Developmental regulation of calcium channel-mediated currents in retinal glial (Müller) cells.
Whole cell voltage-clamp recordings of freshly isolated cells were used to study changes in the currents through voltage-gated Ca(2+) channels during the postnatal development of immature radial glial cells into Müller cells of the rabbit retina. Using Ba(2+) or Ca(2+) ions as charge carriers, currents through transient low-voltage-activated (LVA) Ca(2+) channels were recorded in cells from early postnatal stages, with an activation threshold at -60 mV and a peak current at -25 mV. To increase the amplitude of currents through Ca(2+) channels, Na(+) ions were used as the main charge carriers, and currents were recorded in divalent cation-free bath solutions. Currents through transient LVA Ca(2+) channels were found in all radial glial cells from retinae between postnatal days 2 and 37. The currents activated at potentials positive to -80 mV and displayed a maximum at -40 mV. The amplitude of LVA currents increased during the first postnatal week; after postnatal day 6, the amplitude remained virtually constant. The density of LVA currents was highest at early postnatal days (days 2-5: 13 pA/pF) and decreased to a stable, moderate level within the first three postnatal weeks (3 pA/pF). A significant expression of currents through sustained, high-voltage-activated Ca(2+) channels was found after the third postnatal week in approximately 25% of the investigated cells. The early and sole expression of transient currents at high-density may suggest that LVA Ca(2+) channels are involved in early developmental processes of rabbit Müller cells.
Bringmann
A
A
Department of Neurophysiology, Paul Flechsig Institute of Brain Research, University of Leipzig, D-04109 Leipzig, Germany. bria@server3.medizin.uni-leipzig.de
Schopf
S
S
Reichenbach
A
A
D000375:Aging / Q000502:physiology; D000818:Animals; D001464:Barium / Q000378:metabolism / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism*; D020747:Calcium Channels, T-Type / Q000378:metabolism; D002478:Cells, Cultured; D003300:Copper / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D018507:Gene Expression Regulation, Developmental; D008274:Magnesium / Q000378:metabolism / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000235:genetics / Q000502:physiology; D009457:Neuroglia / Q000166:cytology / Q000378:metabolism*; D009532:Nickel / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011817:Rabbits; D012160:Retina / Q000166:cytology / Q000254:growth & development / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D020747:Calcium Channels, T-Type; D002104:Cadmium; D001464:Barium; D003300:Copper; D009532:Nickel; D012964:Sodium; D008274:Magnesium; D002118:Calcium