These mice showed a reduction or delay in synapse formation and a high reduction in the amount of key proteins in the synapses, such as the glutamate receptors, which are ion channels that detect glutamate released from the presynaptic neurons to activate the postsynaptic neurons. To further explore how Prickle regulates synapse numbers, the Zou lab generated mice that mimic a human mutation of Prickle2, which is known to cause autism. When these genes were deleted in adulthood, 70-80% of the synapses disappeared. When these genes were deleted in early development, 70-80% of the synapses failed to form. After Prickle1 and Prickle2 were specifically knocked out in the hippocampus and the prefrontal cortex, the researchers found a 70-80% reduction in the number of glutamatergic synapses. In the new study, the Zou lab focused on the role of a key PCP component called Prickle, which in mice features four family members. 'Building on a previous study where we initially showed the function of the members of the PCP signaling pathway in synapse formation, this new paper further highlights the significance of this pathway in controlling synapse numbers in both the developing and mature brain.' 'One main conclusion of this paper is that the planar cell polarity pathway is responsible for the formation and maintenance of a very large majority of glutamatergic synapses,' said Zou. 6 in the journal Science Advances that the 'planar cell polarity,' or PCP, a powerful signaling pathway that systematically polarizes cells and tissues along the plane of the tissues, is a widely used mechanism for the formation and maintenance of a large number of synapses. Postdoctoral Scholar Yue Ban, Professor Yimin Zou and their colleagues provide promising new evidence Oct. Scientists at the University of California San Diego have been piecing together the mechanisms that appear to plug this gap in neurobiological knowledge. A longstanding missing piece of the synapse puzzle has been an explanation for how glutamatergic synapses are assembled and maintained, leading to further questions about whether a common development mechanism, or pathway, even exists for the large numbers and many types of glutamatergic synapses.

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