The Downstream Influence of Synaptotagmin on Axon Branching found by Changing Levels of Calcium

Posted June 24th, 2010 at 12:57 pm.

Abstract: Nikitha Ashok
Mentor: Dr. Greif
Neurotransmission is the mechanism by which neurons communicate with one another through signaling with the release of chemicals known as neurotransmitters. These neurotransmitters are packaged into synaptic vesicles and released by exocytosis, the fusion of the vesicles with the cell membrane, from the presynaptic neuron. Calcium is an essential ion for the proper functioning of this process. The protein synaptotagmin (syt) acts a calcium sensor to mediate this process. While many studies have established the role of syt in mature neurons at the synapse, we hope to study other possible functions of this protein in developing neurons.

In order to understand why syt is expressed in developing neurons before the neurons have made any synapses, embryonic day 8 chicken forebrain neurons are cultured to yield neurons in early development. Thus far, we have found that changes in the levels of syt alter the branching and filopodia of developing axon. The next step is to study the role of calcium in mediating this process. We hypothesize that changing levels of Ca2+ will influence syt’s regulation of axon outgrowth, filopodia and lamellipodia, neurite outgrowth membrane consisting of microtubulin and actin filaments that might act as precursors to axon branches. To determine if syt preferentially adds membrane to the areas of high calcium concentration, it is necessary to establish conditions that allow us to manipulate Ca2+ levels while maintaining cell viability. Ca2+ influx will be blocked using calcium chelators and elevated using ionophores to examine how changes in calcium levels interact with syt.

This research is supported by grants from NIH, Bryn Mawr College and Drexel University.

Filed under: 2010,Ashok, Nikitha,Greif, Dr. Karen Tags: by Lisa Klinman

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