UBneuro Researchers unravel controversial role of Complexin in Neuronal Synapse

In a groundbreaking study, scientists have clarified the long-debated function of Complexin within the neuronal synapse, shedding light on its crucial role in various neurological conditions

Neurotransmission, a complex phenomenon central to nervous system function, has long perplexed researchers due to the intricate interactions of proteins involved, occurring within milliseconds. Among these proteins, Complexin has been a subject of intense scrutiny due to its association with conditions like schizophrenia, Alzheimer’s, and Parkinson’s. Conflicting findings in previous studies had clouded its role, with some suggesting it activates neurotransmitter release while others indicate the opposite effect, particularly in specific synapses. However, attributing these discrepancies to experimental variations or species differences has now been disproven.

Unlocking the Enigma: Complexin’s Dual Role Revealed in Central Synapses

Recently published in PNAS, a collaborative effort between researchers from UBneuro, IDIBELL, and the Max-Planck Institute of Multidisciplinary Sciences (MPI-NAT) has provided clarity by revealing Complexin’s dual role. Leveraging cutting-edge electrophysiology techniques and building upon the groundwork laid by Drs. Holger Taschenberger and Kun-Han Lin, along with the expertise of Profs. Nils Brose and Erwin Neher, a Nobel laureate in Physiology or Medicine, the team elucidated Complexin’s function across various central synapses. Through meticulous analysis and the development of a sophisticated mathematical model, they demonstrated that Complexin serves as both a regulator, ensuring proper vesicle preparation prior to nerve stimulation, and a facilitator, promoting vesicle fusion upon stimulation. Its absence disrupts the protein machinery, leading to abnormal neurotransmitter release, out of sync with nerve impulses.

Dr. Francisco López-Murcia, lead author of the study and principal investigator at UBneuro, IDIBELL, and the Max-Planck Institute satellite group, predicts that this research will be a landmark in neurobiology.

Establishing a Satellite Group at the Max-Planck Institute

Dr. López-Murcia, having completed his postdoctoral work at Prof. Nils Brose’s lab at MPI-NAT, has recently joined the cellular and molecular neurobiology research group at UBneuro and IDIBELL. For the next five years, this group will remain affiliated with the Max Planck Institute as a satellite group, benefiting from collaborative opportunities and funding support. Dr. López-Murcia aims to leverage this partnership, alongside his own grants, to advance understanding of nervous system disorders linked to Complexin and other synaptic proteins.

Reference Article

Francisco José López-Murcia et al. Complexin has a dual synaptic function as checkpoint protein in vesicle priming and as a promoter of vesicle fusion. PNAS. 2024.