Effects of Calneuron I and CaMKIIβ on Neurotransmission
Date Issued
2015
Date
2015
Author(s)
He, Yun
Abstract
The complex patterns of Calcium (Ca2+) signals in neuronal physiology can be largely attributed to calcium binding proteins (CaBPs) which participates in Ca2+ signaling pathway. CaBP8, also referred to as calneuron I (CalnI), is involved in transduction of Ca2+ signaling and inhibiting N-type Ca2+ channel currents. Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays an important role in regulating synaptic development and plasticity. According to a previous study in our lab, a possible interaction between CalnI and CaMKIIβ was indicated by Yeast Two-Hybrid screening. To verify the effects of CalnI on neurotransmission, CalnI and related mutants were overexpressed in primary cultured neurons, and calcium imaging experiments were applied to characterize neurotransmission. In addition, CalnI overexpressed neurons were analyzed by Sholl analysis to investigate if there were any changes in morphology. In addition, CFP-CalnI and YFP-CaMKIIβ co-expressed HEK293T cells were examined to determine whether CalnI affects the localization of CaMKIIβ. The overexpression of CalnI in neurons caused significant deficits in neurotransmission, also decreased the Ca2+ responses in calcium-induced calcium release (CICR) and metabotropic glutamate receptor (mGluR) signaling pathway. In neuronal morphology, the distal branches of neurites in CalnI overexpressed neurons were obviously decreased. Moreover, the fluorescence imaging of CFP-CalnI and YFP-CaMKIIβ co-expressed HEK293T cells shows that the expression of CalnI does affect the localization of CaMKIIβ. Taken together, CalnI may regulate Ca2+ channels to influence neurotransmission, and possibly interacts with CaMKIIβ to further affect the synaptic development or plasticity.
Subjects
CICR
HEK293T cell
synaptic transmission
Type
thesis
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