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G9a influences neuronal subtype specification in striatum.

Ian Maze¹, Dipesh Chaudhury², David M Dietz³

¹Laboratory of Chromatin Biology and Epigenetics, The Rockefeller University, New York, New York, USA.

Nature Neuroscience

|March 4, 2014

Summary

Cocaine affects histone methyltransferase G9a in specific brain neurons, altering gene expression and neuronal identity. This epigenetic regulation influences how mice respond to repeated cocaine exposure.

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Area of Science:

Neuroscience
Epigenetics
Molecular Biology

Background:

Cocaine addiction involves changes in gene expression within the brain.
Histone methyltransferase G9a (HMT G9a) is implicated in cellular responses to chronic cocaine.
HMT G9a repression by cocaine occurs in both striatonigral and striatopallidal neurons.

Purpose of the Study:

To investigate the role of HMT G9a in distinct neuronal subtypes.
To understand how HMT G9a regulates neuronal identity and cocaine-induced behaviors.
To explore the impact of cell type-specific histone methylation on behavioral responses.

Main Methods:

Ribosomal affinity purification to identify neurons affected by G9a repression.
Conditional knockout and overexpression of G9a in Drd1 and Drd2 expressing neurons.
Analysis of transcriptional programs, projection patterns, and electrophysiological properties.

Main Results:

Cocaine-induced G9a repression occurs in both Drd1 and Drd2 medium spiny neurons.
Altering G9a levels in specific neuronal types leads to divergent behavioral responses to cocaine.
Developmental deletion of G9a in Drd2 neurons caused a 'switching' of neuronal identity towards Drd1-like properties.

Conclusions:

G9a plays a crucial role in maintaining neuronal subtype identity.
Cell type-specific histone methylation patterns are critical for regulating behavioral responses to stimuli like cocaine.
Epigenetic modifications by G9a offer potential targets for understanding and treating substance use disorders.