title: Effect of sodium dimercaptopropanesulfonate on antagonism of tetramethylenedisulphotetramine to GABA receptor.
abstract: OBJECTIVE
  To study effects of sodium dimercaptopropanesulfonate (DMPS) on the antagonism of tetramethylenedisulphotetramine (TETS) to gamma-aminobutyric acid (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. Autoradiography was used to observe the [3H]GABA bindings in the rat brain slices 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 DMPS control group and TETS control group compared with DMPS protection group and NS control group [micromol/g: (2.09 +/- 0.05) and (2.67 +/- 0.15) vs (2.40 +/- 0.10 (micromol/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) micromol/g in NS control group, DMPS control group, TETS control group, and DMPS protection group, respectively. The OD value of autoradiograms decreased in TETS group compared with buffer control group in cortex, hippocampus, diencephalon, and brainstem [(0.084 +/- 0.008), (0.081 +/- 0.009), (0.094 +/- 0.006) and (0.081 +/- 0.006), vs (0.102 +/- 0.003), (0.109 +/- 0.005), (0.128 +/- 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 areas [(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), (0.128 +/- 0.007), and (0.125 +/- 0.008), respectively].
  
  
  CONCLUSIONS
  The inhibitory effects of DMPS on the antagonism of TETS to GABA receptor are due to the increase in the GABA binding to its receptors in brain caused by DMPS
authors.affiliation: Department of Pharmacology, Wenzhou Medical College, Wenzhou 325027, China.
authors.forename: C Y
authors.initials: CY
authors.lastname: Zhang
authors.forename: T J
authors.initials: TJ
authors.lastname: Zhu
authors.forename: G X
authors.initials: GX
authors.lastname: Hu
authors.forename: X Y
authors.initials: XY
authors.lastname: Chen
authors.forename: D X
authors.initials: DX
authors.lastname: Liu
authors.forename: Z K
authors.initials: ZK
authors.lastname: Chen
mesh_terms: D000818:Animals; D000931:Antidotes / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D001952:Bridged-Ring Compounds / Q000494:pharmacology*; D004347:Drug Interactions; D005260:Female; D018756:GABA Antagonists / Q000494:pharmacology*; D005998:Glycine / Q000378:metabolism; D008297:Male; D051379:Mice; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D018079:Receptors, GABA / Q000378:metabolism*; D012378:Rodenticides; D012640:Seizures / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism; D014494:Unithiol / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D000931:Antidotes; D001952:Bridged-Ring Compounds; D018756:GABA Antagonists; D018079:Receptors, GABA; D012378:Rodenticides; D014494:Unithiol; C010349:tetramethylenedisulfotetramine; D005998:Glycine