{'fraction_non_alphanumeric': 0.028066528066528068, 'fraction_numerical': 0.031185031185031187, 'mean_word_length': 5.506756756756757, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Modulation of SKF38393 and clonidine on expressed GABA(A) receptors in Xenopus oocytes].

AIM AND METHODS
The present research is performed on Xenopus oocytes injected with rat DRG mRNA. Modulatory effects of SKF38393 and Clonidine on GABAS(A) receptors expressed in Xenopus oocytes was investigated by two-electrodes voltage-clamp technique, and it is compared with the neurons fresh isolated.


RESULTS
It is found that SKF38393 and Clonidine inhibitable GABA(A) receptor function obviously by a concentration-dependent manner. There is an interaction between SKF38393- and Clonidine-induced currents. The inhibition of SKF38393 and Clonidine on GABA(A) receptors is noncompetitive and voltage-independent.


CONCLUSIONS
The results suggest that the inhibition by SKF38393 and clonidine of GABA-activated current might be a result of phosphorylation of GABA(A) receptor following action of second messenger and the thereby mediated intracellular transduction.