Effect of sodium dimercaptopropanesulfonate on antagonism of tetramethylenedisulphotetramine to GABA receptor

AIM: To study effects of sodium dimercaptopropanesulfonate (DMPS) on the an tagonism of tetramethylenedisulphotetramine (TETS) to gamma -aminobutyric a cid (GABA) receptor. METHODS: Acute toxicity experiments were conducted to observe the effects of DMPS and TETS on mice. Contents of free amino acids in mouse brain were determined with automatic analyzer for amino acids. Aut oradiography was used to observe the [H-3]GABA bindings in the rat brain sl ices under different conditions. RESULTS: After icv and ip DMPS, the number of mice experiencing convulsions reduced from 20 in control group to 4 and 2 respectively in TETS poisoned mice. The content of GABA was altered in D MPS control group and TETS control group compared with DMPS protection grou p and NS control group [mu mol/g: (2.09 +/-0.05) and (2.61 +/- 0.15) vs (2. 40 +/- 0.10 (mu mol/g)) and (2.41 +/- 0.21)]; the content of glutamic acid was (12.3 +/- 1.2), (12.0 +/- 0.8), (10.2 +/- 0.6), and (11.8 +/- 1.0) mu m ol/g in NS control group, DMPS control group, TEIS control group, and DMPS protection group, respectively. The OD value of autoradiograms decreased in TETS group compared with buffer control group in cortex, hippocampus, dien cephalon, and brainstem [(0.084 +/- 0.008), (0.081 +/- 0.009), (0.091 +/- 0 .006) and (0.081 +/- 0.006), vs (0.102 +/- 0.003), (0.109 +/- 0.005), (0.12 8 +/- 0.007), and (0.125 +/- 0.008), respectively]. OD value was maintained or higher than the normal level in DMPS + TETS group in the four brain are as [(0.116 +/- 0.008), (0.125 +/- 0.011), (0.129 +/- 0.005), and (0.128 +/- 0.010) vs (0.102 +/- 0.003), (0.109 +/- 0.005), (0. 28 +/- 0.007), and (0. 125 +/- 0.008), respectively]. CONCLUSION: The inhibitory effects of DMPS o n the antagonism of TETS to GABA receptor are due to the increase in the GA BA binding to its receptors in brain caused by DMPS.