Human and animal studies have found that brains go through substantialsynaptic pruning during childhood, removing approximately half of all synapses until puberty. While the pruning of synapses is a natural process, some researchers have theorized that schizophrenia arises from excessive pruning (Siekmeier & Hoffman, 2002). Presuming schizophrenia is a disorder of disruptions in neural connectivity caused by excessive pruning, then efforts to prevent the onset of psychosis and other symptoms of schizophrenia should being prior to adolescence. Identification of likely prodromes should therefore occur as early as possible in development.

Identifying the areas of the brain and specific neurotransmitters that play a role in pruning, in particular pruning likely specific to schizophrenia is an important step to keep those areas from being pruned unnecessarily. One possible prevention strategy could be to stimulate glutamate receptors on pyramidal neurons during childhood or before the heightened rate of pruning. Great care would need to be taken to be sure that only areas with excessive synaptic pruning be targeted. Animal studies could help to locate which agonist will bind to the correct receptors. Some early research is encouraging, as a study on amphibians found that after chronic NMDA treatment, changes in the magnitude of NMDA currents were detected in glutamatergic synaptic currents (Hickmott & Constantive-Paton, 1997). It will likely take many years to be confident that the introduction of pharmacological treatments to prevent unnecessary pruning will have benefits that outweigh the risks.

Animal research can and has helped to identify novel treatments for a number of diseases. For more information on how to support humane animal research go to http://www.ucla-pro-test.org/

References

Hickmott, P. W., & Constantine-Paton, M. (1997). Experimental down-regulation of the NMDA channel associated with synapse pruning. The Journal of Neurophysiology, 78, 1096-1107.

Siekmeier, P. J., Hoffman, R. E. (2002). Enhanced semantic priming in schizophrenia: a computer model based on excessive pruning of local connections in association cortex. British Journal of Psychiatry, 180, 345-350.