Two new studies provide insight into “dendritic spines” on neurons and schizophrenia. People with this mental disorder have a lower density of these spines in several brain areas when compared to those without schizophrenia. It appears that certain proteins regulate the number of spines. In recent animal studies, researchers explored what happens if these proteins are reduced.

Dendritic spines play a crucial role in transmission of information among neurons (brain cells). A neuron communicates through dendrites that extend from the cell body; they look like intricate, spreading tree branches. Tiny nubs called spines stick out from the dendrite surface and connect the “listening” neuron with the one doing the “talking.” As the primary site of excitatory neurotransmission, dendritic spines are crucial to nearly every aspect of brain function.

A prominent theory about schizophrenia suggests that a lower density of spines leads to reduced transmission of information, which in turn contributes to symptoms such as cognitive deficits. In two separate studies, researchers reduced the levels of two proteins that may play a role in schizophrenia, providing clues about what may go wrong in the illness.

The first study, published October 22nd in Neuron, reports that the protein ankyrin-G is important for maintaining the proper number of spines. Spines are dynamic structures, especially during development, appearing and disappearing over time in response to the amount of communication they receive. Lead study author and two-time NARSAD Young Investigator Grantee Peter Penzes, Ph.D., of Northwestern University, and colleagues found that reducing the levels of ankyrin-G in neurons decreased the number of spines present and led to less excitatory neurotransmission. Also involved in this study was NARSAD Young Investigator Grantee Geoffrey Swanson, Ph.D.

In the second study, published October 8th in The Journal of Neuroscience, Li Zheng, Ph.D., and colleagues at the National Institute of Mental Health examined the spines from mice that lacked the protein dysbindin. The scientists found that, like ankyrin-G, dysbindin is critical for the preservation of spines; deletion of the protein resulted in too many spines disappearing.

Read the abstract for these research papers:

• Journal: Cell
• The Journal of Neuroscience

Read more about this research on the Schizophrenia Research Forum.