Cracking the code of addiction

Welberg, Leonie

doi:10.1038/nrn2921

Research Highlight
Published: 15 September 2010

Addiction

Cracking the code of addiction

Leonie Welberg

Nature Reviews Neuroscience volume 11, page 668 (2010)Cite this article

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In the first paper, Deng et al. used lentivirus-mediated knock down and overexpression of Mecp2 in the nucleus accumbens (NAc) — a striatal area involved in reward processing — of adult mice. In a conditioned place-preference test, Mecp2-knockdown mice showed an increased preference for the chamber that had been paired with amphetamine administration, whereas overexpressing Mecp2 eliminated this preference. This suggests that MeCP2 in the NAc negatively regulates the rewarding properties of amphetamine.

Perhaps surprisingly, mutant mice that constitutively expressed a truncated form of MeCP2 showed no preference for the amphetamine-paired chamber and also showed evidence of reduced reward processing in a sucrose-preference test. This indicates that MeCP2 has a role in reward processing, but the precise effect of manipulating MeCP2 function might depend on the brain area and on developmental effects of MeCP2 on the organization of striatal synapses. Indeed, the mutant mice also had increased immunoreactivity for presynaptic markers of GABA (γ-aminobutyric acid)-ergic synapses in the NAc. Moreover, after amphetamine treatment, they did not show the increased spine density on glutamatergic neurons in this area that is observed in wild-type mice. These findings suggest that MeCP2 affects both the development and adult plasticity of striatal synapses.

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ORIGINAL RESEARCH PAPERS

Deng, J. V. et al. MeCP2 in the nucleus accumbens contributes to neural and behavioral responses to psychostimulants. Nature Neurosci. 13, 1128–1136 (2010)
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Im, H. -I. et al. MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212. Nature Neurosci. 13, 1120–1127 (2010)
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