PRRT2: from Paroxysmal Disorders to Regulation of Synaptic Function

Flavia Valtorta, F. Benfenati, Federico Zara, Jacopo Meldolesi

Research output: Contribution to journalReview articlepeer-review


In the past few years, proline-rich transmembrane protein (PRRT)2 has been identified as the causative gene for several paroxysmal neurological disorders. Recently, an important role of PRRT2 in synapse development and function has emerged. Knock down of the protein strongly impairs the formation of synaptic contacts and neurotransmitter release. At the nerve terminal, PRRT2 endows synaptic vesicle exocytosis with Ca2+ sensitivity by interacting with proteins of the fusion complex and with the Ca2+ sensors synaptotagmins (Syts). In the postsynaptic compartment, PRRT2 interacts with glutamate receptors. The study of PRRT2 and of its mutations may help in refining our knowledge of the process of synaptic transmission and elucidating the pathogenetic mechanisms leading to derangement of network function in paroxysmal disorders.

Original languageEnglish
Pages (from-to)668-679
Number of pages12
JournalTrends in Neurosciences
Issue number10
Publication statusPublished - Oct 1 2016


  • dyskinesia
  • epilepsy
  • neuronal development
  • synaptic transmission
  • synaptopathies

ASJC Scopus subject areas

  • Neuroscience(all)


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