RT Journal Article
SR Electronic
T1 Extracellular ATP modulates calcium uptake and transmitter release at the neuromuscular junction
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1567
OP 1573
DO 10.1523/JNEUROSCI.07-05-01567.1987
VO 7
IS 5
A1 CA Lindgren
A1 DO Smith
YR 1987
UL http://www.jneurosci.org/content/7/5/1567.abstract
AB Adenosine, AMP, ADP, and ATP were tested for their ability to modulate evoked quantal transmitter release at excitor-opener nerve terminals in the crayfish walking leg. Only ATP was found to have a significant effect, inhibiting release by 43%. To determine whether the effects of extracellular ATP on transmitter release were related to changes in free Ca2+ levels in the nerve terminal, net 45Ca uptake was measured in regions of the nerve near the terminal; although resting 45Ca uptake was increased by 5 mM exogenous ATP. Thus, extracellular ATP normally inhibits evoked transmitter release; this is associated with reduced stimulation-induced net Ca2+ uptake into the synaptic terminal. To explore the possibility that metabolic factors might be involved, nerve ATP levels were reduced by greater than or equal to 50% by omitting glucose from the bathing solution. Although quantal content and synaptic delay were unaffected by reduced intracellular ATP, under these conditions 5 mM exogenous ATP failed to reduce quantal release. Five millimolars of ATP did increase synaptic facilitation, however, which is consistent with a reduced ability to regulate intracellular free Ca2+. Therefore, under conditions of reduced intracellular ATP, the increased resting Ca2+ uptake produced by 5 mM ATP is not buffered completely. This leads to elevated free Ca2+ levels in the nerve terminal, increasing the amount of transmitter released following an action potential.