Lei, Saobo, William F. Dryden, and Peter A. Smith. Regulation of N- and L-type Ca2+ channels in adult frog sympathetic ganglion B cells by nerve growth factor in vitro and in vivo. J. Neurophysiol. 78: 3359–3370, 1997. To examine mechanisms responsible for the long-term regulation of Ca2+-channels in an adult neuron, changes in whole cell Ba2+ current ( I Ba) were examined in adult bullfrog sympathetic ganglion B cells in vitro. Cells were cultured at low density in defined, serum free medium. After 15 days, total I Ba was similar to the initial value, whereas I Ba density was reduced by ∼36%, presumably due to an increase in neuronal surface area. By contrast, I Ba density remained constant after 6–15 days in the presence of murine β-NGF (200 ng/ml), and total I Ba was almost doubled. Inclusion of cytosine arabinoside (Ara-C; 10 μM) to inhibit proliferation of nonneuronal cells, did not affect the survival of neurons in the absence of nerve growth factor (NGF) nor did it attenuate I Ba. Ara-C did not prevent the effect of NGF on I Ba. There were three independent components to the action of NGF; during 6–9 days, it increased ω-conotoxin-GVIA–sensitive N-type I Ba ( I Ba,N); increased nifedipine-sensitive L-type I Ba ( I Ba,L) and decreased inactivation of the total Ba2+ conductance ( g Ba). The latter effect involved a selective decrease in the amplitude of one of the four kinetic components that describe the inactivation process. Total I Ba was also 55.8% larger than control in the somata of B cells acutely dissociated from leopard frogs that had received prior subcutaneous injections of NGF. By contrast, injection of NGF antiserum decreased total I Ba by 29.4%. There was less inactivation of g Ba in B cells from NGF-injected animals than in cells from animals injected with NGF antiserum ( P < 0.001). These data suggest that NGF-like molecule(s) play(s) a role in the maintenance of I Ba in an adult amphibian sympathetic neuron; the presence of NGF may allow the neuron to maintain a constant relationship between cell size and current density. They also show that I Ba inactivation in an adult neuron can be modulated in a physiologically relevant way by an extracellular ligand.
Calcium Sensors STIM1 and STIM2 Regulate Different Calcium Functions in Cultured Hippocampal Neurons