AI Article Synopsis
- Researchers found that genetic variation in the Grm2 gene, which affects a receptor for glutamate, influences alcohol preference in animal models.
- A specific mutation (Grm2 *407) leads to a lack of this receptor and is linked to increased alcohol consumption in specially bred rats.
- The study suggests mGluR2 plays a crucial role in determining alcohol preference and could be a target for treatments related to alcohol consumption.
Article Abstract
Identification of genes influencing complex traits is hampered by genetic heterogeneity, the modest effect size of many alleles, and the likely involvement of rare and uncommon alleles. Etiologic complexity can be simplified in model organisms. By genomic sequencing, linkage analysis, and functional validation, we identified that genetic variation of Grm2, which encodes metabotropic glutamate receptor 2 (mGluR2), alters alcohol preference in animal models. Selectively bred alcohol-preferring (P) rats are homozygous for a Grm2 stop codon (Grm2 *407) that leads to largely uncompensated loss of mGluR2. mGluR2 receptor expression was absent, synaptic glutamate transmission was impaired, and expression of genes involved in synaptic function was altered. Grm2 *407 was linked to increased alcohol consumption and preference in F2 rats generated by intercrossing inbred P and nonpreferring rats. Pharmacologic blockade of mGluR2 escalated alcohol self-administration in Wistar rats, the parental strain of P and nonpreferring rats. The causal role of mGluR2 in altered alcohol preference was further supported by elevated alcohol consumption in Grm2 (-/-) mice. Together, these data point to mGluR2 as an origin of alcohol preference and a potential therapeutic target.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800985 | PMC |
| http://dx.doi.org/10.1073/pnas.1309839110 | DOI Listing |
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