Effects of hypothalamic peptides on electrical activity and membrane currents of ‘patch perforated’ clamped GH₃ anterior pituitary cells

Abstract

INTROBLJCTIONElectrophysiological recordings from GH, cells using conventional high resistance micro-electrodes have revealed that somatosrarin (SS) depresses [l] and TRH enhances cell excitability, The effect of TRH is quite complex, consisting of Rf) initial phase of transient hyperpolarization 12-S] followed by a second phase in wlrich mcmbranc conductance is decreased while both the rate of production and the length of APs are increased (2,3,5-71. This second phase causes a plateau of elevated intracellular Ca 2'* due to influx of extracellular Ca'+ ([&lo] for review see [I 13) and coincides with a sustained increase in secretion [9,12-161. The importance of Ca* + in this sustained secretion is controversial [9,11,12], and it has been suggested that this cation is only necessary at low TRH concentrations when the increases in diacylglycerol are submaximal

Pharmacology of high‐threshold calcium currents in GH4C1 pituitary cells and their regulation by activation of human D2 and D4 dopamine receptors

“…Thyrotropin-releasing hormone mobilizes intracellular calcium in pituitary cells and can regulate Ca2l-activated K channel activity in both GH3 and GH4C, cells (Dubinsky & Oxford, 1985;Barros et al, 1991). Rat D2 receptors have been reported to suppress the intracellular calcium mobilisation caused by activation of receptors to thyrotropin releasing hormone in GH4C1 cells (Valar et al, 1990).…”

Okadaic acid and calyculin A enhance the effect of thyrotropin‐releasing hormone on GH3 rat anterior pituitary cells excitability

“…Other Materials and Methods were identical to those described in [5,13]. AP's frequency was determined in periods of at least 80 s either before or 2-5 min after the start of the indicated treatments.…”

“…These two phases are paralleled by changes in cell excitability, consisting of an initial phase of transient hyperpolarization followed by a second phase in which both the rate of production and the length of action (APs) are increased [4][5][6]. The mechanisms and conductance pathways responsible for the increased production of APs are not well known.…”

“…The mechanisms and conductance pathways responsible for the increased production of APs are not well known. It has been suggested that inhibition of various outward currents, including the transient outward current named IK~ and IK(~) [7][8][9], the voltage-and Ca2+-activated K ÷ curret~t [5,10,11], or the inwardly rectifying K + current [12,13], is the cause of the second phase of hyperexcitability. It has also been suggested that phosphorylation by protein kinase C (PKC) is involved in modulation of the K ÷ channel activity which determines the firing rate [1,2,4,14,15].…”

“…Given the very different structures of OKA and CL-A, the combined use of both inhibitors has been regarded as a way to strengthen the evidence that a cellular process is controlled by phosphorylation [I 8]. We have recently shown that electrical responses to TRH are fully preserved when patch-perforated current-clamped GHa cells are studied [5]. On the other hand, recent experiments from our laboratory indicated that treatment of GH3 cells with OKA specifically potentiates the reductions caused by TRH on inward rectifying K ÷ currents [13].…”