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. 1988;101(2):119-31.
doi: 10.1007/BF01872827.

Calmodulin acts as an intermediary for the effects of calcium on gap junctions from crayfish lateral axons

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Calmodulin acts as an intermediary for the effects of calcium on gap junctions from crayfish lateral axons

R O Arellano et al. J Membr Biol. 1988.

Abstract

Lateral axons from the abdominal nerve cord of crayfish were internally perfused with the calcium receptor calmodulin (CaM) in solutions with low (pCa greater than 7.0) or high (pCa 5.5) calcium concentrations and studied electrophysiologically and morphologically. Results from these experiments show that when the internal solution contains calcium-activated calmodulin (Ca2+-CaM) the junctional resistance between the axons increases from control values of about 60 to 500-600 k omega in 60 min. In contrast, axons perfused with calmodulin in low calcium solutions maintain their junctional resistance at control levels during the 60-min perfusion. Similar results are obtained when only one or both coupled axons are perfused. The morphological study shows that in the perfused axons the axoplasmic organelles are replaced or grossly perturbed by the perfusion solution up to the region of the synapses. Additionally, in axons perfused with Ca2+-CaM there are regions where the synaptic gap between the membranes decreases from a control 4-6 to 2-3 nm. Both electrophysiological and morphological results can be interpreted as indicating that calcium-activated calmodulin acts directly on the junctional channels to induce their closure.

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References

    1. Arch Biochem Biophys. 1976 Jan;172(1):301-11 - PubMed
    1. J Physiol. 1981 Aug;317:509-18 - PubMed
    1. Pflugers Arch. 1987 Apr;408(4):379-85 - PubMed
    1. Biochem Biophys Res Commun. 1985 Jan 31;126(2):825-32 - PubMed
    1. J Gen Physiol. 1961 Nov;45:267-308 - PubMed

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