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The binding and unbinding constants describing interaction of ω-CTx-GVIA with N-type Ca2+ channels were calculated based on the time course of the blocking action of the toxin. The experiments were carried out on
pyramidal neurons freshly dissociated from theCA3 region of the rat hippocampus using a “concentration-clamp” technique and a patch-clamp technique in the whole-cell configuration.
The bindingk
1 and unbindingk
−1 constants were evaluated as 0.32 (μM·sec)−1 and 0.004 sec−1, respectively. The dissociation constantK
D kinetically derived from the ratiok
−1/k
1 was 0.012 μM. These values allow us to interpret the apparent “irreversibility” of the toxin action. 相似文献
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The effects of NMDA receptor agonists on voltage-dependent Ca2+ channels were studied in pyramidal neurons freshly dissociated from theCA3 region of the rat hippocampus. In a fraction of investigated cells (18 of 26), application of NMDA receptor agonists resulted
in a rapid increase in the amplitude of whole-cell Ca2+ channel currents (Ca2+CC). This effect immediately disappeared on return to the control solution. The current-voltage relationship for the whole-cell
Ca2+ channel currents was not shifted under this action of NMDA receptor agonists. It was shown that neither T-, nor L-type Ca2+CC were facilitated by NMDA receptor agonists. The experiments with specific blockers of various types (ω-CgTxGVIA, ω-Aga-IVA,
and ω-CgTxMVIIC) showed that N-, P-, and Q-types of Ca2+ channels were not potentiated by NMDA receptor agonists. The involvement of other types of Ca2+ CC (R type, in particular) in the modulatory action of NMDA receptor agonists is considered. 相似文献
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Fisyunov A. I. Lozovaya N. A. Tsyntsadze T. Sh. Yatsenko N. M. Chatterjee S. Krishtal O. A. 《Neurophysiology》2001,33(1):5-10
A modulating action of hyperforin (an active compound of the extract from Hypericum perforatum) on a high-threshold component of the calcium current, sensitive to application of 100 nM -Aga-IVA toxin and identified as P current, was studied on freshly isolated Purkinje neurons with the use of a patch-clamp technique in the whole-cell configuration. It was shown that extracellular application of 0.8 M hyperforin caused a shift of the current-voltage (I-V) relationship of P current by -(8 ± 2) mV, slowdown of the activation kinetics, and a decrease in the amplitude of this current. The shift of the I-V relationship and slowdown of activation kinetics developed for less than 10 sec, while the P-current amplitude decreased for a much longer time (several minutes) and depended on the intracellular concentration of Ca2+ ions. -Aga-IVA toxin at the concentration of 100 nM completely blocked the recorded inward current in the presence of 0.8 M hyperforin. In experiments with intracellular perfusion of Purkinje neurons, we found that interaction of hyperforin with its binding site occurs at the external side of the cell membrane. The study of the mechanisms involved in the hyperforin-induced P-current modulation revealed that 1 mM GTPS (activating GTs proteins, as well as activating or blocking GMs proteins) or 1-2 mM GDPS (blocking GTs and GMs proteins) in the intracellular solution did not affect the hyperforin-induced modulation of P current. Hyperforin-induced Ca2+-independent shift of the I-V relationship and slowdown of the activation kinetics of P current were abolished in the presence of 0.5 M calmidazolium in the extracellular medium. 相似文献
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