu, Ji Hea, Baek, Ahreum, Shin, Yoon-Kyum, Lee, Hoo Young, Choi, Ja Young, Cho, Sung-Rae
Format: Article
Language:English
Subjects:
Assessments
Blood flow
Brain damage
Cages
calcium channels
Cerebral cortex
Encephalopathy
Enrichment
environmental enrichment
Gene expression
Hypoxia
hypoxic–ischemic encephalopathy
Ischemia
Neonates
Neuroplasticity
Neuroprotection
Neurotransmitter release
Neurotransmitters
Oxygen enrichment
Presynaptic plasticity
Protein expression
Proteins
synaptic plasticity
Traumatic brain injury
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22073414