Scientists from Columbia University discovered that social memory impairments may be linked to schizophrenia and likely stem from a decrease in the number of inhibitory neurons in a region of the brain that underwent limited exploration. The findings will help scientists better understand the underlying mechanisms that stimulate the severe symptoms of schizophrenia, such as emotional blunting, social withdrawal and hindered motivation.
Schizophrenia, which affects approximately one in every 100 adults in the world, is believed to stem from problems in the hippocampus, the area of the brain that is responsible for memory and spatial navigation. Although this area of the brain has been studied extensively for connections to schizophrenia, the one region left unexamined in the hippocampus is a small area known as CA2.
"Smaller and less well-defined than other parts of the hippocampus, CA2 was like a small island that was depicted on old maps but remained unexplored," said Vivien Chevaleyre, lead author of the paper, in a press release.
Previous studies have shown that CA2 is linked to vasopressin, a hormone that is involved in sexual bonding and other social behaviors and is typically impaired in those with schizophrenia. Furthermore, postmortem examinations of schizophrenic patients found that their CA2 neurons experienced a significant reduction in inhibitory neurons.
The current team of researchers examined levels of CA2 inhibitory neurons in a mouse model of schizophrenia and compared the control group of healthy mice to the schizophrenia group. The results showed similar patterns to the postmortem examinations — the schizophrenia group was severely lacking in CA2 inhibitory neurons. Furthermore, the group also showed a reduction in social memory capacity in comparison to the control group, pointing to CA2 as a factor in controlling the social behavior changes in those with schizophrenia.
"Even the timing of the emergence of symptoms in the mice, during young adulthood, parallels the onset of schizophrenia in humans," said Joseph Gogos, lead author of the paper.
"We can now examine the effects of schizophrenia at the cellular level and at the behavioral level," said Steven Siegelbaum, co-author of the paper. "This essentially opens up a whole new avenue for research that could lead to earlier diagnosis and more effective treatments for schizophrenia."
The results were published in the Jan. 6 issue of Neuron.
