Kinetic and pharmacological properties of Ca(2+) currents in postganglionic sympathetic neurones projecting to muscular and cutaneous effectors.
Voltage-gated Ca(2+) channels are expressed in neurones and greatly influence neuronal activity by activating Ca(2+)-dependent K(+) channels. The whole cell patch-clamp technique was used to compare the kinetic and pharmacological properties of voltage-dependent Ca(2+) currents in two groups of sympathetic neurones identified by the fluorescent tracer Fast Blue: putative muscular sympathetic neurones (MSN) and putative cutaneous sympathetic neurones (CSN). The tracer was injected into the muscular part of the diaphragm (to mark MSN) and into the skin of the ear (to mark CSN). The capacitance of MSN (23.0 pF) was larger than the capacitance of CSN (12.6 pF). The maximum current in MSN (1.3 nA) was also larger than in CSN (0.93 nA). However, the current density was larger in CSN (77. 3 pA/pF) than in MSN (57.7 pA/pF) and the current activation rate was faster in CSN (0.27 nA/ms) than in MSN (0.19 nA/ms). V(1/2) and slope factors of activation and inactivation were not significantly different for MSN and CSN. The majority of Ca(2+) current was available for activation in both categories of neurones at resting membrane potential. Ca(2+) currents in MSN and CSN were blocked by nifedipine (7.0 and 3.6%, respectively), omega-Agatoxin-IVA (23.0 and 25.6%, respectively) and omega-conotoxin-GVIA (67.0 and 65.1%, respectively). We found that CSN are twice as small, have higher Ca(2+) current density and their Ca(2+) activation rate is faster in comparison to MSN. Such properties may lead to faster rise of Ca(2+) concentration in the cytoplasm of the CSN comparing to MSN and more effectively dampen their activity due to more effective activation of Ca(2+)-dependent K(+) current. Both kinds of neurones express high proportion of N and P/Q Ca(2+) current.
The Medical University of Warsaw, Department of Experimental and Clinical Physiology, Warsaw, Poland.
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Kukwa
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Macioch
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Rola
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Szulczyk
D000818:Animals; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004553:Electric Conductivity; D005728:Ganglia, Sympathetic / Q000166:cytology / Q000502:physiology*; D006706:Homeostasis; D007700:Kinetics; D008297:Male; D018482:Muscle, Skeletal / Q000294:innervation*; D009424:Nervous System Physiological Phenomena; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D012867:Skin / Q000294:innervation*; D009435:Synaptic Transmission / Q000502:physiology*; D020867:omega-Agatoxin IVA / Q000494:pharmacology; D020866:omega-Conotoxin GVIA / Q000494:pharmacology
D002121:Calcium Channel Blockers; D020867:omega-Agatoxin IVA; D020866:omega-Conotoxin GVIA; D009543:Nifedipine; D002118:Calcium