Abstract
Background
Myocyte enhancer factor 2 (MEF2) transcription factors play critical roles in diverse
cellular processes during central nervous system development. Studies attempting to
address the role of MEF2 in brain have largely relied on overexpression of a constitutive
MEF2 construct that impairs memory formation or knockdown of MEF2 function that increases
spine numbers and enhances memory formation. Genetic deletion of individual MEF2 isoforms
in brain during embryogenesis demonstrated that Mef2c loss negatively regulates spine numbers resulting in learning and memory deficits,
possibly as a result of its essential role in development.
Methods
To investigate MEF2C function in brain further, we genetically deleted Mef2c during postnatal development in mice. We characterized these conditional Mef2c knockout mice in an array of behavioral paradigms and examined the impact of postnatal
loss of Mef2c on long-term potentiation.
Results
We observed increased spine numbers in hippocampus of the conditional Mef2c knockout mice. However, the postnatal loss of Mef2c did not impact learning and memory, long-term potentiation, or social and repetitive
behaviors.
Conclusions
Our findings demonstrate a critical role for MEF2C in the regulation of spine numbers
with a dissociation of learning and memory, synaptic plasticity, and measures of autism-related
behaviors in postnatal brain.
Keywords
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Article info
Publication history
Published online: October 08, 2015
Accepted:
September 24,
2015
Received in revised form:
September 4,
2015
Received:
July 24,
2015
Identification
Copyright
© 2015 Society of Biological Psychiatry. Published by Society of Biological Psychiatry All rights reserved.
