title: Early environmental experience alters baseline and ethanol-induced cognitive impulsivity: relationship to forebrain 5-HT1A receptor binding.
abstract: The relationship between impulsivity and drug abuse is poorly understood despite evidence that impulsive behaviour both predicts, and is a consequence of, drug use. Moreover, although there are clear individual differences in the propensity to addiction, this relationship has not been investigated with respect to impulsive behaviour. We tested whether early environmental experience would influence behavioural measures of impulsivity, and further, whether this experience would alter impulsive choice following ethanol intoxication. Thirty-six male, Long-Evans rats were reared in either isolated (1 rat/cage), standard (2 rats/cage), or enriched (group housed with toys) conditions. After a 3-month rearing period, animals were tested in two operant tasks measuring either motor (go/no-go) or cognitive (delay-to-reinforcement) impulsivity. Rats were then re-tested following 0, 0.3, 0.6, 0.9, and 1.2 g/kg ethanol. Forebrain 5-HT1A binding was assessed post-mortem using in vitro receptor autoradiography with the agonist [3H]8-OH-DPAT (3H-8-hydroxy-2-[di-n-propylamino]tetralin). Rearing condition did not influence baseline motor impulsivity, but isolation rearing led to decreased baseline cognitive impulsivity. Ethanol did not affect motor impulsivity, but dose-dependently increased impulsive choice in the delay-to-reinforcement task. Enriched rats were more impulsive overall, and isolation-reared rats only showed a shift in impulsive behaviour after 1.2 g/kg. Isolation rearing decreased, and enrichment rearing increased 5-HT1A binding in the frontal pole of the cortex following experience in the delay-to-reinforcement task. Isolation-reared rats also showed a significant decrease in 5-HT1A binding in the dentate gyrus of the ventral hippocampus following experience in the delay-to-reinforcement relative to the go/no-go task. These data indicate that differential rearing has a significant influence on cognitive impulsivity, and that altered serotonergic function may underlie these differences.
authors.affiliation: Department of Psychology, Queen's University, Kingston, Ont., Canada K7L 3N6.
authors.forename: Kim G C
authors.initials: KG
authors.lastname: Hellemans
authors.forename: José N
authors.initials: JN
authors.lastname: Nobrega
authors.forename: Mary C
authors.initials: MC
authors.lastname: Olmstead
mesh_terms: D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001070:Appetitive Behavior / Q000187:drug effects; D003071:Cognition / Q000187:drug effects*; D004193:Discrimination Learning / Q000187:drug effects; D000431:Ethanol / Q000494:pharmacology*; D007175:Impulsive Behavior / Q000139:chemically induced / Q000503:physiopathology* / Q000523:psychology; D007206:Individuality; D008297:Male; D009474:Neurons / Q000187:drug effects; D016548:Prosencephalon / Q000166:cytology / Q000187:drug effects*; D011897:Random Allocation; D051381:Rats; D020318:Rats, Long-Evans; D044282:Receptor, Serotonin, 5-HT1A / Q000187:drug effects*; D012054:Reinforcement, Psychology; D012931:Social Environment
chemical_list: D044282:Receptor, Serotonin, 5-HT1A; D000431:Ethanol