
doi: 10.1038/265246a0
pmid: 319366
CALCIUM ions, which enter presynaptic nerve terminals during depolarisation, trigger transmitter release from the terminals of both peripheral1 and central2 neurones. The subsequent disposition of the entering Ca is not entirely settled. Although this Ca must eventually be extruded in order for the neurones to return to the steady state, some of it may be temporarily retained and sequestered in intra-terminal organelles. We now present evidence for an intraterminal, ATP-dependent Ca storage system which may help to regulate internal ionised Ca concentrations. This latent Ca sequestering system has been revealed by lysis of pinched-off presynaptic nerve terminals (“synaptosomes”) in hypotonic media, followed by measurements of ATP-dependent Ca uptake from media containing mitochondrial inhibitors. These observations provide an alternative to the suggestion3,4 that intraterminal mitochondria may be the primary Ca storage sites.
Cerebral Cortex, Nerve Endings, Oxalates, Biological Transport, Active, Mitochondria, Rats, Adenosine Triphosphate, Synapses, Animals, Calcium, Calcimycin, Dinitrophenols, Synaptosomes
Cerebral Cortex, Nerve Endings, Oxalates, Biological Transport, Active, Mitochondria, Rats, Adenosine Triphosphate, Synapses, Animals, Calcium, Calcimycin, Dinitrophenols, Synaptosomes
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