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Journal of Neuroscience, Vol 16, 1668-1678, Copyright © 1996 by Society for Neuroscience
Characterization of an M-like current modulated by thyrotropin- releasing hormone in normal rat lactotrophs
S Sankaranarayanan and SM Simasko
Department of Veterinary Comparative Anatomy, College of Veterinary Medicine, Washington State University, Pullman 99164-6520, USA.
In rat pituitary lactotrophs, a component of thyrotropin-releasing hormone
(TRH)-induced prolactin secretion is dependent on extracellular calcium and
is associated with an increase in action-potential firing. The mechanism
underlying the TRH-induced increase in firing frequency was investigated
using the perforated-patch variation of the whole-cell patch-clamp
technique. TRH was found to inhibit a voltage-dependent, noninactivating K+
current that was similar to M-currents originally identified in neurons.
The TRH-modulated M-like current started to activate at approximately -60
mV and had a V0 of -28 mV and thus would be active under the normal resting
potentials of lactotrophs (-35 to - 45 mV). Exponential fits to
deactivating tail currents revealed a fast and a slow component. The
deactivation rates of the M-like current and the ratio of the fast to the
slow component of deactivation were found to increase with more
hyperpolarized potentials. In addition, increasing the duration of command
potentials led to the conversion of the fast component to the slow
component of deactivation. The M-like current in lactotrophs was partially
sensitive to 4-aminopyridine and tetraethylammonium. TRH inhibition of this
current was associated with acceleration of deactivation rates and a
depolarizing shift in the voltage of activation (V0 = -17 mV). The effect
of TRH on the M-like current was lost in whole-cell voltage-clamp
conditions, suggesting the requirement of an important cytosolic component
that mediates the effect of TRH.
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