Date of Award




Document Type


Degree Name

Doctor of Philosophy (PhD)


Department of Biological Sciences

Content Description

1 online resource (viii, 101 pages)

Dissertation/Thesis Chair

Gregory A Lnenicka

Committee Members

Helmut Hirsch, Haijun Chen, Li Niu


homeostasis, neuromuscular junction, postsynaptic calcium, Calcium ions, Cellular signal transduction, Neural transmission, Homeostasis, Myoneural junction, Drosophila

Subject Categories

Biology | Neuroscience and Neurobiology


Postsynaptic [Ca2+]i has been proposed to play an important role in both synaptic plasticity and synaptic homeostasis. Postsynaptic Ca2+ signals appear to regulate synaptic transmission at the Drosophila larval NMJ; however, they have not been characterized at a NMJ. We were interested in examining the postsynaptic Ca2+ signals in this system and determining its influence on synaptic strength. The muscle Ca2+ transients were recorded by injecting the muscle fibers with Ca2+ indicators; discrete postsynaptic Ca2+ transients were observed along the NMJ during evoked and spontaneous transmitter release. The magnitude of the Ca2+ signals was correlated with synaptic efficacy, terminals producing larger excitatory post synaptic potentials (EPSPs) were also seen to produce larger Ca2+ signals per terminal length. The muscle plasma membrane Ca2+-ATPase (PMCA) was seen to participate in extruding Ca2+ from the postsynaptic region of the muscle. Various PMCA isoforms are predicted for this system; an RT-PCR approach was used to identify the specific transcripts expressed in Drosophila melanogaster larvae. These Ca2+ transients could serve as a gauge of synaptic efficacy and be involved in synaptic regulation. We investigated the effect of increasing postsynaptic Ca2+ on synaptic transmission. This was conducted by either directly injecting Ca2+ into the muscle or by inhibiting the muscle PMCA. In both instances we noticed a decrease in synaptic strength, EPSP amplitudes were drastically reduced and the resting membrane potential (RMP) was hyperpolarized due to activation of the slow Ca2+-dependent K+ conductance (gCS). Our studies indicated the involvement of the gCS during physiological levels of synaptic activity. This conductance was also shown to be activated by Ca2+ entering through the glutamate receptors alone. Altogether this is suggestive of gCS providing negative feedback on synaptic strength and thus being involved in fine tuning the synapse. This would function as a rapid form of homeostasis unlike previous models which are more developmental slow acting. I observed that a high frequency stimulation results in an increase in quantal size, possibly representing a mechanism for synaptic enhancement, but a decrease in the minEPSP amplitude most likely due to gCS induced decrease in muscle input resistance.