Journal of Neuroscience, Vol 7, 3623-3632, Copyright © 1987 by Society for Neuroscience
Alpha bag cell peptide directly modulates the excitability of the neurons that release it
JA Kauer, TE Fisher and LK Kaczmarek
Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06510.
Brief electrical or hormonal stimulation of the bag cell neurons of Aplysia
triggers a long-lasting discharge during which alpha bag cell peptide
(alpha-BCP) and other neuropeptides are released from the cells. We have
carried out experiments, using both intact abdominal ganglia and isolated
neurons, demonstrating that alpha-BCP acts directly on the bag cell neurons
to influence cAMP levels and voltage- dependent potassium currents.
Exposure of the bag cell neurons within intact ganglia to alpha-BCP, at
concentrations greater than 1 nM, inhibited an ongoing discharge. alpha-BCP
also significantly reduced both basal and forskolin-stimulated levels of
cAMP in bag cell clusters. The inhibition of the discharge by alpha-BCP
could be prevented and reversed by pharmacological elevation of
intracellular cAMP levels. Immunohistochemical staining of neurons
maintained in cell culture showed that all isolated bag cell neurons
exhibit immunoreactivity with antisera against alpha-BCP. Application of
the adenylate cyclase activator forskolin to such isolated cells, in the
presence of a phosphodiesterase inhibitor, attenuates the amplitude of the
delayed voltage-dependent outward currents measured in voltage- clamp
experiments. Pretreatment of the cells with alpha-BCP significantly reduced
the ability of forskolin to attenuate these currents, demonstrating that
alpha-BCP acts directly at autoreceptors on bag cell neurons. Experiments
with the isolated cells showed that a second autoreceptor-mediated effect
of alpha-BCP was the enhancement of an inwardly rectifying potassium
current that was activated at potentials more negative than -40 mV. The
reversal potential and conductance of the current induced by alpha-BCP were
dependent on the external K+ concentration. This response to alpha-BCP
could be blocked by rubidium, cesium, and barium ions. Our data demonstrate
that alpha- BCP can exert inhibitory biochemical and electrophysiological
actions on the bag cell neurons that release it and suggest that
autoreceptors for alpha-BCP play an important role in the termination of a
discharge in the bag cell neurons.
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