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Resources » Paper

Qiang Liu et al. (2004) East Coast Worm Meeting "CaM KII Regulates Neurotransmitter Release at the C. elegans Neuromuscular Junction"

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00010699

    Qiang Liu, & Zhao-Wen Wang (2004). CaM KII Regulates Neurotransmitter Release at the C. elegans Neuromuscular Junction presented in East Coast Worm Meeting. Unpublished information; cite only with author permission.

    Ca 2+ /calmodulin-dependent kinase II (CaM KII) plays an important role in synaptic plasticity and development of the nervous system. Malfunction of CaM KII is associated with a variety of diseases including epilepsy. In the nervous system, CaM KII is expressed at both pre- and post-synaptic sites. Little is known about the potential role of CaM KII in neurotransmitter release. We have embarked on a project to study the function of CaM KII in neurotransmitter release using C. elegans as model system. C. elegans has a single CaM KII gene, unc-43 . Both gain-of-function and loss-of-function mutants are available for analysis. To evaluate the function of CaM KII in neurotransmitter release, miniature and evoked postsynaptic currents (mPSCs and ePSCs) were recorded at the neuromuscular junction with the postsynaptic body-wall muscle cell clamped at -60 mV. We initially analyzed mPSCs and ePSCs in unc-43(n498) , a gain-of-function mutant. Compared with the wild-type, the mutant showed a significant reduction in the amplitude of ePSCs (wild-type 1579 +/- 129 pA, n = 8; n-498 721 +/- 79 pA, n = 12) and in the frequency of mPSCs (wild-type 50.6 +/- 3.4 Hz, n = 22; n-498 22.6 +/- 3.4 Hz, n = 6). Postsynaptic receptor sensitivity appeared normal in the mutant since the amplitude of mPSCs did not change (wild-type 27.4 +/- 1.6 pA, n = 22; n-498 28.4 +/- 4.3 pA, n = 6). These results suggest that a normal function of CaM KII is to regulate neurotransmitter release. Experiments are under way to determine 1) whether unc-43 loss-of-function mutants show opposite changes of mPSCs and ePSCs compared with the gain-of-function mutant; 2) whether the apparent effect on neurotransmitter release is due to an action of presynaptic CaM KII, or a retrograde signal generated by postsynaptic CaM KII; and 3) what are the phosphorylation targets of CaM KII in regulating neurotransmitter release.


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