TY - JOUR
T1 - Re-evaluation of phorbol ester-induced potentiation of transmitter release from mossy fibre terminals of the mouse hippocampus
AU - Honda, Izumi
AU - Kamiya, Haruyuki
AU - Yawo, Hiromu
N1 - Copyright:
Copyright 2007 Elsevier B.V., All rights reserved.
PY - 2000/12/15
Y1 - 2000/12/15
N2 - 1. To investigate the mechanisms by which phorbol esters potentiate transmitter release from mossy fibre terminals we used fura dextran to measure the intraterminal Ca2+ concentration in mouse hippocampal slices. 2. A phorbol ester, phorbol 12,13-diacetate (PDAc), potentiated the field excitatory post-synaptic potential (fEPSP) slope. PDAc also enhanced the stimulation-dependent increase of [Ca2+]i in the mossy fibre terminal (Δ[Ca2+]pre). The magnitude of the PDAc-induced fEPSP potentiation (463 ± 57% at 10 μM) was larger than that expected from the enhancement of Δ[Ca2+]pre (153 ± 5%). 3. The Δ[Ca2+]pre was suppressed by ω-agatoxin IVA (ω- AgTxIVA, 200 nM), a P/Q-type Ca2+ channel-specific blocker, by 31%. The effect of PDAc did not select between ω-AgTxIVA-sensitive and - resistant components. 4. The PDAc-induced potentiation of the fEPSP slope was partially antagonized by the protein kinase C (PKC) inhibitor bisindolymaleimide I (BIS-I, 10 μM), whereas the Δ[Ca2+]pre was completely blocked by BIS-I. Although the BIS-I-sensitive fEPSP potentiation was accompanied by a reduction of the paired-pulse ratio (PPR), the BIS-I-resistant component was not. 5. Whole-cell patch clamp recording from a CA3 pyramidal neuron in a BIS-I-treated slice demonstrated that PDAc (10 μM) increased the frequency of miniature excitatory postsynaptic currents (mEPSCs, 259 ± 33% of control) without a noticeable change in their amplitude (102 ± 5% of control). 6. These results suggest that PKC potentiates transmitter release by at least two distinct mechanisms, one Δ[Ca2+]pre dependent and the other Δ[Ca2+]pre independent. In addition, some phorbol ester-mediated potentiation of synaptic transmission appears to occur without activating PKC.
AB - 1. To investigate the mechanisms by which phorbol esters potentiate transmitter release from mossy fibre terminals we used fura dextran to measure the intraterminal Ca2+ concentration in mouse hippocampal slices. 2. A phorbol ester, phorbol 12,13-diacetate (PDAc), potentiated the field excitatory post-synaptic potential (fEPSP) slope. PDAc also enhanced the stimulation-dependent increase of [Ca2+]i in the mossy fibre terminal (Δ[Ca2+]pre). The magnitude of the PDAc-induced fEPSP potentiation (463 ± 57% at 10 μM) was larger than that expected from the enhancement of Δ[Ca2+]pre (153 ± 5%). 3. The Δ[Ca2+]pre was suppressed by ω-agatoxin IVA (ω- AgTxIVA, 200 nM), a P/Q-type Ca2+ channel-specific blocker, by 31%. The effect of PDAc did not select between ω-AgTxIVA-sensitive and - resistant components. 4. The PDAc-induced potentiation of the fEPSP slope was partially antagonized by the protein kinase C (PKC) inhibitor bisindolymaleimide I (BIS-I, 10 μM), whereas the Δ[Ca2+]pre was completely blocked by BIS-I. Although the BIS-I-sensitive fEPSP potentiation was accompanied by a reduction of the paired-pulse ratio (PPR), the BIS-I-resistant component was not. 5. Whole-cell patch clamp recording from a CA3 pyramidal neuron in a BIS-I-treated slice demonstrated that PDAc (10 μM) increased the frequency of miniature excitatory postsynaptic currents (mEPSCs, 259 ± 33% of control) without a noticeable change in their amplitude (102 ± 5% of control). 6. These results suggest that PKC potentiates transmitter release by at least two distinct mechanisms, one Δ[Ca2+]pre dependent and the other Δ[Ca2+]pre independent. In addition, some phorbol ester-mediated potentiation of synaptic transmission appears to occur without activating PKC.
UR - http://www.scopus.com/inward/record.url?scp=0034671168&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034671168&partnerID=8YFLogxK
U2 - 10.1111/j.1469-7793.2000.00763.x
DO - 10.1111/j.1469-7793.2000.00763.x
M3 - Article
C2 - 11118504
AN - SCOPUS:0034671168
VL - 529
SP - 763
EP - 776
JO - Journal of Physiology
JF - Journal of Physiology
SN - 0022-3751
IS - 3
ER -