Since their clinical application in the 1840s,the greatest mystery surrounding general anesthesia(GA)is how different kinds of general anesthetics cause reversible unconsciousness,and the precise neural mechanisms und...Since their clinical application in the 1840s,the greatest mystery surrounding general anesthesia(GA)is how different kinds of general anesthetics cause reversible unconsciousness,and the precise neural mechanisms underlying the processes.Over past years,although many studies revealed the roles of cortex,thalamus,brainstem,especially the sleep-wake circuits in GA-induced loss of consciousness(LOC),the full picture of the neural circuit mechanism of GA is still largely unknown.Recent studies have focused on the importance of other brain regions.Here,we report that the activity of glutamatergic(Glu)neurons in the piriform cortex(PC),a critical brain region for odor encoding,began to increase during the LOC of GA and gradually recovered after recovery of consciousness.Chemical lesions of the anterior PC(APC)neurons accelerated the induction time of isoflurane anesthesia.Chemogenetic and optogenetic activation of APcGlu neurons prolonged isoflurane and sevoflurane anesthesia induction,whereas APcclu neuron inhibition displayed the opposite effects.Moreover,the modification of APcclu neurons did not affect the induction or emergence time of propofol GA.In addition,odor processing may be partially involved in the induction of isoflurane and sevofurane GA regulated by APCclu neurons.In conclusion,our findings reveal a critical role of APCGlu neurons in inhalational GA induction.展开更多
Abstract The expression of early developmental markers such as doublecortin （DCX） and the polysialylated-neural cell adhesion molecule （PSA-NCAMIp has been used to identify immature neurons within canonical neuroge...Abstract The expression of early developmental markers such as doublecortin （DCX） and the polysialylated-neural cell adhesion molecule （PSA-NCAMIp has been used to identify immature neurons within canonical neurogenic niches. Additionally, DCX/PSA-NCAM ＋ immature neurons reside in cortical layer II of the paleocortex and in the paleo- and entorhinal cortex of mice and rats, respectively. These cells are also found in the neocortex of guinea pigs, rabbits, some afrotherian mammals, cats, dogs, non-human primates, and humans. The population of cortical DCX/PSA-NCAM ＋ immature neurons is generated prenatally as conclusively demonstrated in mice, rats, and guinea pigs. Thus, the majority of these cells do not appear to be the product of adult proliferative events. The immature neurons in cortical layer II are most abundant in the corlLices of young individuals, while very few DCX/PSA-NCAM ＋ cortical neurons can be detected in aged mammals. Maturation of DCX/PSA-NCAM ＋ cells into glutamatergic and GABAergic neurons has been proposed as an explanation for the age-dependent reduction in their population over time. In this review, we compile the recent information regarding the age-related decrease in the number of cortical DCX/PSA-NCAM ＋ neurons. We compare the distribution and fates of DCX/PSA-NCAM ＋ neurons among mammalian species and speculate their impact on cognitive function. To respond to the diversity of adult neurogenesis research produced over the last number of decades, we close this review by discussing the use and precision of the term ＂adult non-canonical neurogenesis.＂展开更多
目的研究生长休止蛋白(Growth arrest-specific protein 7,Gas7)在大鼠梨状皮质发育过程中的表达。方法采用逆转录聚合酶链反应(RT-PCR)方法和免疫组织化学方法检测Gas7核酸与蛋白在SD大鼠胚胎第18.5天(E18.5)、E20.5、出生当天(P0)、...目的研究生长休止蛋白(Growth arrest-specific protein 7,Gas7)在大鼠梨状皮质发育过程中的表达。方法采用逆转录聚合酶链反应(RT-PCR)方法和免疫组织化学方法检测Gas7核酸与蛋白在SD大鼠胚胎第18.5天(E18.5)、E20.5、出生当天(P0)、生后第7天(P7)、P14、P21和成年(Adult)各时期梨状皮质中的表达。结果 RT-PCR结果显示Gas7核酸在大鼠梨状皮质各发育时期均有表达,在P14时表达最强;免疫组织化学方法显示梨状皮质在E18.5时即出现Gas7免疫阳性产物,至P7时出现清晰的Gas7免疫阳性细胞,至P14时细胞数达到峰值,免疫阳性反应最强,P21细胞数少于P14(P<0.05),Adult细胞数少于P21(P<0.05)。结论 Gas7在梨状皮质的表达具有时间上的差异性,提示Gas7可能在梨状皮质结构形成和功能成熟方面起着重要的调控作用。展开更多
c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions....c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, Neu N immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction.展开更多
基金the National Natural Science Foundation of China(82060224,81971298,81571026)Scientific Project of Guizhou Province(Qian Comprehensive Basic Science[2020]1Y088,[2017]5733-066,[2020]-002)+1 种基金Joint Bidding Project by Zunyi City and Zunyi Medical University(ZSKH-HZ[2021]-194)PhD Research Startup Foundation of Zunyi Medical University(F-958).
