“Blocking the formation of neurons in the hippocampus blocks the behavioral effects of antidepressants in mice, say researchers funded by the National Institutes of Health (NIH). Their finding lends new credence to the proposed role of such neurogenesis in lifting mood. It also helps to explain why antidepressants typically take a few weeks to work, note Rene Hen, Ph.D., Columbia University, and colleagues, who report on their study in the August 8th Science.” EurekAlert!
You heard it here first; we are in the midst of a fundamental paradigm shift reconceptualizing how psychiatric medications work and, by extension, the nature of psychiatric disease. For more than fifty years, since the advent of the modern psychopharmaceutical age, mechanisms of action of these drugs have been conceived of in terms of their effects on neurotransmitters at the synapses between neurons. This filtered down to the lay public as the “chemical imbalance” notion of psychiatric illness. As my diatribe here about Peter Breggin’s diatribe against biological psychiatry last week suggests, this model for psychiatric illness and drug action has not lent itself readily to empirical validation and the CNS remained a black box. As far as it has gone and as far as it has been believed, the neurotransmitter theories of mental illneess have functioned in the same way that mythology does. I don’t mean that this is useless, but it has no ready answers to the agnostics’ challenges.
But I suggested that Breggin’s critique was a straw man agrument, railing against a reductionist and outmoded version of psychiatric knowledge without much relationship to contemporary findings. Findings like the one discussed in this news item take us into a realm where we understand that structural, as well as functional, changes in numbers, connectivity and vitality of neurons in specfic brain regions underpin psychaitric conditions, and that the medications known to be effective against those diseases can be demonstrated to protect against or reverse those neuronal-structural changes. Even Breggin suggested that he might be persuaded by pretty pictures demonstrating the reality of psychiatric illness.
This is true not only for depression and antidepressants, as discussed in this study, but for other major mental illnesses as well. In schizophrenia research, for example, a new focus has emerged in the last decade or so on the neurotransmitter NMDA, now considered a widespread and crucial excitatory agent in the brain but virtually unstudied just several decades before when I went to medical school. NMDA is important not only in the classical neurotransmitter sense (of its level of activity underlying the functional state of various neuronal circuits in the brain) but because it is an “excitotoxin”, causing neuronal injury. There are ways in which life stresses injure or destroy neurons, and there are ways in which health-promoting activities (medications but also exercise, stress reduction, nutrition, rest, etc.) protect against or reverse such damage, visibly, demonstrably. The perennial tortured efforts to bridge the longstanding gulf between the physiological and the psychological in psychiatry by suggesting pie-in-the-sky models of how experience might be transduced into brain changes are finally bearing empirical fruit, and with that advance will fall the last vestiges of the artificial distinctions betwen brain and mind.
