TY - JOUR
T1 - Effects of scorpion toxin on excitatory and inhibitory presynaptic terminals
AU - Akaike, Hironari
AU - Shin, Min chul
AU - Kubo, Chiharu
AU - Akaike, Norio
N1 - Funding Information:
The authors thank to Dr. M. Yoshimura and Dr. M. Andresen for their valuable comments and advice. This work is supported by a grant to N. Akaike from the Project for Promoting Industry-Academic Collaborative Research.
PY - 2009/10/29
Y1 - 2009/10/29
N2 - The effects of scorpion toxin (STX) on both spontaneous and evoked glycinergic and glutamatergic postsynaptic currents were studied by using both the mechanically dissociated single SDCN neuron (synaptic bouton preparation) and the 'focal electrical stimulation technique'. In the experimental condition where Na+ channels on postsynaptic soma membrane were blocked by intracellular perfusion of QX-314, STX increased dose-dependently the frequency of spontaneous glycinergic and glutamatergic postsynaptic currents (sIPSC and sEPSC, respectively) without affecting the amplitude, suggesting STX acts on inhibitory and excitatory presynaptic nerve terminal. Such a facilitatory effect of STX on sIPSC was stronger than that on sEPSC. On the other hand, STX significantly enhanced the averaged current amplitude and decreased the failure rate (Rf) of both evoked inhibitory and excitatory postsynaptic currents (eIPSC and eEPSC, respectively), indicating that STX increases not only the release frequency of glycine and glutamate but also the amount of their release from the both presynaptic nerve endings. These effects of STX were completely removed by adding Na+ or Ca2+ channel blockers, indicating that STX increases Ca2+ influx through Ca2+ channels triggered by activating voltage-dependent Na+ channels on the nerve terminals. In addition, the difference of STX actions on the amplitude of spontaneous and evoked currents was discussed.
AB - The effects of scorpion toxin (STX) on both spontaneous and evoked glycinergic and glutamatergic postsynaptic currents were studied by using both the mechanically dissociated single SDCN neuron (synaptic bouton preparation) and the 'focal electrical stimulation technique'. In the experimental condition where Na+ channels on postsynaptic soma membrane were blocked by intracellular perfusion of QX-314, STX increased dose-dependently the frequency of spontaneous glycinergic and glutamatergic postsynaptic currents (sIPSC and sEPSC, respectively) without affecting the amplitude, suggesting STX acts on inhibitory and excitatory presynaptic nerve terminal. Such a facilitatory effect of STX on sIPSC was stronger than that on sEPSC. On the other hand, STX significantly enhanced the averaged current amplitude and decreased the failure rate (Rf) of both evoked inhibitory and excitatory postsynaptic currents (eIPSC and eEPSC, respectively), indicating that STX increases not only the release frequency of glycine and glutamate but also the amount of their release from the both presynaptic nerve endings. These effects of STX were completely removed by adding Na+ or Ca2+ channel blockers, indicating that STX increases Ca2+ influx through Ca2+ channels triggered by activating voltage-dependent Na+ channels on the nerve terminals. In addition, the difference of STX actions on the amplitude of spontaneous and evoked currents was discussed.
UR - http://www.scopus.com/inward/record.url?scp=70349210045&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70349210045&partnerID=8YFLogxK
U2 - 10.1016/j.tox.2009.08.010
DO - 10.1016/j.tox.2009.08.010
M3 - Article
C2 - 19686797
AN - SCOPUS:70349210045
VL - 264
SP - 198
EP - 204
JO - Toxicology
JF - Toxicology
SN - 0300-483X
IS - 3
ER -