目的观察恩氟烷、异氟烷的遗忘作用与NMDA受体的关系。方法小鼠分别腹腔注射恩氟烷(0.4ml.kg-1)或异氟烷(0.3ml.kg-1)建立遗忘模型,在跳台实验和避暗实验中分别观察不同剂量NMDA(25、50、75ng)侧脑室注射(intracerebroventricular injec...目的观察恩氟烷、异氟烷的遗忘作用与NMDA受体的关系。方法小鼠分别腹腔注射恩氟烷(0.4ml.kg-1)或异氟烷(0.3ml.kg-1)建立遗忘模型,在跳台实验和避暗实验中分别观察不同剂量NMDA(25、50、75ng)侧脑室注射(intracerebroventricular injection,icv)对遗忘小鼠错误次数(error times,ETs)、跳台潜伏期(step down latency,SDL)、步入潜伏期(step through latency,STL)的影响。结果侧脑室注射NMDA(50、75ng)可减少恩氟烷、异氟烷所致遗忘小鼠的ETs,延长SDL和STL。结论侧脑室注射NMDA可部分改善恩氟烷、异氟烷的遗忘作用,NMDA受体是二者所致遗忘作用的重要靶位。展开更多
N-methyl-D-aspartate receptors(NMDARs)play crucial roles in neuronal plasticity and brain function by sensing key neurotransmitters,such as glutamate and glycine.In a tour-de-force,Zhang et al.[1]provide the first ima...N-methyl-D-aspartate receptors(NMDARs)play crucial roles in neuronal plasticity and brain function by sensing key neurotransmitters,such as glutamate and glycine.In a tour-de-force,Zhang et al.[1]provide the first images of native NMDARs directly extracted from rat brains,revealing key aspects of NMDAR assembly and diversity.展开更多
Growth arrest DNA damage-inducible protein 45β(GADD45B)has been reported to be a regulatory factor for active DNA demethylation and is implicated in the modulation of synaptic plasticity and chronic stress-related ps...Growth arrest DNA damage-inducible protein 45β(GADD45B)has been reported to be a regulatory factor for active DNA demethylation and is implicated in the modulation of synaptic plasticity and chronic stress-related psychopathological processes.However,its precise role and mechanism of action in stress susceptibility remain elusive.In this study,we found a significant reduction in GADD45B expression specifically in the ventral,but not the dorsal hippocampal CA1(dCA1)of stress-susceptible mice.Furthermore,we demonstrated that GADD45B negatively regulates susceptibility to social stress and NMDA receptor-dependent long-term potentiation(LTP)in the ventral hippocampal CA1(vCA1).Importantly,through pharmacological inhibition using the NMDA receptor antagonist MK801,we provided further evidence supporting the hypothesis that GADD45B potentially modulates susceptibility to social stress by influencing NMDA receptor-mediated LTP.Collectively,these results suggested that modulation of NMDA receptor-mediated synaptic plasticity is a pivotal mechanism underlying the regulation of susceptibility to social stress by GADD45B.展开更多
文摘目的观察恩氟烷、异氟烷的遗忘作用与NMDA受体的关系。方法小鼠分别腹腔注射恩氟烷(0.4ml.kg-1)或异氟烷(0.3ml.kg-1)建立遗忘模型,在跳台实验和避暗实验中分别观察不同剂量NMDA(25、50、75ng)侧脑室注射(intracerebroventricular injection,icv)对遗忘小鼠错误次数(error times,ETs)、跳台潜伏期(step down latency,SDL)、步入潜伏期(step through latency,STL)的影响。结果侧脑室注射NMDA(50、75ng)可减少恩氟烷、异氟烷所致遗忘小鼠的ETs,延长SDL和STL。结论侧脑室注射NMDA可部分改善恩氟烷、异氟烷的遗忘作用,NMDA受体是二者所致遗忘作用的重要靶位。
文摘N-methyl-D-aspartate receptors(NMDARs)play crucial roles in neuronal plasticity and brain function by sensing key neurotransmitters,such as glutamate and glycine.In a tour-de-force,Zhang et al.[1]provide the first images of native NMDARs directly extracted from rat brains,revealing key aspects of NMDAR assembly and diversity.
基金supported by the National Natural Science Foundation of China(82201667,82371195,and 82304474)the Research Fund of Jianghan University(2023JCYJ15).
文摘Growth arrest DNA damage-inducible protein 45β(GADD45B)has been reported to be a regulatory factor for active DNA demethylation and is implicated in the modulation of synaptic plasticity and chronic stress-related psychopathological processes.However,its precise role and mechanism of action in stress susceptibility remain elusive.In this study,we found a significant reduction in GADD45B expression specifically in the ventral,but not the dorsal hippocampal CA1(dCA1)of stress-susceptible mice.Furthermore,we demonstrated that GADD45B negatively regulates susceptibility to social stress and NMDA receptor-dependent long-term potentiation(LTP)in the ventral hippocampal CA1(vCA1).Importantly,through pharmacological inhibition using the NMDA receptor antagonist MK801,we provided further evidence supporting the hypothesis that GADD45B potentially modulates susceptibility to social stress by influencing NMDA receptor-mediated LTP.Collectively,these results suggested that modulation of NMDA receptor-mediated synaptic plasticity is a pivotal mechanism underlying the regulation of susceptibility to social stress by GADD45B.
