Multiple types of calcium channels in acutely isolated rat neostriatal neurons.
Voltage-activated high- and low-threshold Ca2+ currents were studied using whole-cell voltage-clamp techniques and fura-2 fluorescence measurements of intracellular Ca2+ in neurons acutely isolated from rat neostriatum. High-threshold Ca2+ currents activated around -40 mV and were present in at least 95% of neostriatal neurons. The maximum current, 736 +/- 44 pA (mean +/- SEM, n = 141), was observed around 0 mV. In 70% of neurons, high-threshold Ca2+ currents exhibited both inactivating and noninactivating components. The majority of the high-threshold Ca2+ currents appeared to belong neither to the "L-type" nor the "N-type" classification, since omega-conotoxin (5 microM) decreased this current by only 29% and nimodipine (10 microM) decreased the noninactivating component of this current by only 17%. A low-threshold transient (T-type) Ca2+ current was observed in 40% of neurons. When both T-type and high-threshold Ca2+ currents were present, their maximum amplitudes were 78 +/- 7 pA and 800 +/- 57 pA, respectively (mean +/- SEM, n = 58). At a holding potential of -100 mV, the T-type Ca2+ current activated around -60 mV, with maximum current near -40 mV. Steady-state inactivation of the T-type Ca2+ current was observed at holding potentials positive to -125 mV, and the current was half-inactivated at -88 mV. Recovery from inactivation to 90% of maximum occurred within 800 msec. Mn2+ or Co2+ (3 mM) blocked both high-threshold and T-type Ca2+ currents, whereas Cd2+ (25 microM) or verapamil (50 microM and 150 microM) preferentially blocked high-threshold over T-type Ca2+ currents. In response to depolarization by 50 mM K+, fura-2 fluorescence measurements showed increased intracellular Ca2+ in both the soma and the proximal dendrites of neostriatal neurons that was markedly reduced by 25 microM Cd2+. These findings suggest that high-threshold Ca channels are present in both the soma and proximal dendrites of neostriatal neurons.
Neuroscience Research Group, University of Calgary, Alberta, Canada.
K
K
Hoehn
T W
TW
Watson
B A
BA
MacVicar
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D002122:Calcium Chloride / Q000494:pharmacology; D003342:Corpus Striatum / Q000502:physiology*; D004558:Electric Stimulation; D004594:Electrophysiology / Q000379:methods; D016257:Fura-2; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009553:Nimodipine / Q000494:pharmacology; D010456:Peptides, Cyclic / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013050:Spectrometry, Fluorescence; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D020960:omega-Conotoxins
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D010456:Peptides, Cyclic; D013757:Tetraethylammonium Compounds; D020960:omega-Conotoxins; D002104:Cadmium; C053423:Conus magus toxin; D013779:Tetrodotoxin; D009553:Nimodipine; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D002122:Calcium Chloride; D002118:Calcium; D016257:Fura-2