Advanced Search

Browse by Discipline

Scientific Societies

E-print Alerts

Add E-prints

E-print Network

  Advanced Search  

Cellular/Molecular Autapses and Networks of Hippocampal Neurons Exhibit

Summary: Cellular/Molecular
Autapses and Networks of Hippocampal Neurons Exhibit
Distinct Synaptic Transmission Phenotypes in the Absence
of Synaptotagmin I
Huisheng Liu,1 Camin Dean,1 Christopher P. Arthur,2 Min Dong,1 and Edwin R. Chapman1
1Howard Hughes Medical Institute and Department of Physiology, University of Wisconsin, Madison, Wisconsin 53706, and 2Department of Cell Biology,
Scripps Research Institute, La Jolla, California 92037
Synaptotagmin-I (syt-I) is required for rapid neurotransmitter release in mouse hippocampal neurons. However, contradictory results
have been reported regarding evoked and spontaneous secretion from syt-I knock-out (KO) neurons. Here, we compared synaptic
transmission in two different hippocampal neuron preparations: autaptic cultures in which a single isolated cell innervates itself, and
dissociated mass cultures in which individual cells are innervated by neighboring cells. In autaptic cultures, the total extent of evoked
release, size of readily releasable pool of synaptic vesicles, and release probability were unchanged in syt-I KO neurons. In contrast, in
cultures containing multiple interconnected neurons, total evoked release, the number of docked vesicles, and release probability, were
the frequency of spontaneous synaptic vesicle fusion events (minis) was unchanged in syt-I KO neurons when two or fewer cells were
in syt-I KO neurons compared with wild type. Moreover, interneuronal synapses exhibited higher rates of spontaneous release than
autaptic synapses. This higher rate was attributable to an increase in release probability because excitatory hippocampal neurons in
micronetworks formed a set number of synapses per cell regardless of the number of connected neurons. Thus, aspects of synaptic
transmission differ between autaptic and dissociated cultures, and the synaptic transmission phenotype, resulting from loss of syt-I, is


Source: Alford, Simon - Department of Biological Sciences, University of Illinois at Chicago


Collections: Biology and Medicine