By stimulating dead brain tissue, neuroscientists have concluded that a specific receptor found in the outer layer of neurons functions differently in schizophrenic brains. Schizophrenia, a disorder affecting about 1 percent of Americans, stems partly from genetic factors. Current treatments alleviate only a small fraction of the symptoms, which may include hallucinations, paranoia and disorganized behavior.
The N-methyl-D-aspartate (NMDA) receptor is one of several which bind to glutamate, a key neurotransmitter. In schizophrenic brains, scientists believe the function of NMDA receptors, which normally play a critical role in many neural processes, may be disrupted. How this dysfunction in binding contributes to schizophrenia is unclear, but this latest examination provides the first direct evidence of a correlation to diminished NMDA-receptor function.
The work, led in part by Chang-Gyu Hahn, professor of psychiatry at the University of Pennsylvania, also reveals that decreased NMDA-receptor function coincides with increased activation of another receptor, erbB4. This second receptor is activated by the neurotransmitter neuregulin-1, which is produced by a gene, variations of which indicate an increased probability of schizophrenia. Hahn says that a drug designed to suppress erbB4 activation might alleviate symptoms of schizophrenia better than current treatments do.
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Although understanding molecular dynamics using dead brain tissue seems implausible, Hahn and his colleagues invented a means to stimulate the tissue and measure the resulting activation of receptors—in this case, in 28 brains at autopsy. Previous techniques measured only the quantity of receptors. “We hope that this technique will open new avenues of research,” Hahn says.