RT Journal Article
SR Electronic
T1 Ryanodine-Sensitive Component of Calcium Transients Evoked by Nerve Firing at Presynaptic Nerve Terminals
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 6703
OP 6712
DO 10.1523/JNEUROSCI.16-21-06703.1996
VO 16
IS 21
A1 Peng, Yan-yi
YR 1996
UL http://www.jneurosci.org/content/16/21/6703.abstract
AB Whether Ca2+ released from stores within the presynaptic nerve terminals also contributes to the Ca2+elevation evoked by action potentials was tested in intact bullfrog sympathetic ganglia. Intraterminal Ca2+ transients (Δ[Ca2+]i) were evoked by electrical shocks to the presynaptic nerves at 20 Hz and were monitored by fura-2 fluorimetry. Ca2+ released through intraterminal ryanodine-sensitive channels accounted for 46% of the peak Ca2+ elevation. Moreover, in half of the terminals when intraterminal release was blocked by ryanodine, Δ[Ca2+]i reached a plateau at 200 ± 24 nm. Because 20 Hz is a frequency favorable for the release of a neuropeptide, luteinizing hormone releasing hormone (LHRH) from these presynaptic nerve terminals, and because the threshold level for LHRH release is 186 nm, intraterminal Ca2+release during nerve firing is likely to play a major role in regulating LHRH release. The intraterminal ryanodine channels were facilitated by caffeine as in other tissue. The releasable ryanodine-sensitive store could elevate the intraterminal [Ca2+] by an amount as high as 1.6 μm at a rate as fast as 250 nm/sec. The store could be refilled within 100 sec after a maximal discharge of its content by 20 Hz firing. Oscillation of [Ca2+]i evoked by 20 Hz nerve firing occurred in normal Ringer solution, in ryanodine, and in caffeine with a periodicity of ∼10 sec. Besides the facilitatory effects on the ryanodine-sensitive channels, caffeine also had inhibitory effects on Δ[Ca2+]i via its action on a different process.