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The Journal of Neuroscience, October 26, 2005, ():

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Na+-Dependent Sources of Intra-Axonal Ca2+ Release in Rat Optic Nerve during In Vitro Chemical Ischemia
J. Neurosci. Nikolaeva et al. 25: 9960

Supplemental data

Files in this Data Supplement:

  • supplemental material - Fig. S1 Hypothetical model summarizing the three sources of intra-axonal Ca2+ release. During ischemia Na+ enters axons mainly (but not exclusively) through nodal Nav1.6. An increase in axoplasmic [Na+] may 1) positively modulate ryanodine receptors; 2) drive mitochondrial Na+- Ca2+ exchange to export Ca2+ from the matrix, and 3) promote reverse operation of one or several Na+-coupled neurotransmitter transport systems. These transmitters may activate metabotropic receptors (mXR), stimulating PLC to generate IP3 and thus promote Ca2+ release from IP3 receptors. “AR”: axoplasmic reticulum, the axonal analog of endoplasmic reticulum and the putative Ca2+ storage organelle in myelinated fibers.



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