Recently, increased neuronal activity in nucleus reuniens (Re) has been linked to hyperexcitability within hippocampal-thalamo-cortical networks in the J20 mouse model of amyloidopathy. Here in vitro whole-cell patch clamp recordings were used to compare old pathology-bearing J20 mice and wild-type controls to examine whether altered intrinsic electrophysiological properties could contribute to the amyloidopathy-associated Re hyperactivity. A greater proportion of Re neurons display hyperpolarized membrane potentials in J20 mice without changes to the incidence or frequency of spontaneous action potentials. Re neurons recorded from J20 mice did not exhibit increased action potential generation in response to depolarizing current stimuli but an increased propensity to rebound burst following hyperpolarizing current stimuli. Increased rebound firing did not appear to result from alterations to T-type Ca2+ channels. Finally, in J20 mice, there was an ~8% reduction in spike width, similar to what has been reported in CA1 pyramidal neurons from multiple amyloidopathy mice. We conclude that alterations to the intrinsic properties of Re neurons may contribute to hippocampal-thalmo-cortical hyperexcitability observed under pathological beta-amyloid load.

中文翻译：

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阿尔茨海默病小鼠模型核团核的神经生理学改变

最近，在 J20 淀粉样病变小鼠模型中，团核 (Re) 中增加的神经元活动与海马-丘脑-皮质网络内的过度兴奋有关。在这里，体外全细胞膜片钳记录被用来比较旧的携带病理学的 J20 小鼠和野生型对照，以检查改变的内在电生理特性是否会导致淀粉样变性相关的 Re 过度活跃。在 J20 小鼠中，更大比例的 Re 神经元显示超极化膜电位，而自发动作电位的发生率或频率没有变化。从 J20 小鼠记录的 Re 神经元在去极化电流刺激下没有表现出动作电位产生增加，但在超极化电流刺激后反弹爆发的倾向增加。T 型 Ca2+ 通道的改变似乎并未导致反弹发射增加。最后，在 J20 小鼠中，尖峰宽度减少了约 8%，类似于在多只淀粉样病变小鼠的 CA1 锥体神经元中所报道的情况。我们得出结论，Re 神经元内在特性的改变可能导致在病理性 β-淀粉样蛋白负荷下观察到的海马-丘脑-皮质过度兴奋。