title: Effects of scorpion toxin on excitatory and inhibitory presynaptic terminals.
abstract: 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 Ca(2+) channel blockers, indicating that STX increases Ca(2+) influx through Ca(2+) 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.
authors.affiliation: Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. hakaike@kumamoto-hsu.ac.jp
authors.forename: Hironari
authors.initials: H
authors.lastname: Akaike
authors.forename: Min-Chul
authors.initials: MC
authors.lastname: Shin
authors.forename: Chiharu
authors.initials: C
authors.lastname: Kubo
authors.forename: Norio
authors.initials: N
authors.lastname: Akaike
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects*; D018698:Glutamic Acid / Q000378:metabolism; D005998:Glycine / Q000378:metabolism; D053444:Inhibitory Postsynaptic Potentials / Q000187:drug effects*; D007700:Kinetics; D017729:Presynaptic Terminals / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012604:Scorpion Venoms / Q000633:toxicity*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism; D013127:Spinal Nerves / Q000187:drug effects* / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D012604:Scorpion Venoms; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D018698:Glutamic Acid; D005998:Glycine