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Journal of Neuroscience, Vol 9, 657-666, Copyright © 1989 by Society for Neuroscience
G proteins couple alpha-adrenergic and GABAb receptors to inhibition of peptide secretion from peripheral sensory neurons
GG Holz 4th, RM Kream, A Spiegel and K Dunlap
Department of Physiology, Tufts University School of Medicine-New England Medical Center, Boston, Massachusetts 02111.
Regulation of neuronal calcium channels by GTP-binding proteins (G
proteins) is likely to be an important mechanism by which inhibitory
transmitters influence excitation-secretion coupling in presynaptic nerve
endings. Here, we report that in peripheral sensory neurons from embryonic
chick dorsal root ganglia (DRG), the G protein-mediated inhibition of
voltage-dependent calcium channels may best explain how norepinephrine (NE)
and GABA inhibit the electrically evoked, calcium- dependent release of
substance P (SP). As is the case for the previously reported inhibitory
actions of these transmitters on DRG cell calcium channels, we demonstrate
that NE and GABA inhibit peptide secretion through activation of
alpha-adrenergic and GABAb receptors that are functionally coupled to
pertussis toxin (PTX)-sensitive G proteins. Pretreatment of DRG cell
cultures with PTX blocked the ability of NE and GABA to inhibit the release
of SP, an action correlated with PTX-catalyzed ADP-ribosylation of membrane
proteins with apparent molecular weight (Mr) of 40-41 kDa. Western
immunoblot analysis of chick DRG cell membrane proteins using antisera
directed against synthetic peptides corresponding to amino acid sequences
predicted from cDNAs for PTX-sensitive G protein alpha subunits revealed a
minimum of 2 Gi-like proteins (Mr 40 and 41 kDa) and a third Go-like
protein (Mr 40 kD). Significantly, these findings implicate Gi- and/or
Go-like GTP-binding proteins as mediators of presynaptic inhibition in
peripheral sensory neurons.
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