Our latest issue of the Neuroscientist, in its regular survey of the field of neuroscience, comments on an article in the Proceedings of the National Academy of Sciences about the effect of stimulant medication on subsequent learning capacity. It was found that “[p]rior treatment with amphetamine or cocaine interfered with the ability of experience in a complex environment to increase dendritic arborization and spine density.” [Ref. 1] Yet it had been established previously that stimulant medication all by itself is capable of increasing dendritic branching and spine density.

It appears that we have to ask more subtle questions than simply whether stimulants provoke neural growth. It may be that if the growth is not shaped or mediated by learning experience then the growth is not much good to us. It may be more like kudzu in Louisiana. Even more ominously, randomly promoted growth may preempt the more useful neural growth on which learning depends. It could even account for the “neuropsychological deficits seen in amphetamine and cocaine addicts.” In sum, then, it may not be good news to discover that stimulant medication promotes neural growth. If not, then we are back to the model that the salutary benefit of stimulants relates to the immediate state change, not to any lingering induced physiological change.

A similar issue has arisen with respect to anti-depressants as well. A recent issue of Science [Laura Helmuth, In Sickness or in Health?, Science, 302, p808, Oct 31, 2003] reports that neural growth in the hippocampus can be documented upon administration of anti-depressants. Is this a case of neural growth being “pushed” or promoted by the presence of the anti-depressant, or may this be the secondary consequence of recovery from depression, namely the resumption of healthy dendritic proliferation. In the latter case, the significant step is not the dendritic budding, but the retention of the buds because they are reinforced by virtue of being integrated into normal functioning. If it is the former, then we may have to modify our partitioning of the structure-versus-function dichotomy in depression. If it is the latter, then we would expect such resumption of growth to accompany successful neurofeedback as well.

One straw in the wind is that if neurogenesis is blocked in rats, then anti-depressants don’t work. That certainly suggests neurogenesis lies within the causal chain of events in recovery from depression, and could even account for the fact that recovery with meds takes weeks to effect, even though the chemical effect of the drugs is essentially immediate. However, another factor to consider is that ECT also causes neurogenesis to increase, and in this case the recovery from depression does not take weeks to occur. It appears unlikely that either depression or ADHD will yield to simple neurochemical models or even simple neural growth models.

I’m glad we have neurofeedback for depression…
Researchers are beginning to investigate approaches to depression that bark up the same tree: repetitive Transcranial Magnetic Stimulation and Vagal Nerve Stimulators. If only Sterman hadn’t discovered neurofeedback thirty years too soon. If it were discovered now, it would be given a fresh look by scientists because it would be seen as a freshly minted gift from the future instead of as a fossil from the past. As it is, we have to brush off the accumulated “Schmutz” from our messy history, get our story together, and learn to sing with one voice.

Reference 1. Kolb B, Gorny G., Li Y, Samaha A-N, Robinson T. 2003. Amphetamine or cocaine limits the ability of later experience to promote structural plasticity in the neocortex and nucleus accumbens. PNAS 100: 10523-8
As referenced in: Neuroscientist, 10, #2, p.91, April 200

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