首页> 外文期刊>Behavioural Brain Research: An International Journal >Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells
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Vestibular stimulation enhances hippocampal long-term potentiation via activation of cholinergic septohippocampal cells

机译:前庭刺激通过激活胆碱能性海马海马细胞增强海马长时程增强

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Vestibular stimulation induced acetylcholine release in the hippocampus, and acetylcholine is known to facilitate long-term potentiation (LTP) in the hippocampus. Thus, we hypothesize that vestibular stimulation enhances LTP in CA1 in freely behaving rats, and this enhancement depends on the activation of septohippocampal cholinergic neurons. Field excitatory postsynaptic potentials were recorded in CA1 area of behaving rats following stimulation of the basal dendritic afferents. LTP was induced by a single stimulation train (100 pulses at 200. Hz) during passive whole-body rotation or during awake-immobility. LTP induced during rotation was significantly larger than that induced during immobility. Pretreatment with cholinergic antagonist atropine sulfate (50. mg/kg i.p.) abolished the facilitation of LTP during rotation as compared to immobility. Selective lesion of cholinergic cells in the medial septum (MS) with 192 IgG-saporin (0.49. μg in 1.4. μl) also abolished the difference in LTP induced during rotation and immobility, which was found in sham-lesion rats. 192 IgG-saporin lesioned rats, as compared to sham-lesion rats, revealed a depletion of MS cells immunopositive to choline acetyltransferase and paling of acetylcholinesterase staining in the hippocampus, without significant change in the number of parvalbumin-immunopositive cells. We conclude that enhancement of LTP during vestibular stimulation is mediated by the activation of cholinergic septohippocampal cells. This is the first direct evidence that vestibular stimulation facilitates hippocampal synaptic plasticity via a cholinergic input.
机译:前庭刺激诱导海马中的乙酰胆碱释放,并且已知乙酰胆碱可促进海马中的长期增强(LTP)。因此,我们假设前庭刺激在行为自由的大鼠中增强了CA1中的LTP,而这种增强取决于海马区胆碱能神经元的激活。在刺激基础树突状传入神经后,在行为大鼠的CA1区域记录了野外兴奋性突触后电位。 LTP是由单个刺激序列(在200.Hz处有100个脉冲)在被动的全身旋转过程中或在清醒不动时诱导的。旋转过程中诱导的LTP明显大于固定时诱导的LTP。与固定性相比,用胆碱能拮抗剂硫酸阿托品(50 mg / kg i.p.)预处理消除了旋转过程中LTP的促进作用。用192 IgG-saporin(1.4.μl中的0.49.μg)在中隔(MS)中对胆碱能细胞的选择性损伤也消除了在假性损伤大鼠中发现的旋转和固定过程中诱导的LTP的差异。与假手术损伤大鼠相比,192 IgG-saporin损伤的大鼠揭示了对胆碱乙酰转移酶免疫阳性的MS细胞的消耗和海马中的乙酰胆碱酯酶染色的变色,而小白蛋白免疫阳性细胞的数量没有明显变化。我们得出结论,前庭刺激过程中LTP的增强是由胆碱能性海马海马细胞的激活介导的。这是第一个直接证据表明前庭刺激通过胆碱能输入促进海马突触可塑性。

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