Cm. Richardson et al., NOVEL PHARMACOLOGICAL SENSITIVITY OF THE PRESYNAPTIC CALCIUM CHANNELSCONTROLLING ACETYLCHOLINE-RELEASE IN SKATE ELECTRIC ORGAN, Journal of neurochemistry, 64(2), 1995, pp. 944-947
The presynaptic terminals of skate (Raja montagui) electric organ were
tested for their sensitivity to calcium channel antagonists. Acetylch
oline (ACh) release and the elevation of intraterminal Ca2+ concentrat
ions triggered by K+ depolarisation were studied. ACh release was meas
ured as H-3 efflux from slices of organ prelabelled with [H-3]choline.
Depolarisation caused a marked, Ca2+-dependent increase in H-3 efflux
that was completely blocked by 100 mu M Cd2+ and by 300 nM omega-cono
toxin-MVIIC (MVIIC). Inhibition by MVIIC was concentration dependent (
IC50 of similar to 20 nM) and reversible. No inhibition was seen with
nifedipine (5 mu M) or the two other peptide antagonists studied. omeg
a-conotoxin-GVIA (GVIA) at 5 mu M and omega-agatoxin-IVA (Aga-IVA) at
1 mu M. In a ''nerve plate'' preparation (a presynaptic plexus of nerv
e fibres, Schwann cells, and nerve terminals) changes in intraterminal
Ca2+ concentrations were measured by microfluorimetry using fluo-3. A
n increase in fluorescence, indicating a rise in the free [Ca2+], rapi
dly followed K+ depolarisation, and this change was restricted to the
nerve terminals. This response was insensitive to nifedipine (5 mu M),
GVIA(5 mu M), and Aga-IVA (300 nM) but almost completely abolished by
MVIIC (1 mu M) MVIIC inhibition was concentration dependent and parti
ally reversible. These results show that the nerve terminals in skate
electric organ have calcium channels with a pharmacological sensitivit
y that is markedly different from the established L, N, and P types in
other systems but shares some, but not all, of the features of the re
cently described Q type.