The inward rectifier in a model of corticotroph electrical activity
Paul R. Shorten, A. Bruce Robson, Alan E. McKinnon and David J.N. Wall
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Abstract
Pituitary corticotrophcells generate repetitive action potentials and associated Ca2+ transients in response to the agonist corticotropin releasing hormone (CRH). There is indirect evidence suggesting that the agonist, by way of complex intracellular mechanisms, modulates the voltage sensitivity of the L-type Ca2+ channels embedded in the plasma membrane. We have previously constructed a Hodgkin-Huxley type model of this process, which indicated that an increase in the Ltype Ca2+ current is sufficient to generate repetitive action potentials [LeBeau et al. (1997). Biophysical Journal 73, 1263-1275]. The agonist is also believed to inhibit an inwardly rectifying K+ current in the action potential firing frequency and membrane excitability. We have found that a CRH-induced inhibition of the inwardly rectifying K+ current increases the action potential firing frequency and membrane excitability. This structural alteration to the model along with parametric changes bring the model firing frequency in line with experimental data. We also show that the model exhibits experimentally observed bursting behaviour, where the depolarization spike is followed by small oscillations in the membrane potential.
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