Hypothermia pretreatment improves cognitive impairment via enhancing synaptic plasticity in a traumatic brain injury model
| Autor: | Bingjin Liu, Xin-Wen Zhou, Lin Wang, Qing Tian, Fang-Xiao Shi, Yun Cao, Wei-Qi Xu |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male Traumatic brain injury Hippocampus Hypothermia Neuroprotection 03 medical and health sciences Mice 0302 clinical medicine Postsynaptic potential Hypothermia Induced Memory Brain Injuries Traumatic medicine Memory impairment Animals Learning Cognitive Dysfunction Molecular Biology Cerebral Cortex Neurons Neuronal Plasticity General Neuroscience Long-term potentiation medicine.disease nervous system diseases Mice Inbred C57BL 030104 developmental biology nervous system Anesthesia Brain Injuries Synaptic plasticity Models Animal Neurology (clinical) medicine.symptom Psychology Cognition Disorders 030217 neurology & neurosurgery Developmental Biology |
| Zdroj: | Brain research. 1672 |
| ISSN: | 1872-6240 |
| Popis: | Posttraumatic hypothermia attenuates cognitive deficits caused by TBI when it is administered at an early stage. However, little is known regarding the effect of hypothermia pretreatment on cognitive deficits one month after TBI. In the current study, the behavior test revealed that hypothermia pretreatment mitigates the learning and memory impairment induced by TBI in mice. Hypothermia treatment significantly increased the expression of PSD93, PSD95 and NR2B one month after TBI in the cortex and hippocampus compared with the normothermia group. Hypothermia pretreatment also restored the decreased spine number and the impairment in LTP and decreased the number of activated microglia one month after TBI. On the other hand, hypothermia pretreatment increased glucose metabolism in TBI mice. Taken together, these data suggested that hypothermia pretreatment is an effective method with which to prevent spine loss, maintain normal LTP and preserve learning and memory function after TBI. The neuroprotective role might be associated with the preservation of postsynaptic protein expression, the inhibition of activated microglia and the increase in glucose metabolism. |
| Databáze: | OpenAIRE |
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