Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Calcium channels in solitary retinal ganglion cells from post‐natal rat.

Calcium channels in solitary retinal ganglion cells from post‐natal rat. 1. Calcium currents from identified, post‐natal retinal ganglion cell neurones from rat were studied with whole‐cell and single‐channel patch‐clamp techniques. Na+ and K+ currents were suppressed with pharmacological agents, allowing isolation of current carried by either 10 mM‐Ca2+ or Ba2‐ during whole‐cell recordings. For cell‐attached patch recordings, the recording pipette contained 96‐110 mM‐BaCl2 while the bath solution consisted of isotonic potassium aspartate in order to zero the neuronal membrane potential. 2. A transient component, present in approximately one‐third of the whole‐cell recordings resembles closely the T‐type calcium current observed previously in other tissues. This component activates at low voltages (‐40 to ‐50 mV from holding potentials negative to ‐80 mV), inactivates with a time constant of 10‐30 ms at 35 degrees C, and is carried equally well by Ba2+ or Ca2+. In single‐channel recordings small (8 pS) channels are observed whose aggregate microscopic kinetics correspond well to the macroscopic current obtained during whole‐cell measurements. 3. During whole‐cell recordings, a more prolonged component activates in all retinal ganglion cells at ‐40 to ‐20 mV from a holding potential of ‐90 mV. This component is substantially larger when equimolar Ba2+ replaces Ca2+ as the charge carrier, and is sensitive to the dihydropyridine agonist Bay K8644 (5 microM) and antagonists nifedipine (1‐10 microM) and nimodipine (1‐10 microM). Thus, the dihydropyridine pharmacology of this prolonged component resembles that of the L‐type calcium current found in dorsal root ganglion neurones and in heart cells. Also reminiscent of the L‐current, the prolonged component in this preparation is less inactivated at depolarized holding potentials (‐60 to ‐40 mV) than the transient component. In cell‐attached recordings, large (20 pS) channels are observed with activation properties similar to those of the prolonged portion of the whole‐cell current. 4. omega‐Conotoxin fraction GVIA (omega‐CgTX VIA), a peptide from the venom of the snail Conus geographus, produces a readily reversible blockade of all components of the calcium current in these central mammalian neurones. This finding is in contrast to that of other preparations in which this toxin is responsible for an ephemeral block of T‐current but a long‐lasting block of other components of calcium current. 5. In summary, at least two components of calcium current with discrete underlying unitary events are present in post‐natal retinal ganglion cells from rat. One component closely resembles the T or transient current observed in other cell types.(ABSTRACT TRUNCATED AT 400 WORDS) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Calcium channels in solitary retinal ganglion cells from post‐natal rat.

The Journal of Physiology , Volume 418 (1) – Nov 1, 1989

Loading next page...
 
/lp/wiley/calcium-channels-in-solitary-retinal-ganglion-cells-from-post-natal-mbfMFXLoNp

References (42)

Publisher
Wiley
Copyright
© 2014 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1113/jphysiol.1989.sp017847
Publisher site
See Article on Publisher Site

Abstract

1. Calcium currents from identified, post‐natal retinal ganglion cell neurones from rat were studied with whole‐cell and single‐channel patch‐clamp techniques. Na+ and K+ currents were suppressed with pharmacological agents, allowing isolation of current carried by either 10 mM‐Ca2+ or Ba2‐ during whole‐cell recordings. For cell‐attached patch recordings, the recording pipette contained 96‐110 mM‐BaCl2 while the bath solution consisted of isotonic potassium aspartate in order to zero the neuronal membrane potential. 2. A transient component, present in approximately one‐third of the whole‐cell recordings resembles closely the T‐type calcium current observed previously in other tissues. This component activates at low voltages (‐40 to ‐50 mV from holding potentials negative to ‐80 mV), inactivates with a time constant of 10‐30 ms at 35 degrees C, and is carried equally well by Ba2+ or Ca2+. In single‐channel recordings small (8 pS) channels are observed whose aggregate microscopic kinetics correspond well to the macroscopic current obtained during whole‐cell measurements. 3. During whole‐cell recordings, a more prolonged component activates in all retinal ganglion cells at ‐40 to ‐20 mV from a holding potential of ‐90 mV. This component is substantially larger when equimolar Ba2+ replaces Ca2+ as the charge carrier, and is sensitive to the dihydropyridine agonist Bay K8644 (5 microM) and antagonists nifedipine (1‐10 microM) and nimodipine (1‐10 microM). Thus, the dihydropyridine pharmacology of this prolonged component resembles that of the L‐type calcium current found in dorsal root ganglion neurones and in heart cells. Also reminiscent of the L‐current, the prolonged component in this preparation is less inactivated at depolarized holding potentials (‐60 to ‐40 mV) than the transient component. In cell‐attached recordings, large (20 pS) channels are observed with activation properties similar to those of the prolonged portion of the whole‐cell current. 4. omega‐Conotoxin fraction GVIA (omega‐CgTX VIA), a peptide from the venom of the snail Conus geographus, produces a readily reversible blockade of all components of the calcium current in these central mammalian neurones. This finding is in contrast to that of other preparations in which this toxin is responsible for an ephemeral block of T‐current but a long‐lasting block of other components of calcium current. 5. In summary, at least two components of calcium current with discrete underlying unitary events are present in post‐natal retinal ganglion cells from rat. One component closely resembles the T or transient current observed in other cell types.(ABSTRACT TRUNCATED AT 400 WORDS)

Journal

The Journal of PhysiologyWiley

Published: Nov 1, 1989

There are no references for this article.