title: Low-voltage-activated calcium current does not regulate the firing behavior in paired mechanosensory neurons with different adaptation properties.
abstract: Low-voltage-activated Ca(2+) currents (LVA-I(Ca)) are believed to perform several roles in neurons such as lowering the threshold for action potentials, promoting burst firing and oscillatory behavior, and enhancing synaptic excitation. They also may allow rapid increases in intracellular Ca(2+) concentration. We discovered LVA-I(Ca) in both members of paired mechanoreceptor neurons in a spider, where one neuron adapts rapidly (Type A) and the other slowly (Type B) in response to a step stimulus. To learn if I(Ca) contributed to the difference in adaptation behavior, we studied the kinetics of I(Ca) from isolated somata under single-electrode voltage-clamp and tested its physiological function under current clamp. LVA-I(Ca) was large enough to fire single action potentials when all other voltage-activated currents were blocked, but we found no evidence that it regulated firing behavior. LVA-I(Ca) did not lower the action potential threshold or affect firing frequency. Previous experiments have failed to find Ca(2+)-activated K(+) current (I(K(Ca))) in the somata of these neurons, so it is also unlikely that LVA-I(Ca) interacts with I(K(Ca)) to produce oscillatory behavior. We conclude that LVA-Ca(2+) channels in the somata, and possible in the dendrites, of these neurons open in response to the depolarization caused by receptor current and by the voltage-activated Na(+) current (I(Na)) that produces action potential(s). However, the role of the increased intracellular Ca(2+) concentration in neuronal function remains enigmatic.
authors.affiliation: Department of Physiology and Biophysics, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada.
authors.forename: S I
authors.initials: SI
authors.lastname: Sekizawa
authors.forename: A S
authors.initials: AS
authors.lastname: French
authors.forename: P H
authors.initials: PH
authors.lastname: Torkkeli
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D001464:Barium / Q000493:pharmacokinetics; D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020747:Calcium Channels, T-Type / Q000502:physiology*; D005260:Female; D007700:Kinetics; D008297:Male; D008465:Mechanoreceptors / Q000737:chemistry / Q000502:physiology*; D009475:Neurons, Afferent / Q000737:chemistry / Q000502:physiology*; D009532:Nickel / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D013112:Spiders / Q000502:physiology*; D019789:Tetraethylammonium / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D020866:omega-Conotoxin GVIA / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D002104:Cadmium; D001464:Barium; D013779:Tetrodotoxin; D019789:Tetraethylammonium; D009532:Nickel; D020866:omega-Conotoxin GVIA; D015761:4-Aminopyridine; D009543:Nifedipine; D002118:Calcium