Mathematical Biology Seminar
Joel Tabak
Department of Biological Science, Florida State university
Wednesday Jan. 16, 2008
3:05pm in LCB 215
"Fast potassium currents can
stimulate calcium influx and hormone secretion
in pituitary cells
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Abstract:
Dopamine (DA) released from the hypothalamus tonically inhibits
pituitary
lactotrophs. DA opens potassium channels, hyperpolarizing the
lactotrophs
and thus preventing the calcium influx that triggers prolactin hormone
release. Surprisingly, at concentrations ~1000 lower (sub nM), DA can
increase intracellular calcium ([Ca++]i) and stimulate prolactin
secretion. Can an increase in a K+ current mediate this stimulatory
effect?
To answer this question, we added either an inactivating (IA) or a
non-inactivating (IBK) fast K+ current to a minimal lactotroph model.
Both currents transformed the activity pattern of the model from
spiking to bursting. This transition to bursting resulted in larger
amplitude [Ca++]i oscillations. However, while IBK also caused a
reliable increase in mean [Ca++]i, IA generally did not. The reason
for this difference will be explained using fast/slow analysis.
In the cases where IA did increase mean [Ca++]i, we observed that
the
bursting mechanism was no longer dependent on the slow variable
[Ca++]i. Bursting could continue after [Ca++]i was clamped and
therefore did not rely on the usual combination of bistability and a
slow variable. The slow bursting time scale is unexpectedly caused by
a transient pulse of IA at the beginning of each burst. We believe
that this is the first example of a physiologically based,
single-compartmental model of bursting with no slow subsystem.
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Mathematical Biology Program
Department of Mathematics
University of Utah
155 South 1400 East Room 233
Salt Lake City, UT 84112
rasmusse@math.utah.edu
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