Frequency-dependent decay of calcium spikes in cultured spinal cord neurons.
Calcium-dependent action potentials were recorded from cultured (dissociated) spinal cord neurons in the presence of extracellular tetrodotoxin and tetraethylammonium in the mouse. The plateau portion of these action potentials underwent pronounced frequency-dependent decay with repetitive depolarizing current injections. Interstimulus intervals as long as 5 min were often required to ensure reproducible spike durations. This decay was not due to recurrent inhibition or intracellular calcium accumulation. It may be due to accumulation of either voltage-dependent inactivation of the calcium spike or of voltage-dependent outward currents. Any manipulation that prolonged the duration of the spike resulted in an apparent enhancement of the decay; however, this may simply be a consequence of the hyperbolic relationship between spike duration and the slope of the spike decay. It does not necessarily imply an effect on the mechanisms underlying frequency-dependent decay. Caution should, therefore, be exercised in interpreting the effects of drugs upon these calcium-dependent spikes.
D000200:Action Potentials; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004533:Egtazic Acid / Q000494:pharmacology; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D051379:Mice; D009433:Neural Inhibition; D009543:Nifedipine / Q000494:pharmacology; D013116:Spinal Cord / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission; D013779:Tetrodotoxin / Q000494:pharmacology
D007473:Ion Channels; D013779:Tetrodotoxin; D004533:Egtazic Acid; D009543:Nifedipine; D002118:Calcium