title: [Effects of acetamide at different doses on expression of amino acids in cerebral cortex of rats with acute tetramine poisoning].
abstract: OBJECTIVE
  To investigate the effects of acetamide at different doses on the expression of inhibitory amino acids (gamma-aminobutyric acid, GABA) and excitatory amino acid (glutamate, Glu) in the cerebral cortex of rats with acute tetramine (TET) poisoning.
  
  
  METHODS
  Eighty Sprague-Dawley rats (SPF) were randomly divided into five groups, with 16 rats in each group: saline control group, dimethyl sulfoxide (DMSO) control group, TET exposure group, high-dose (2.8 g/kg/d) acetamide treatment group, and super-high-dose (5.6 g/kg/d) acetamide treatment group. Rats in the exposure group and treatment groups were exposed to TET by intragastric administration after fasting, and were then intramuscularly injected with saline or different doses of acetamide in the following 5 days. The cortex of the temporal lobe was collected at 3 h, 12 h, 48 h, or 7 d after treatment. The expression levels of GABA and Glu in the cortex of the temporal lobe were determined by average optical density (OD) values in immunohistochemistry.
  
  
  RESULTS
  1) Expression of GABA: The OD value of GABA in TET exposure group started to increase at 12 h after treatment, reached the peak at 48 h, and decreased to the normal level at 7 d. In the high-dose acetamide treatment group, the increase in OD at 12 h was not so significant as that in the TET exposure group, OD value decreased to the normal level at 48 h and was lower than that in the exposure group, and the changes were more like those in the control groups. In the super-high-dose acetamide treatment group, OD value began to increase significantly at 3 h and was significantly higher than that in the TET exposure group (P < 0.01), it reached the peak at 12 h, and was restored to the normal value at 48 h. 2) Expression of Glu: The OD value of Glu in TET exposure group at 3 h after treatment was significantly lower than those in the two control groups, it increased gradually from 12 h to 48 h, and recovered to the normal level at the 7th d. The changes in the high-dose acetamide treatment group were similar to those in the TET exposure group, but became more like those in the control groups after 48 h; the OD value in super-high-dose acetamide treatment group was significantly higher than that in the TET exposure group at 3 h after treatment (P < 0.01), while no significant difference was found at 12 h; it was significantly lower than those of all other groups at 48 h and 7 d (P < 0.01).
  
  
  CONCLUSIONS
  Treatment with high dose of acetamide has some curative effect on TET poisoning-induced central nervous lesion, while the effect of super-high-dose acetamide on expression of neurotransmitters is too complex to evaluate.
authors.affiliation: Department of Emergency Medicine, the second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Xia
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Emergency Medicine, the second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Yingping
authors.initials: Y
authors.lastname: Tian
authors.affiliation: Department of Emergency Medicine, the second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Dongqi
authors.initials: D
authors.lastname: Yao
authors.affiliation: Department of Emergency Medicine, the second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Hengbo
authors.initials: H
authors.lastname: Gao
authors.affiliation: Department of Emergency Medicine, the second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Jianling
authors.initials: J
authors.lastname: Su
authors.affiliation: Department of Emergency Medicine, the second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
authors.forename: Hanwen
authors.initials: H
authors.lastname: Shi
mesh_terms: D000081:Acetamides / Q000494:pharmacology*; D000818:Animals; D001952:Bridged-Ring Compounds / Q000506:poisoning*; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D000081:Acetamides; D001952:Bridged-Ring Compounds; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; C030686:acetamide; C010349:tetramethylenedisulfotetramine