Selective attention and place navigation in rats treated prenatally with methylazoxymethanol.
Prenatal treatment of rats on gestation day 15 with methylazoxymethanol (MAM) caused forebrain microencephaly. The behavioral analyses included measures of spontaneous motor activity and tests for cognitive deficits, and were performed when the rats had reached adult age. Female MAM-treated rats failed to demonstrate contextual control of latent inhibition, which confirms earlier findings with male rats. Male MAM-treated rats demonstrated a notable impairment of place navigation in a swim-maze, but showed as strong sensory preconditioning as the control animals. Biochemical analyses indicated considerable increases in catecholamine levels in the cerebral cortex, hippocampus and striatum. The cognitive deficits, characterised by the various conditioning (taste-aversion) and instrumental learning (swim-maze) tasks, suggested that the MAM rats are deficient in their capacity to attend selectively to the relevant stimulus in complex arrangements of the stimulus situation.
D000014:Abnormalities, Drug-Induced / Q000523:psychology*; D000818:Animals; D001288:Attention; D001391:Azo Compounds / Q000633:toxicity*; D001921:Brain / Q000002:abnormalities*; D003072:Cognition Disorders / Q000139:chemically induced*; D005260:Female; D007266:Inhibition, Psychological; D007859:Learning Disabilities / Q000139:chemically induced; D008746:Methylazoxymethanol Acetate / Q000031:analogs & derivatives / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D011930:Reaction Time; D013028:Space Perception
D001391:Azo Compounds; D008746:Methylazoxymethanol Acetate; C030667:methylazoxymethanol