Date of Award

Spring 5-2020

Document Type

Honors Thesis

Degree Name

Bachelor of Science





Advisor/Committee Chair

Gregory Lnenicka, Ph.D.

Committee Member

Ben Szaro, Ph.D.


Following an action potential in the presynaptic neuron there is evoked release of neurotransmitter into the synapse which activates ionotropic transmembrane receptors on the postsynaptic membrane that cause depolarizations in voltage that get recorded as excitatory postsynaptic potentials (EPSPs). In the absence of an action potential there is spontaneous release of neurotransmitter that postsynaptically gets recorded as miniature excitatory postsynaptic potentials (mEPSPs). According to the quantal hypothesis, postulated by Bernard Katz, the mEPSPs are allor- none changes in potential caused by a single quantum of neurotransmitter, which when added up create EPSPs. Following studies have found that these two modes of vesicle release have differences in molecular mechanisms, vesicle recycling, and extracellular conditions of operation. Spontaneous release by itself is sufficient to maintain synaptic homeostasis and is involved in longterm potentiation. New data from our lab suggests that mEPSP frequency depresses after sustained stimulation of the presynaptic cell suggesting some feedback mechanism coming from the postsynaptic cell. In this study, following experimental observation that optical frequency from postsynaptic calcium sensor (GCaMP6) activation does not correlate with mEPSP frequency, we looked at what we call missing minis. Simultaneously recording optical and electrophysiological data we have found that certain fluorescence GCaMP6 flashes coming from glutamate receptor activation do not coincide with electrophysiological mEPSP events.