TY - JOUR
T1 - Pancreatic polypeptide inhibits calcium channels in rat sympathetic neurons via two signaling pathways
AU - Wollmuth, L. P.
AU - Shapiro, M. S.
AU - Hille, B.
PY - 1995
Y1 - 1995
N2 - 1. We studied modulation of N-type Ca2+ channels in adult rat superior cervical ganglion (SCG) neurons by pancreatic polypeptide (PP) using whole cell clamp. In large (>20 pF) SCG neurons, PP inhibited I(Ca) (35 ± 2%, mean ± SE) in a concentration-dependent fashion, with one-half maximal inhibition at 19 nM. 2. One-third of the inhibition was blocked by pertussis toxin, about one-half was blocked by N-ethylmaleimide (NEM) treatments, and about one-half was voltage dependent. The NEM-insensitive component of the PP inhibition was voltage independent and not significantly blocked by intracellular Ca2+ chelators. 3. The NEM-insensitive component was only weakly attenuated by GDP-β-S, and moderately reversible with guanosine 5'- triphosphate (GTP)-γ-S, in the whole cell pipette, leaving open the possibility that it is not mediated by a G protein. 4. Hence, PP inhibits I(Ca) via two mechanisms: one G-protein-mediated and the other possibly G- protein independent. The former pathway is sensitive to pertussis toxin (PTX) and NEM, voltage dependent, and shared by several other transmitters in these cells. The latter pathway is PTX-and NEM-insensitive, not voltage dependent, and not affected by the presence of intracellular Ca2+ chelators.
AB - 1. We studied modulation of N-type Ca2+ channels in adult rat superior cervical ganglion (SCG) neurons by pancreatic polypeptide (PP) using whole cell clamp. In large (>20 pF) SCG neurons, PP inhibited I(Ca) (35 ± 2%, mean ± SE) in a concentration-dependent fashion, with one-half maximal inhibition at 19 nM. 2. One-third of the inhibition was blocked by pertussis toxin, about one-half was blocked by N-ethylmaleimide (NEM) treatments, and about one-half was voltage dependent. The NEM-insensitive component of the PP inhibition was voltage independent and not significantly blocked by intracellular Ca2+ chelators. 3. The NEM-insensitive component was only weakly attenuated by GDP-β-S, and moderately reversible with guanosine 5'- triphosphate (GTP)-γ-S, in the whole cell pipette, leaving open the possibility that it is not mediated by a G protein. 4. Hence, PP inhibits I(Ca) via two mechanisms: one G-protein-mediated and the other possibly G- protein independent. The former pathway is sensitive to pertussis toxin (PTX) and NEM, voltage dependent, and shared by several other transmitters in these cells. The latter pathway is PTX-and NEM-insensitive, not voltage dependent, and not affected by the presence of intracellular Ca2+ chelators.
UR - http://www.scopus.com/inward/record.url?scp=0028952258&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028952258&partnerID=8YFLogxK
U2 - 10.1152/jn.1995.73.3.1323
DO - 10.1152/jn.1995.73.3.1323
M3 - Article
C2 - 7608776
AN - SCOPUS:0028952258
VL - 73
SP - 1323
EP - 1328
JO - Journal of Neurophysiology
JF - Journal of Neurophysiology
SN - 0022-3077
IS - 3
ER -