{"title":"Behavioral correlates of soman-induced neuropathology: deficits in DRL acquisition.","authors":"J H McDonough, R F Smith, C D Smith","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Rats (N = 45) pretrained to lever press for milk reinforcement on a continuous reinforcement (CRF) schedule were injected with 100-110 micrograms/kg of the anticholinesterase soman (N = 24) or saline (N = 21) SC. Subjects exposed to soman experienced moderate to severe acute symptoms of anticholinesterase intoxication. After a 3 week recovery period, all surviving subjects were retrained on CRF, then given 45 training sessions on a differential reinforcement of low rates (DRL) 20 sec schedule, followed by 10 sessions of extinction. Brains of all subjects were then examined for evidence of neuropathology. Subjects exposed to soman showed no improvement over sessions in the number of reinforcements earned on the DRL schedule due to an inefficient patterning of responses. There were no differences between groups in the number of total DRL responses or terminal extinction responses. Neuropathology was most evident in dorsal thalamic areas, primary olfactory/piriform cortex and amygdala of subjects exposed to soman. There were significant correlations between the severity of acute intoxication scores, degree of neuropathology, and deficits in DRL performance. The results demonstrate that exposure to high doses of this anticholinesterase agent can result in neural damage and persistent decrements in performance of certain operant tasks.</p>","PeriodicalId":19112,"journal":{"name":"Neurobehavioral toxicology and teratology","volume":"8 2","pages":"179-87"},"PeriodicalIF":0.0000,"publicationDate":"1986-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurobehavioral toxicology and teratology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Rats (N = 45) pretrained to lever press for milk reinforcement on a continuous reinforcement (CRF) schedule were injected with 100-110 micrograms/kg of the anticholinesterase soman (N = 24) or saline (N = 21) SC. Subjects exposed to soman experienced moderate to severe acute symptoms of anticholinesterase intoxication. After a 3 week recovery period, all surviving subjects were retrained on CRF, then given 45 training sessions on a differential reinforcement of low rates (DRL) 20 sec schedule, followed by 10 sessions of extinction. Brains of all subjects were then examined for evidence of neuropathology. Subjects exposed to soman showed no improvement over sessions in the number of reinforcements earned on the DRL schedule due to an inefficient patterning of responses. There were no differences between groups in the number of total DRL responses or terminal extinction responses. Neuropathology was most evident in dorsal thalamic areas, primary olfactory/piriform cortex and amygdala of subjects exposed to soman. There were significant correlations between the severity of acute intoxication scores, degree of neuropathology, and deficits in DRL performance. The results demonstrate that exposure to high doses of this anticholinesterase agent can result in neural damage and persistent decrements in performance of certain operant tasks.