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Direct Observation of Serotonin 5‐HT 3 Receptor‐Induced Increases in Calcium Levels in Individual Brain Nerve Terminals
Author(s) -
Nichols Robert A.,
Mollard Patrice
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.67020581.x
Subject(s) - depolarization , biophysics , agonist , chemistry , calcium , synaptosome , 5 ht receptor , striatum , medicine , endocrinology , receptor , serotonin , biology , biochemistry , dopamine , organic chemistry
Confocal microscopy was used to assess internal calcium level changes in response to presynaptic receptor activation in individual, isolated nerve terminals (synaptosomes) from rat corpus striatum, focusing, in particular, on the serotonin 5‐HT 3 receptor, a ligand‐gated ion channel. The 5‐HT 3 receptor agonist‐induced calcium level changes in individual synaptosomes were compared with responses evoked by K + depolarization. Using the fluorescent dye fluo‐3 to measure relative changes in internal free Ca 2+ concentration ([Ca 2+ ] i ), K + ‐induced depolarization resulted in variable but rapid increases in apparent [Ca 2+ ] i among the individual terminals, with some synaptosomes displaying large transient [Ca 2+ ] i peaks of varying size (two‐ to 12‐fold over basal levels) followed by an apparent plateau phase, whereas others displayed only a rise to a sustained plateau level of [Ca 2+ ] i (two‐ to 2.5‐fold over basal levels). Agonist activation of 5‐HT 3 receptors induced slow increases in [Ca 2+ ] i (rise time, 15–20 s) in a subset (∼5%) of corpus striatal synaptosomes, with the increases (averaging 2.2‐fold over basal) being dependent on Ca 2+ entry and inhibited by millimolar external Mg 2+ . We conclude that significant increases in brain nerve terminal Ca 2+ , rivaling that found in response to excitation by depolarization but having distinct kinetic properties, can therefore result from the activation of presynaptic ligand‐gated ion channels.