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Journal of Neuroscience, Vol 8, 2544-2555, Copyright © 1988 by Society for Neuroscience
Inositol trisphosphate releases intracellularly stored calcium and modulates ion channels in molluscan neurons
LA Fink, JA Connor and LK Kaczmarek
Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06510.
Stimulation of the bag cell neurons of Aplysia triggers a long-lasting
afterdischarge in these cells. In vivo, such a discharge causes the onset
of a sequence of reproductive behaviors. We have found that treatments that
trigger discharges in vitro stimulate the hydrolysis of phosphoinositides
in the bag cell neurons, as measured by increased incorporation of
3H-inositol into fractions containing membrane lipids and water-soluble
inositol phosphates. The electrophysiological effects of inositol
trisphosphate, one of the products of phosphoinositide turnover that has
been shown to mobilize intracellular calcium in non- neuronal cells, were
investigated using isolated bag cell neurons in cell culture.
Microinjection of inositol trisphosphate into cultured bag cell neurons
caused a transient hyperpolarization of the membrane (approximately 35
sec), together with an increase in conductance. This effect of inositol
trisphosphate was abolished by 50 mM tetraethylammonium ions. Inositol
trisphosphate also reduced the amplitude of action potentials. Injection of
calcium ions directly into bag cell neurons mimicked these responses seen
after inositol trisphosphate injection. Using the cell-attached patch-clamp
technique in conjunction with inositol trisphosphate microinjection, we
observed that inositol trisphosphate evoked increases in the activity of a
channel carrying outward current at the resting potential and more positive
potentials. The estimated slope conductance of the channel modulated by
inositol trisphosphate was approximately 40 pS, and its reversal potential
was close to that predicted for potassium ions. The increased opening of
this channel in response to inositol trisphosphate injection appeared to
result from a transient shift of its voltage- dependence to more negative
potentials. In a few cases, inositol trisphosphate injection also elicited
an increase in the activity of a channel passing inward current at rest.
Direct measurements of changes in intracellular calcium in response to
inositol trisphosphate were made using digital imaging of isolated neurons
loaded with the fluorescent calcium indicator fura-2. These revealed that
injection of inositol trisphosphate significantly elevated intracellular
calcium levels, and that this inositol trisphosphate-induced rise in
cytosolic calcium was not affected by removal of extracellular calcium. In
contrast to the effects of trains of action potentials in calcium-
containing media, which produced increases in calcium primarily in
neurites, the inositol trisphosphate-induced elevation of calcium appeared
more localized to the somata of these neurons.(ABSTRACT TRUNCATED AT 400
WORDS)
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