Neurons are able to detect the loss of autaptic synapsis -established by themselves- and recover the reduction of nervous neurotransmission through the formation and promotion of new connections. This is the main conclusion of the new article published in the journal Communications Biology, by researchers Artur Llobet and Cecília Velasco, members of the Faculty of Medicine and Health Sciences, the Institute of Neurosciences of the UB (UBNeuro) and the Bellvitge Institute for Biomedcal Research (IDIBELL).
The team led by Llobet had described in previous studies the ability of SPARC protein -secreted factor by glial cells in the nervous system- to remove synapsis. However, there were many doubts on the used mechanism by this protein and the target synapses.
Surprisingly, a series of following experiments to study the activity of SPARC protein revealed that those neurons exposed to the action of this factor showed an early fall into neurotransmission, an ability that could be then recovered with the present SPARC. Therefore, neurons expressed a new homeostatic presynaptic plasticity mechanism, which contributes to maintain the right neurotransmission levels in the neural circuits.
According to the lecturer Llobet, “we wanted to describe the action selectivity of SPARC on the synapses and we ended up doing research on a new plasticity mechanism”. The fast recovery of autaptic synapses in the experimental trials “shows that neurons could use these contacts to detect a reduction in the neurotransmission and therefore, create new synapses to re-establish the base levels”, notes Cecília Velasco, first author of the study.
Universitat de Barcelona