Impaired delay but normal trace eyeblink conditioning in PLCβ4 mutant mice

被引:48
|
作者
Kishimoto, Y
Hirono, M
Sugiyama, T
Kawahara, S
Nakao, K
Kishio, M
Katsuki, M
Yoshioka, T
Kirino, Y [1 ]
机构
[1] Univ Tokyo, Sch Pharmaceut Sci, Lab Neurobiophys, Bunkyo Ku, Tokyo 1130033, Japan
[2] Waseda Univ, Adv Res Inst Sci & Engn, Shinjuku Ku, Tokyo 1698555, Japan
[3] Waseda Univ, Sch Human Sci, Dept Mol Neurobiol, Tokorozawa, Saitama 3591192, Japan
[4] Univ Tokyo, Inst Med Sci, Ctr Med Expt, Lab DNA Biol & Embryo Engn,Minato Ku, Tokyo 1088639, Japan
关键词
cerebellar LTD; classical eyeblink conditioning; phospholipase C beta 4;
D O I
10.1097/00001756-200109170-00033
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To elucidate the functional role of phospholipase C beta4 (PLC beta4), which is highly expressed in the Purkinje cells of the rostral cerebellum, cerebellar long-term depression (LTD) and delay and trace eyeblink conditioning were investigated in PLC beta4-deficient mice. Rostral cerebellar LTD and delay eyeblink conditioning were severely impaired, whereas trace eyeblink conditioning was not. These results indicate that PLC beta4 is essential for LTD in the rostral cerebellum and delay conditioning, but not trace conditioning. Rostral cerebellar LTD may be required as a neural substrate for delay conditioning, but is not required for trace conditioning. NeuroReport 12:2919-2922 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:2919 / 2922
页数:4
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