Deletion of the endogenous TrkB.T1 receptor isoform restores the number of hippocampal CA1 parvalbumin-positive neurons and rescues long-term potentiation in pre-symptomatic mSOD1(G93A) ALS mice.

Deletion of the endogenous TrkB.T1 receptor isoform restores the number of hippocampal CA1 parvalbumin-positive neurons and rescues long-term potentiation in pre-symptomatic mSOD1(G93A) ALS mice.
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删除内源性 TrkB.T1 受体亚型可恢复海马 CA1 小清蛋白阳性神经元的数量,并挽救症状前 mSOD1(G93A) ALS 小鼠的长期增强作用。

DOI:
10.1016/j.mcn.2018.03.010
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发表时间:
2018
期刊:
Molecular and cellular neurosciences
影响因子:
--
通讯作者:
Minciacchi,Diego
Minciacchi,Diego
中科院分区:
--
文献类型:
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作者:
Quarta,Eros;Fulgenzi,Gianluca;Bravi,Riccardo;Cohen,ErezJames;Yanpallewar,Sudhirkumar;Tessarollo,Lino;Minciacchi,Diego

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