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Impaired delay but normal trace eyeblink conditioning in PLCbeta4 mutant mice
Y Kishimoto1, M Hirono, T Sugiyama
1Laboratory of Neurobiophysics, School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan.
Neuroreport
|October 6, 2001
Summary
Phospholipase Cbeta4 (PLCbeta4) is crucial for cerebellar long-term depression (LTD) and delay conditioning. PLCbeta4-deficient mice showed impaired LTD and delay eyeblink conditioning, but not trace conditioning.
Area of Science:
- Neuroscience
- Molecular Biology
- Cellular Biology
Background:
- Phospholipase Cbeta4 (PLCbeta4) is highly expressed in Purkinje cells of the rostral cerebellum.
- The precise functional role of PLCbeta4 in cerebellar circuits remains to be fully elucidated.
Purpose of the Study:
- To investigate the functional role of PLCbeta4 in cerebellar long-term depression (LTD) and eyeblink conditioning.
- To determine if PLCbeta4 is essential for delay and trace eyeblink conditioning paradigms.
Main Methods:
- Utilized PLCbeta4-deficient mice for experimental investigation.
- Assessed cerebellar LTD in the rostral cerebellum.
- Evaluated performance in delay and trace eyeblink conditioning tasks.
Main Results:
- Rostral cerebellar LTD was severely impaired in PLCbeta4-deficient mice.
- Delay eyeblink conditioning was also severely impaired in these mice.
- Trace eyeblink conditioning remained unaffected in PLCbeta4-deficient mice.
Conclusions:
- PLCbeta4 is essential for LTD in the rostral cerebellum.
- PLCbeta4 plays a critical role in delay eyeblink conditioning.
- Rostral cerebellar LTD is a necessary neural substrate for delay conditioning but not for trace conditioning.