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| English: synapse diagram: cells communicate by electrical messages passed from the axon of one nerve cell to the dendrite of another. This transmission is not electrical, but is mediated by chemicals called neurotransmitters such as serotonin and dopamine released into the synapse -- the space between the axon and the dendrite. An imbalance --either too much or too little -- can result in improper communication and physical or psychological symptoms. (Photo credit: Wikipedia) |
Scientists have identified one potentially key type of cocaine-related change that appears to last for many months after the last cocaine exposure, and perhaps longer: an alteration in the physical structure of nerve cells in the NAc. Chronic cocaine exposure causes these cells to extend and sprout new offshoots on their dendrites (Nestler, 2001; Robinson and Berridge, 2001). Dendrites are the branch-like fibers that grow out from nerve cell bodies and collect incoming signals from other nerve cells. Just as a bigger antenna picks up more radio waves, more dendrite branches in the NAc theoretically will collect a greater volume of nerve signals coming from other regions—for example, the hippocampus, amygdala, and frontal cortex. This will give those other regions an enhanced influence over the NAc, which could drive some of the very long-lived behavioral changes associated with addiction. For example, enhanced inputs from the hippocampus and amygdala could be responsible for the intense craving that occurs when drug-associated memories are stimulated (e.g., by drug paraphernalia).
While we do not yet know how cocaine triggers NAc nerve cells to grow and sprout new offshoots, ΔFosB appears to be involved. Recall that one of the genes stimulated by ΔFosB is CDK5, a known regulator of nerve cell growth. When laboratory animals are treated with a compound that deactivates CDK5 in the NAc and then are given cocaine, the nerve cell growth normally associated with exposure to the drug does not occur.
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