文摘Since their clinical application in the 1840s,the greatest mystery surrounding general anesthesia(GA)is how different kinds of general anesthetics cause reversible unconsciousness,and the precise neural mechanisms underlying the processes.Over past years,although many studies revealed the roles of cortex,thalamus,brainstem,especially the sleep-wake circuits in GA-induced loss of consciousness(LOC),the full picture of the neural circuit mechanism of GA is still largely unknown.Recent studies have focused on the importance of other brain regions.Here,we report that the activity of glutamatergic(Glu)neurons in the piriform cortex(PC),a critical brain region for odor encoding,began to increase during the LOC of GA and gradually recovered after recovery of consciousness.Chemical lesions of the anterior PC(APC)neurons accelerated the induction time of isoflurane anesthesia.Chemogenetic and optogenetic activation of APcGlu neurons prolonged isoflurane and sevoflurane anesthesia induction,whereas APcclu neuron inhibition displayed the opposite effects.Moreover,the modification of APcclu neurons did not affect the induction or emergence time of propofol GA.In addition,odor processing may be partially involved in the induction of isoflurane and sevofurane GA regulated by APCclu neurons.In conclusion,our findings reveal a critical role of APCGlu neurons in inhalational GA induction.
文摘Abstract The expression of early developmental markers such as doublecortin （DCX） and the polysialylated-neural cell adhesion molecule （PSA-NCAMIp has been used to identify immature neurons within canonical neurogenic niches. Additionally, DCX/PSA-NCAM ＋ immature neurons reside in cortical layer II of the paleocortex and in the paleo- and entorhinal cortex of mice and rats, respectively. These cells are also found in the neocortex of guinea pigs, rabbits, some afrotherian mammals, cats, dogs, non-human primates, and humans. The population of cortical DCX/PSA-NCAM ＋ immature neurons is generated prenatally as conclusively demonstrated in mice, rats, and guinea pigs. Thus, the majority of these cells do not appear to be the product of adult proliferative events. The immature neurons in cortical layer II are most abundant in the corlLices of young individuals, while very few DCX/PSA-NCAM ＋ cortical neurons can be detected in aged mammals. Maturation of DCX/PSA-NCAM ＋ cells into glutamatergic and GABAergic neurons has been proposed as an explanation for the age-dependent reduction in their population over time. In this review, we compile the recent information regarding the age-related decrease in the number of cortical DCX/PSA-NCAM ＋ neurons. We compare the distribution and fates of DCX/PSA-NCAM ＋ neurons among mammalian species and speculate their impact on cognitive function. To respond to the diversity of adult neurogenesis research produced over the last number of decades, we close this review by discussing the use and precision of the term ＂adult non-canonical neurogenesis.＂
基金supported by Hallym University Research Fund,No.01-2012-10
文摘c-Fos is a good biological marker for detecting the pathogenesis of central nervous system disorders. Few studies are reported on the change in myocardial infarction-induced c-Fos expression in the paralimbic regions. Thus, in this study, we investigated the changes in c-Fos expression in the rat cingulate and piriform cortices after myocardial infarction. Neuronal degeneration in cingulate and piriform cortices after myocardial infarction was detected using cresyl violet staining, Neu N immunohistochemistry and Fluoro-Jade B histofluorescence staining. c-Fos-immunoreactive cells were observed in cingulate and piriform cortices at 3 days after myocardial infarction and peaked at 7 and 14 days after myocardial infarction. But they were hardly observed at 56 days after myocardial infarction. The chronological change of c-Fos expression determined by western blot analysis was basically the same as that of c-Fos immunoreactivity. These results indicate that myocardial infarction can cause the chronological change of immediate-early response gene c-Fos protein expression, which might be associated with the neural activity induced by myocardial infarction.
