Abstract
Several neurotransmitters including noradrenaline (NA), gamma-aminobutyric acid (GABA) and serotonin (5-HT), and also certain peptides, decrease the duration of the Na+-Ca2+ action potential recorded in cell bodies of embryonic chick dorsal root ganglion neurones maintained in cell culture. To determine if these agents decreased action potential duration by affecting Ca2+ channels (inward current) or K+ channels (outward current) membrane currents were recorded in voltage-clamped sensory neurone somata. 1. Depolarization produced a prominent inward Na+ current and a smaller and slower inward Ca2+ current (ICa). The inactivation of ICa was not simply dependent on membrane potential but apparently required prior entry of Ca2+. Two components of outward current, voltage-activated and Ca2+-activated, were evident in most cells. 2. The effect of NA, and also of GABA and 5-HT, was shown to result from a direct effect on ICa because: NA decreased the TTX-resistant tail current recorded at EK and also the inward current recorded in the presence of 125 mM-TEA and TTX (in which Na+ and K+ currents were blocked). 3. The decrease in ICa is most likely due to an effect on the number of available Ca2+ channels and/or the single Ca2+ channel conductance rather than to a shift in either the kinetics of channel activation or the Ca2+ equilibrium potential. 4. No effect of the several transmitters on the voltage-dependent Na+ and K+ currents was observed. 5. Implications of ICa modulation for the phenomenon of presynaptic inhibition are discussed.
MeSH Terms
Action Potentials/drug effects
Animals
Calcium/physiology
Cells, Cultured
Chick Embryo
Ion Channels/drug effects
Kinetics
Membrane Potentials/drug effects
Neurons, Afferent/physiology
Neurotransmitter Agents/pharmacology
Norepinephrine/pharmacology
Serotonin/pharmacology
gamma-Aminobutyric Acid/pharmacology
Chemicals
Ion Channels
Neurotransmitter Agents
Serotonin
gamma-Aminobutyric Acid
Calcium
Norepinephrine
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Dunlap K
Fischbach G D
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