RT Journal Article
SR Electronic
T1 Calcium signaling of glial cells along mammalian axons
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 4229
OP 4245
DO 10.1523/JNEUROSCI.13-10-04229.1993
VO 13
IS 10
A1 Kriegler, S
A1 Chiu, SY
YR 1993
UL http://www.jneurosci.org/content/13/10/4229.abstract
AB Glial [Ca2+]i signaling was examined in a mammalian white matter lacking neuronal cell bodies and synapses. Rat optic nerves (postnatal days 2 and 7) were stained with calcium indicator dyes and confocal images of [Ca2+bdi were recorded at approximately 25 degrees C or approximately 37 degrees C. Glial cell bodies showed spiking or sustained [Ca2+], response to bath-applied glutamate (50–500 microM). The metabotropic glutamate agonist trans-ACPD elicited transient, sometimes spiking, [Ca2+], responses, whereas ionotropic agonists kainate and AMPA elicited a 6,7-dinitroquinoxaline-2,3-dione-sensitive, mostly sustained [Ca2+]i response. Transient and spiking glial [Ca2+]i responses also were elicited by adenosine and ATP (0.1–100 microM). Repetitive nerve stimulation (10–20 Hz) elicited [Ca2+bdi spiking in 15–25% of glial cells in postnatal day 7 nerves, with spiking typically occurring 15–60 sec after onset of nerve stimulation. At 37 degrees C, the frequency of glial [Ca2+]i spikes increased from approximately 0.06 Hz to approximately 0.11 Hz when axonal stimulation was increased from 10 to 20 Hz. This activity-dependent glial spiking was inhibited by TTX, could not be mimicked by increasing the bath K+ by 20 mM, and occurred when nerves were stimulated in the absence of bath calcium. Activity-dependent and glutamate-induced glial spiking could be mimicked by altering ionic gradients known to favor release of glutamate via glutamate transporters, including elevation of intracellular Na+ by veratridine concurrent with external K+ elevation. We suggest that glial [Ca2+]i spiking observed during electrical activity resulted from activation of glial receptors (e.g., metabotropic glutamate receptor, adenosine receptor) by substances (e.g., glutamate, adenosine) released from the optic nerve in a nonvesicular fashion, possibly through a reversal of sodium-coupled transporters when Na+ and K+ gradients are altered by prolonged nerve activity.