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The Journal of Neurophysiology Vol. 88 No. 2 August 2002, pp. 802-816
Copyright ©2002 by the American Physiological Society
Department of Physiology, University of Wisconsin School of Medicine, Madison, Wisconsin 53706
Verbny, Yakov,
Chuan-Li Zhang, and
Shing
Yan Chiu.
Coupling of Calcium Homeostasis to Axonal Sodium in Axons of
Mouse Optic Nerve. J. Neurophysiol. 88: 802-816, 2002. Axonal populations in neonatal and mature optic
nerves were selectively stained with calcium dyes for analysis of
calcium homeostasis and its possible coupling to axonal Na. Repetitive nerve stimulation causes a rise in axonal
[Ca2+]i the posttetanus
recovery of which is impeded by increasing the number of action
potentials in the tetanus. This effect is augmented in 4-aminopyridine
(4-AP; 1 mM), which dramatically increases the calcium and presumably
sodium load during the tetanus. Increasing axonal
[Na]i with the Na-ionophore monensin (4-50
µM) and ouabain (30 µM) retards posttetanus calcium decline,
suggesting that efficient calcium clearance depends on a low level of
axonal [Na]i. Posttetanus calcium clearance is
not affected by K-mediated depolarization. To further examine coupling
between axonal [Na]i and
[Ca2+]i, the resting
axonal [Ca2+]i was
monitored as axonal
[Na+]i was elevated with
ouabain, veratridine, and monensin. In all cases, elevation of axonal
[Na+]i evokes a calcium
influx into axons. This influx is unrelated to activation of calcium
channels but is consistent with calcium influx via reversal of the
Na/Ca exchanger expected as a consequence of axonal
[Na+]i elevation. In
conclusion, this study demonstrates that calcium homeostasis in the
axons of the optic nerve is strongly coupled to axonal
[Na+]i in a manner
consistent with the Na/Ca exchanger playing a major role in extruding
calcium following nerve activity.
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