title: Calcium channel currents in acutely dissociated intracardiac neurons from adult rats.
abstract: With the use of the whole cell patch-clamp technique, multiple subtypes of voltage-activated calcium channels, as indicated by measuring Ba2+ currents, were pharmacologically identified in acutely dissociated intracardiac neurons from adult rats. All tested neurons that were held at -80 mV displayed only high-voltage-activated (HVA) Ca2+ channel currents that were completely blocked by 100 microM CdCl2. The current density of HVA Ca2+ currents was dependent on the external Ca2+ concentration. The Ba2+ (5 mM) currents were half-activated at -16.3 mV with a slope of 5.6 mV per e-fold change. The steady-state inactivation was also voltage dependent with half-inactivation at -33.7 mV and a slope of -12.1 mV per e-fold change. The most effective L-type channel activator, FPL 64176 (2 microM), enhanced the Ba2+ current in a voltage-dependent manner. When cells were held at -80 mV, the saturating concentration (10 microM) of nifedipine blocked approximately 11% of the control Ba2+ current. The major component of the Ca2+ channels was N type (63%), which was blocked by a saturating concentration (1 microM) of omega-conotoxin GVIA. Approximately 19% of the control Ba2+ current was sensitive to omega-conotoxin MVIIC (5 microM) but insensitive to low concentrations (30 and 100 nM) of omega-agatoxin IVA (omega-Aga IVA). In addition, a high concentration (1 microM) of omega-Aga IVA occluded the effect of omega-conotoxin MVIIC. Taken together, these results indicate that the omega-conotoxin MVIIC-sensitive current represents only the Q type of Ca2+ channels. The current that was insensitive to nifedipine and various toxins represents the R-type current (7%), which was sensitive to 100 microM NiCl2. In conclusion, the intracardiac neurons from adult rats express at least four different subtypes (L, N, Q, and R) of HVA Ca2+ channels. This information is essential for understanding the regulation of synaptic transmission and excitability of intracardiac neurons by different neurotransmitters and neural regulation of cardiac functions.
authors.affiliation: Department of Physiology, Loyola Stritch School of Medicine, Maywood, Illinois 60153, USA.
authors.forename: S W
authors.initials: SW
authors.lastname: Jeong
authors.forename: R D
authors.initials: RD
authors.lastname: Wurster
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects; D006321:Heart / Q000294:innervation*; D066298:In Vitro Techniques; D008297:Male; D008978:Mollusk Venoms / Q000494:pharmacology; D009474:Neurons / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020866:omega-Conotoxin GVIA
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D008978:Mollusk Venoms; D010455:Peptides; D020866:omega-Conotoxin GVIA; D009543:Nifedipine