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Facilitation of the presynaptic calcium current at an auditory synapse in rat brainstem
Author(s) -
Cuttle Matthew F.,
Tsujimoto Tetsuhiro,
Forsythe Ian D.,
Takahashi Tomoyuki
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.723bd.x
Subject(s) - facilitation , chemistry , bapta , egta , neural facilitation , biophysics , neuroscience , depolarization , electrophysiology , calcium , neurotransmission , biology , biochemistry , receptor , organic chemistry
1 The presynaptic calcium current ( I pCa ) was recorded from the calyx of Held in rat brainstem slices using the whole‐cell patch clamp technique. 2 Tetanic activation of I pCa by 1 ms depolarizing voltage steps markedly enhanced the amplitude of I pCa . Using a paired pulse protocol, the second (test) response was facilitated with inter‐pulse intervals of less than 100 ms. The facilitation was greater at shorter intervals and was maximal (about 20 %) at intervals of 5–10 ms. 3 When the test pulse duration was extended, the facilitation was revealed as an increased rate of I pCa activation. From the current‐voltage relationship measured at 1 ms from onset, facilitation could be described by a shift in the half‐activation voltage of about −4 mV. 4 IpCa facilitation was not attenuated when guanosine‐5′‐ O ‐(3‐thiotriphosphate) (GTPγS) or guanosine‐5′‐ O ‐(2‐thiodiphosphate) (GDPβS) was included in the patch pipette, suggesting that G‐proteins are not involved in this phenomenon. 5 On reducing [Ca 2+ ] o , the magnitude of facilitation diminished proportionally to the amplitude of I pCa . Replacement of [Ca 2+ ] o by Ba 2+ or Na + , or buffering of [Ca 2+ ] i with EGTA or BAPTA attenuated I pCa facilitation. 6 We conclude that repetitive presynaptic activity can facilitate the presynaptic Ca 2+ current through a Ca 2+ ‐dependent mechanism. This mechanism would be complementary to the action of residual Ca 2+ on the exocytotic machinery in producing activity‐dependent facilitation of synaptic responses.