PubMed · 86708
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M W Morgan. 1979-04-28. Adrenal suppression after short-term corticosteroid therapy.. https://doi.org/10.1016/s0140-6736(79)91420-x
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The modulation of IA K+ current by ten trivalent lanthanide (Ln3+) cations spanning the series with ionic radii ranging from 0.99 A to 1.14 A was characterized by the whole-cell patch clamp technique in bovine adrenal zona fasciculata (AZF) cells. Each of the ten Ln3+s reduced IA amplitude measured at +20 mV in a concentration-dependent manner. Smaller Ln3+s were the most potent and half-maximally effective concentrations (EC50s) varied inversely with ionic radius for the larger elements. Estimation of EC50s yielded the following potency sequence: Lu3+ (EC50 = 3.0 microM) approximately Yb3+ (EC50 = 2.7 microM) > Er3+ (EC50 = 3.7 microM) >/= Dy3+ (EC50 = 4.7 microM) > Gd3+ (EC50 = 6.7 microM) approximately Sm3+ (EC50 = 6.9 microM) > Nd3+ (EC50 = 11.2 microM) > Pr3+ (EC50 = 22.3 microM) > Ce3+ (EC50 = 28.0 microM) > La3+ (EC50 = 33.7 microM). Ln3+s altered selected voltage-dependent gating and kinetic parameters of IA with a potency and order of effectiveness that paralleled the reduction of IA amplitude. Ln3+s markedly slowed activation kinetics and shifted the voltage-dependence of IA gating such that activation and steady-state inactivation occurred at more depolarized potentials. In contrast, Ln3+s did not measurably alter inactivation or deactivation kinetics and only slightly slowed kinetics of inactivated channels returning to the closed state. Replacement of external Ca2+ with Mg2+ had no effect on the concentration-dependent inhibition of IA by Ln3+s. In contrast to their action on IA K+ current, Ln3+s inhibited T-type Ca2+ currents in AZF cells without slowing activation kinetics. These results indicate that Ln3+ modulate IA K+ channels through binding to a site on IA channels located within the electric field but which is not specific for Ca2+. They are consistent with a model where Ln3+ binding to negative charges on the gating apparatus alters the voltage-dependence and kinetics of channel opening. Ln3+s modulate transient K+ and Ca2+ currents by two fundamentally different mechanisms.
Immune responses can be modulated by noradrenergic input at (1) hypothalamic (CRF and ACTH release), (2) immune cell (cytokine production), and (3) adrenal cortex (glucocorticoid production) level. Elucitating the basic mechanisms responsible for immunological responses and diseases may be helpful in developing therapeutic approaches for many disorders, such as autoimmune diseases.
Brefeldin A (BFA) is a fungus metabolite (penicillum brefeldanum) that is known to produce the disintegration of the Golgi apparatus in exposed cells, and apoptosis in various cancer cells. This study reports that in rat primary cortical cell cultures BFA also produces apoptosis assessed by the TUNEL method and DAPI (4',6-diemidino-2-phenylindole) staining. The percentages of apoptotic neurons range from 26.9% +/- 8.3 to 43.2 +/- 2.5% in cultures exposed from 4 to 8 h to BFA (10 microg/ml). A double fluorescent staining, using AT8 antibody (phosphorylated tau) or tau1 antibody (dephosphorylated tau) associated with DAPI labeling reveals that tau1 positive neurons are more sensitive to BFA-induced apoptosis compared to AT8 positive neurons. This result and previous results using other apoptosis inducers suggest that tau phosphorylation in the vicinity of the AT8-tau1 epitopes is a marker of resistance or sensitivity to neuronal apoptosis in rat cortical cell cultures.