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Conditioned eyeblink response is impaired in mutant mice lacking NMDA receptor subunit NR2A
Y Kishimoto1, S Kawahara, Y Kirino
1Laboratory of Neurobiophysics, School of Pharmaceutical Sciences, The University of Tokyo, Japan.
Neuroreport
|January 14, 1998
Summary
Mice lacking the NR2A subunit of NMDA receptors showed impaired motor learning. This suggests NR2A is crucial for early learning acquisition, particularly involving the hippocampus and cerebellar deep nuclei.
Area of Science:
- Neuroscience
- Molecular Biology
- Behavioral Genetics
Background:
- NMDA receptor channels, composed of diverse subunits, are vital for synaptic plasticity, learning, and memory.
- Specific subunits, like NR2A and NR2C, may play differential roles in complex cognitive functions such as motor learning.
Purpose of the Study:
- To investigate the specific roles of NR2A and NR2C NMDA receptor subunits in the acquisition of motor learning.
- To determine the involvement of cerebellar and hippocampal pathways in conditioned eyeblink response learning.
Main Methods:
- Utilized gene knockout mice lacking NR2A, NR2C, or both subunits.
- Assessed the acquisition of a classically conditioned eyeblink response using a delayed-conditioning paradigm.
- Correlated behavioral deficits with known subunit distribution in brain regions.
Main Results:
- Mice lacking NR2C showed no significant impairment in motor learning.
- Mice lacking NR2A, or both NR2A and NR2C, exhibited impaired early acquisition of the conditioned eyeblink response.
- Findings suggest NR2A is critical for the initial stages of this motor learning task.
Conclusions:
- Early acquisition of the conditioned eyeblink response is dependent on the NR2A subunit of NMDA receptors.
- The learning process does not rely on NMDA receptors in the cerebellar cortex.
- Involvement of the hippocampus and/or cerebellar deep nuclei is indicated for early motor learning acquisition.