QBI Seminar: Tuning the release kinetics of neurotransmission
Event Details
- Date:
- Monday, 15 September 2014 - Monday, 15 September 2014
- Time:
- 12:00 pm - 1:00 pm
- Room:
- Auditorium, level 7
- UQ Location:
- Queensland Brain Institute (St Lucia)
- URL:
- http://www.qbi.uq.edu.au/neuroscience-seminars
- Event category(s):
Event Contact
- Name:
- Mr Reeza Nazer
- Phone:
- 66353
- Email:
- r.nazer@uq.edu.au
- Org. Unit:
- Queensland Brain Institute
Event Description
- Full Description:
- Speaker: Dr Zhitao Hu
Harvard Medical School, Massachusetts General Hospital
Title: Tuning the release kinetics of neurotransmission
Abstract: Synaptic transmission consists of fast and slow components of neurotransmitter release. Here we show that these components are mediated by distinct exocytic proteins. The C. elegans unc-13 gene is required for SV exocytosis, and encodes long and short isoforms (UNC-13L and S). Fast release was mediated by UNC-13L whereas slow release required both UNC-13 proteins and was inhibited by Tomosyn. The spatial location of each protein correlated with its effect. Proteins adjacent to active zones mediated fast release while those controlling slow release were more distal or diffuse. Two UNC-13L domains accelerated release. C2A, which binds the active zone protein RIM, anchored UNC-13 at active zones and shortened the latency of release. A calmodulin binding site accelerated release but had little effect on UNC-13's spatial localization.
Alteration of release kinetics occurs in autism related gene mutant nrx-1 and nlg-1. Neurexin and Neuroligin mutations are implicated in several psychiatric disorders but how these mutations alter circuit development and function remains uncertain. Here we show that the C. elegans Neurexin (NRX-1) and Neuroligin (NLG-1) mediate a retrograde synaptic signal that inhibits acetylcholine (ACh) release at neuromuscular junctions (NMJs). Retrograde signaling is induced in mutants lacking a muscle microRNA (miR-1) and is blocked in mutants lacking NLG-1 or NRX-1. ACh release becomes more rapid and abbreviated when the retrograde signal is on whereas release is slower and more prolonged when retrograde signaling is blocked. The retrograde signal adjusts the kinetics of ACh release by inhibiting exocytosis of synaptic vesicles that are distal to the site of calcium entry. These results suggest that changes in the kinetics of neurotransmitter release may represent an important pathological mechanism in psychiatric diseases.
Directions to UQ
- Google Map:
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- Directions:
- St Lucia Campus | Gatton campus.
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