ABSTRACT
Whole-cell patch clamp technique was performed on acutely isolated rat dorsal root ganglion (DRG) neurons to investigate the modulatory effect of caffeine on γ-aminobutyric acid (GABA)-activated currents (IGABA). The results showed that the majority of the neurons examined (97.4%, 113/116) were sensitive to GABA. 1-1000 μmol/L GABA activated a concentration-dependent inward current which manifested obvious desensitization. After the neurons were treated with caffeine (0.01-100 μmol/L) prior to the application of GABA (100 μmol/L) for 30 s, GABA-activated membrane currents were obviously inhibited. Caffeine shifted the GABA dose-response curve downward and decreased the maximum response to 57% without changing Kd value. These results indicate that the inhibitory effect is non-competitive. Theophylline showed a similar and stronger inhibitory effect on IGABA. The pretreatment with caffeine (10 μmol/L) inhibited IGABA, which was potentized by diazepam (1 μmol/L). Intracellular application of H-8 almost completely abolished the inhibitory effect of caffeine on IGABA. The present results suggest that caffeine may be able to antagonize the effect of presynaptic inhibition of GABA in primary afferent.
ABSTRACT
The frequency domain of single channel currents is analyzed by the power distribution function (PDF) constructed by the discrete wavelet transform (DWT) and power spectral density (PSD). The result shows that the power distribution function based on DWT is an effective frequency-domain analysis method for single channel currents.
Subject(s)
Humans , Fourier Analysis , Ganglia, Spinal , Physiology , Ion Channels , Physiology , Mathematics , Membrane Potentials , Models, Biological , Signal Processing, Computer-AssistedABSTRACT
The history and current situation of cell membrane ion-channel gating mechanism study were reviewed, with an emphasis on the application and the latest developments of kinetic model in gating mechanism study; the problems in present study and ion-channel gating mechanism kinetics model for future investigations were finally discussed.
Subject(s)
Humans , Cell Membrane , Physiology , Ion Channel Gating , Kinetics , Models, Biological , ResearchABSTRACT
The experiment was performed on neurons freshly isolated from rat DRG by using whole cell patch clamp techniques. When 60 cells responded to GABA were treated with SKF38393, a selective agonist of dopamine Dl receptor, it was found that except one cell which exhibited a slight potentiation( l0.0%,l/60), the inhibition by SKF38393 of GABA-activated current was predominant (88.33%,53/60), while the remainders were of no effect( l.66%,6/60). In 50 neurons tested , when the neurons were treated with R(-)-NPA prior to the application of GABA for 30sec, It was found that GABA-activated membrane currents were inhibited (76%,38/50) , enhanced (2%,l/50) , no effected markedly (22%,11/50). The effect of SKF38393 and R(-)-NPA was dependent on the concentration of SKF38393 and R(-)-NPA . By intracellular application of 10-4mol/L H7, a potent inhibitor of protein kinase , via micropipette the inhibition of SKF38393 and R(-)-NPA was abolished apparently as compared with the control .
ABSTRACT
Whole-cell patch-clamp technique was performed on isolated rat DRG neurons to investigate the modulation of DA onGABA-activated membrane currents. It was found that majority of the examined neurons(40/47) were sensitive to GABA, 10-6～ 103mol/L GABA activated a dose-dependent inward current which had an obvious desensitization. In 26 of 40 neurons sensitiveto GABA DA induced a little outward current which had no desentization at all. Others showed no effect obviously. When theneurons were treated with DA 10-7～10-4 mol/L prior to the application of GABA for 30 s, 68% (27/40) GABA-activated mem-brane currents were inhibited, whereas DA10-5 inhibited markedly(33.3%) (x±s).
ABSTRACT
AIM To study the modulation of AlCl 3 on GABA activated currents in isolated rat dorsal root ganglion (DRG) neurons. METHODS Using whole cell patch clamp technique to investigate the effects of AlCl 3 on GABA activated currents in isolated rat DRG neurons. RESULTS The majority of the neurons examined(46/58) were sensitive to GABA in the concentration range from 1 to 1 000 ?mol?L -1 . In the 46 GABA sensitive cells, responses induced by AlCl 3 manifested three types: (1) outward current(3/46); (2) inward current(5/46) and (3) no detectable response(38/46). As compared with GABA activated current, the amplitude of AlCl 3 activated current was smaller. Preapplication with low concentrations of AlCl 3 (≤100 ?mol?L -1 ), the GABA activated current in majority of the cells(32/38) was potentiated, which was dose dependent, the current in a few cells(4/38) was inhibited, while the remaining two(2/38) showed no effect. At higher concentration( 1 000 ?mol?L -1 ), AlCl 3 inhibited the GABA activated current( n =8). It was found that AlCl 3 potentiated both the peak value of and the steady state value of GABA activated currents. CONCLUSION AlCl 3 can modulate the function of GABA A receptors.