Washington, Dec 7(ANI): That cocaine, a stimulating alkaloid crushed out of the leaves of the coca plant-increases euphoria and energy as well as triggers off a mind-killing addiction in humans, is well known. But researchers have now for the first time shed light on how it causes its effect on the brain, by tracing the hyperactive high of cocaine to interactions between two types of receiving stations in neurons for nerve signals from their neighbours John Wang, of the University of Missouri, Kansas City School of Medicine, and his colleagues who conducted studies in rats found that when the animals received cocaine, a component of a receptor for the neurotransmitter dopamine tends to grab onto a component of a receptor for glutamate. Neurons trigger nerve impulses in their neighbours by launching bursts of chemicals called neurotransmitters at them. The neurotransmitters activate protein receptors on the receiving neurons, which induce the nerve impulses in the receiving cell. These receptors also adjust themselves in complex ways to alter the sensitivity of the receiving neuron to stimulation. The researchers found that in the striatum of the brain the dopamine receptors known as D2 interfered with the normal function of some glutamate receptors--known as NR2B--by blocking their activation. The researchers also analysed whether this interaction between D2R and NR2B affected the rats' behavioural 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 behavioural 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. The study is published in the December 7 issue of the journal Neuron. (ANI)
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