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Cocaine high caused by interference in neuronal receiving stations

between D2R and NR2B occurred specifically in the striatum of the brain—the region known to be responsible for cocaine's stimulating effects.

The researchers also analyzed whether this interaction between D2R and NR2B affected the rats' behavioral response to cocaine—specifically the hyperactivity and intensive sniffing and biting the drug elicits in the animals. They found that drugs that either activated the D2R subunit or inactivated the NR2B subunit tended to enhance such behavioral responses to cocaine.

"These results provide strong evidence supporting a critical role of the D2R-NR2B interaction in mediating cocaine's effect on [kinase binding and phosphorylation] and in constructing a full-scale motor response to cocaine," concluded the researchers.


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Source:Cell Press


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