The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we in...The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we investigated the effects of damage to the inferior alveolar nerve, an important peripheral nerve in the trigeminal sensory pathway, on learning and memory be-haviors and structural changes in related brain regions, in a mouse model of Alzheimer’s disease. Inferior alveolar nerve transection or sham surgery was performed in middle-aged （4-month-old） or elderly （7-month-old） senescence-accelerated mouse prone 8 （SAMP8） mice. When the middle-aged mice reached 8 months （middle-aged group 1） or 11 months （middle-aged group 2）, and the elderly group reached 11 months, step-down passive avoidance and Y-maze tests of learn-ing and memory were performed, and the cholinergic system was examined in the hippocampus （Nissl staining and acetylcholinesterase histochemistry） and basal forebrain （choline acetyltrans-ferase immunohistochemistry）. In the elderly group, animals that underwent nerve transection had fewer pyramidal neurons in the hippocampal CA1 and CA3 regions, fewer cholinergic ifbers in the CA1 and dentate gyrus, and fewer cholinergic neurons in the medial septal nucleus and vertical limb of the diagonal band, compared with sham-operated animals, as well as showing impairments in learning and memory. Conversely, no signiifcant differences in histology or be-havior were observed between middle-aged group 1 or group 2 transected mice and age-matched sham-operated mice. The present ifndings suggest that trigeminal nerve damage in old age, but not middle age, can induce degeneration of the septal-hippocampal cholinergic system and loss of hippocampal pyramidal neurons, and ultimately impair learning ability. Our results highlight the importance of active treatment of trigeminal nerve damage in elderly patients and those with Alzheimer’s disease, and indicate that tooth extract展开更多
目的检测吗啡(morphine,Mo)r点燃条件位置性偏爱(conditioned place preference,CPP)重现大鼠海马CA1区多巴胺(dopamine,DA)递质的变化,揭示海马CA1区DA递质的变化与吗啡点燃诱发CPP重现的关系.方法用恒量法(10mg/kg)给大鼠连续颈背部...目的检测吗啡(morphine,Mo)r点燃条件位置性偏爱(conditioned place preference,CPP)重现大鼠海马CA1区多巴胺(dopamine,DA)递质的变化,揭示海马CA1区DA递质的变化与吗啡点燃诱发CPP重现的关系.方法用恒量法(10mg/kg)给大鼠连续颈背部皮下注射(subcutaneous,SC)吗啡8d建立CPP模型;用生理盐水替代吗啡训练大鼠10d,使形成的CPP逐渐消退;单次SC2.5mg/kg吗啡点燃已消退的CPP.用荧光分光光度法检测吗啡点燃CPP重现大鼠海马CA1区DA递质的变化.结果SC10mg/kg吗啡8d建立CPP,生理盐水训练10d使已形成的CPP消退,小剂量吗啡(2.5mg/kg)使消退的CPP重现;吗啡点燃CPP重现大鼠海马CA1区DA含量与对照组比较显著增加(P<0.05).结论吗啡点燃CPP重现时大鼠海马CA1区DA增加,小剂量吗啡诱发大鼠CPP重现行为可能与海马CA1区中DA含量增加有关.展开更多
目的检测吗啡诱发条件位置性偏爱(conditioned place preference,CPP)大鼠海马CA1区NMDA受体亚型NR2A、NR2B的变化,探讨NR2A、NR2B在吗啡精神依赖形成过程的作用与可能机制.方法采用恒量法(10mg/kg)连续颈背部皮下注射(subcutaneous,SC...目的检测吗啡诱发条件位置性偏爱(conditioned place preference,CPP)大鼠海马CA1区NMDA受体亚型NR2A、NR2B的变化,探讨NR2A、NR2B在吗啡精神依赖形成过程的作用与可能机制.方法采用恒量法(10mg/kg)连续颈背部皮下注射(subcutaneous,SC)吗啡8 d建立大鼠CPP模型.采用免疫组化法测定海马CA1区NR2A、NR2B的表达.结果 SC 10 mg/kg吗啡8 d建立大鼠CPP模型,吗啡组海马CA1区NR2A表达与生理盐水组比较无显著性变化(P>0.05),而NR2B表达较生理盐水对照组增加(P<0.05).结论吗啡诱导大鼠CPP海马CA1区NR2B表达增加,NR2B可能参与吗啡诱导CPP形成.展开更多
基金supported by the National Natural Science Foundation of China,No.81371107,81470760the Natural Science Foundation of Guangdong Province in China,No.S2013010015888+1 种基金the Foundation of Open Laboratory of Sun Yat-sen University in China,No.KF201312a grant from Translational Medicine Center,Guangdong Department of Science&Technology,No.2011A080300002
文摘The tooth belongs to the trigeminal sensory pathway. Dental damage has been associated with impairments in the central nervous system that may be mediated by injury to the trigeminal nerve. In the present study, we investigated the effects of damage to the inferior alveolar nerve, an important peripheral nerve in the trigeminal sensory pathway, on learning and memory be-haviors and structural changes in related brain regions, in a mouse model of Alzheimer’s disease. Inferior alveolar nerve transection or sham surgery was performed in middle-aged （4-month-old） or elderly （7-month-old） senescence-accelerated mouse prone 8 （SAMP8） mice. When the middle-aged mice reached 8 months （middle-aged group 1） or 11 months （middle-aged group 2）, and the elderly group reached 11 months, step-down passive avoidance and Y-maze tests of learn-ing and memory were performed, and the cholinergic system was examined in the hippocampus （Nissl staining and acetylcholinesterase histochemistry） and basal forebrain （choline acetyltrans-ferase immunohistochemistry）. In the elderly group, animals that underwent nerve transection had fewer pyramidal neurons in the hippocampal CA1 and CA3 regions, fewer cholinergic ifbers in the CA1 and dentate gyrus, and fewer cholinergic neurons in the medial septal nucleus and vertical limb of the diagonal band, compared with sham-operated animals, as well as showing impairments in learning and memory. Conversely, no signiifcant differences in histology or be-havior were observed between middle-aged group 1 or group 2 transected mice and age-matched sham-operated mice. The present ifndings suggest that trigeminal nerve damage in old age, but not middle age, can induce degeneration of the septal-hippocampal cholinergic system and loss of hippocampal pyramidal neurons, and ultimately impair learning ability. Our results highlight the importance of active treatment of trigeminal nerve damage in elderly patients and those with Alzheimer’s disease, and indicate that tooth extract
文摘目的检测吗啡(morphine,Mo)r点燃条件位置性偏爱(conditioned place preference,CPP)重现大鼠海马CA1区多巴胺(dopamine,DA)递质的变化,揭示海马CA1区DA递质的变化与吗啡点燃诱发CPP重现的关系.方法用恒量法(10mg/kg)给大鼠连续颈背部皮下注射(subcutaneous,SC)吗啡8d建立CPP模型;用生理盐水替代吗啡训练大鼠10d,使形成的CPP逐渐消退;单次SC2.5mg/kg吗啡点燃已消退的CPP.用荧光分光光度法检测吗啡点燃CPP重现大鼠海马CA1区DA递质的变化.结果SC10mg/kg吗啡8d建立CPP,生理盐水训练10d使已形成的CPP消退,小剂量吗啡(2.5mg/kg)使消退的CPP重现;吗啡点燃CPP重现大鼠海马CA1区DA含量与对照组比较显著增加(P<0.05).结论吗啡点燃CPP重现时大鼠海马CA1区DA增加,小剂量吗啡诱发大鼠CPP重现行为可能与海马CA1区中DA含量增加有关.
