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Spike aftercurrents in R15 of Aplysia: their relationship to slow inward current and calcium influx.

Publication ,  Journal Article
Lewis, DV
Published in: J Neurophysiol
February 1984

Spikes in the bursting neuron, R15, are followed by depolarizing afterpotentials (35) and often by delayed hyperpolarizing afterpotentials as well. Placing the cell in a voltage clamp after a spike allows measurement of the depolarizing aftercurrent (DAC) and hyperpolarizing aftercurrent (HAC) that underlie the afterpotentials. Subthreshold depolarizations give rise to small DACs and HACs. The DAC and the slow inward current (SIC) of R15 are reduced or blocked in a similar manner by many experimental manipulations, e.g., application of dopamine, zero-calcium seawater, zero-sodium seawater, or calcium-channel blockers (Mn2+ and La3+), or cooling the cell from 21-22 degrees C to 10 degrees C. Neither the DAC nor the SIC were blocked by tetrodotoxin (100 uM) and neither was sensitive to altered extracellular potassium. Both the DAC and SIC become larger as the holding potential of the cell is progressively depolarized from -70 to -40 mV. DACs are sensitive to the injection of intracellular calcium chelators (EGTA (ethylene glycol-bis(beta-aminoethyl ether)-N,N1-tetraacetic acid) or EDTA [ethylenedinitrilo)tetraacetic acid]. DAC amplitude is approximately 90% reduced by intracellular EGTA concentration near 1mM. In contrast, the SIC is unchanged or much less affected by the calcium buffers. DACs are also more sensitive to low (1 mM) extracellular calcium than is the SIC. The HAC is also a calcium-dependent current. It is blocked by any experimental manipulation reducing calcium influx or intracellular calcium accumulation, i.e., reduced extracellular calcium, calcium-channel blockers, or intracellular EGTA. We suggest that the DAC and the SIC are carried by the same conductance mechanism. In the case of the DAC, the conductance might be activated by a rise in intracellular calcium activity accompanying the spike and, in the case of the SIC, depolarization per se may be the most important activating condition.

Duke Scholars

Published In

J Neurophysiol

DOI

ISSN

0022-3077

Publication Date

February 1984

Volume

51

Issue

2

Start / End Page

387 / 403

Location

United States

Related Subject Headings

  • Tetrodotoxin
  • Neurons
  • Neurology & Neurosurgery
  • Ganglia
  • Electric Conductivity
  • Dopamine
  • Cold Temperature
  • Chelating Agents
  • Calcium
  • Aplysia
 

Citation

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MLA
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Lewis, D. V. (1984). Spike aftercurrents in R15 of Aplysia: their relationship to slow inward current and calcium influx. J Neurophysiol, 51(2), 387–403. https://doi.org/10.1152/jn.1984.51.2.387
Lewis, D. V. “Spike aftercurrents in R15 of Aplysia: their relationship to slow inward current and calcium influx.J Neurophysiol 51, no. 2 (February 1984): 387–403. https://doi.org/10.1152/jn.1984.51.2.387.
Lewis, D. V. “Spike aftercurrents in R15 of Aplysia: their relationship to slow inward current and calcium influx.J Neurophysiol, vol. 51, no. 2, Feb. 1984, pp. 387–403. Pubmed, doi:10.1152/jn.1984.51.2.387.

Published In

J Neurophysiol

DOI

ISSN

0022-3077

Publication Date

February 1984

Volume

51

Issue

2

Start / End Page

387 / 403

Location

United States

Related Subject Headings

  • Tetrodotoxin
  • Neurons
  • Neurology & Neurosurgery
  • Ganglia
  • Electric Conductivity
  • Dopamine
  • Cold Temperature
  • Chelating Agents
  • Calcium
  • Aplysia