التفاصيل البيبلوغرافية
| العنوان: |
Sevoflurane-induced cognitive effect on α7-nicotine receptor and M1 acetylcholine receptor expression in the hippocampus of aged rats. |
| المؤلفون: |
Ge, Yuan, Ming, Lei, Xu, Dedong |
| المصدر: |
Neurological Research; Jul2024, Vol. 46 Issue 7, p593-604, 12p |
| مصطلحات موضوعية: |
CHOLINERGIC receptors, GENE expression, HIPPOCAMPUS (Brain), NICOTINIC acetylcholine receptors, RATS |
| مستخلص: |
Sevoflurane treatment increases the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD show a decline in cognitive abilities compared to preoperative levels. This study aimed to investigate whether the activation of α7 nicotinic acetylcholine receptor (α7nAChR) and the expression of M1 acetylcholine receptor (mAChR M1) in the hippocampus affects the cognitive function of aged rats. Forty-eight Sprague-Dawley (SD) rats of 1-week- and 12-months-old were divided into eight groups: four groups for α7nAChR and four groups for mAChR M1, respectively. All SD rats received 1.0–02% sevoflurane for α7nAChR and 1.0–02% sevoflurane for mAChR M1 for 2–6 h, respectively. The Y-maze test was used to assess the ability to learn and memory after receiving sevoflurane for 7 days at the same moment portion. RT-PCR was used to determine the expression of α7nAChR and mAChR M1 in the hippocampus of rats. The α7nAChR mitigated the formation of sevoflurane-induced memory impairment by modulating the translocation of NR2B from the intracellular reservoir to the cell surface reservoir within the hippocampus. Next, sevoflurane-induced decline of cognitive function and significantly decreased mAChR M1 expression at mRNA levels. α7nAChR regulates the trafficking of NR2B in the hippocampus of rats via the Src-family tyrosine kinase (SFK) pathway. This regulation is associated with cognitive deficits induced by sevoflurane in hippocampal development. Sevoflurane affects the cognitive function of rats by suppressing the mAChR M1 expression at mRNA levels in the hippocampus. α7nAChR attenuates sevoflurane-induced memory deficits by regulating NR2B. α7nAChR controls NR2B via the SFK in the hippocampus of rats that contribute to sevoflurane-induced cognitive deficits. Sevoflurane may affect cognitive function in rats by suppressing the mAChR M1 expression at the mRNA levels in the hippocampus. Dysregulation of the α7nAChR and mAChR M1 receptors may contribute to cognitive deficits and neurodegenerative disorders. Results provide key insights into the cognitive effects of sevoflurane, a commonly used anesthetic, on the expression of the α7nAChR and mAChR M1 in the hippocampus of aged rats. Activation of α7nAChR may attenuate sevoflurane-induced memory deficits by regulating the trafficking of NR2B in the hippocampus. Sevoflurane administration could temporarily impair cognitive function in rats by suppressing the expression of the mAChR M1 at the mRNA level in the hippocampus. These findings advance our understanding of the mechanisms underlying sevoflurane-induced POCD and provide implications for the prevention and treatment of the cognitive deficits associated with anesthesia in aging populations. [ABSTRACT FROM AUTHOR] |
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