Date of Award

1-1-2014

Language

English

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

College/School/Department

Department of Biological Sciences

Content Description

1 online resource (ix, 97 pages) : illustrations

Dissertation/Thesis Chair

Gregory A Lnenicka

Committee Members

Benjamin G Szaro, Christine K Wagner, Haijun Chen

Keywords

Calcium, drosophila, Potasium, SK channel, synaptic homeostasis, synaptic plasticity, Drosophila, Calcium ions, Cellular signal transduction, Myoneural junction, Neural transmission, Homeostasis

Subject Categories

Biology | Developmental Biology | Neuroscience and Neurobiology

Abstract

Postsynaptic Ca2+ plays an important role in synaptic homeostasis and synaptic plasticity. Postsynaptic Ca2+ signals have been shown to regulate synaptic transmission at the Drosophila larval neuromuscular junction (NMJ), however, these signals have not been well characterized. This will explore how these signals regulate synaptic strength and what channels are involved. In previous lab experiments Ca2+ transients were observed during evoked and spontaneous release (Desai and Lnenicka, 2011). It was further demonstrated that a reduction in synaptic strength occurs following synaptic stimulation. It was hypothesized that the increase in postsynaptic Ca2+ following synaptic stimulation activates the gCS and causes a reduction in synaptic strength. Experiments expressing the Ca2+ buffer parvalbumin in the muscle demonstrated that the gCS is activated by Ca2+ and buffering Ca2+ prevented its activity. Previous studies demonstrated that the gCS in the presynaptic cell is the dSK channel (Abou Tayoun et al., 2011). In this thesis I show that dSK is present in the muscle and is responsible for the reduction in synaptic strength following synaptic stimulation. I will also show that buffering Ca2+ by expressing parvalbumin (PV) in the muscle, does lead to a developmental decrease in synaptic growth. Animals expressing PV show a reduction in synaptic strength not related to a reduction in transmitter release. This decrease in synaptic strength was due to a reduction in motor terminal growth, indicating that buffering postsynaptic Ca2+ prevents the release of a retrograde signal that is used initiate synapse growth. This study will also point to quantal size (minESPC) and not quantal content (minEPSP) as the primary actor in synaptic homeostasis during muscle fiber growth. Larger muscle fibers have lower membrane resistances, whereas smaller fibers have higher membrane resistances. These differences are shown not to be caused by changes in transmitter release; all muscles regardless of size have similar minEPSP amplitudes. However, their minEPSPCs amplitudes were observed to be larger in larger fibers and smaller in smaller fibers. This indicates that quantal size regulates synaptic homeostasis.

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