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The effect of D‐amphetamine, clonidine, and yohimbine on human information processing
Author(s) -
HALLIDAY ROY,
NAYLOR HILARY,
BRANDEIS DANIEL,
CALLAWAY ENOCH,
YANO LOVELLE,
HERZIG KAREN
Publication year - 1994
Publication title -
psychophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.661
H-Index - 156
eISSN - 1469-8986
pISSN - 0048-5772
DOI - 10.1111/j.1469-8986.1994.tb02441.x
Subject(s) - yohimbine , clonidine , amphetamine , psychology , stimulus (psychology) , anxiogenic , placebo , neuroscience , anesthesia , medicine , dopamine , anxiolytic , psychiatry , anxiety , antagonist , cognitive psychology , receptor , alternative medicine , pathology
Twelve subjects were tested with D‐amphetamine, yohimbine, clonidine, and a placebo on a task with two levels of stimulus and two levels of response complexity. The purpose of this study was to test the hypothesis that noradrenergic durgs affect early stimulus processes. D‐amphetamine speeded reaction time (RT), clonidine slowed it, and yohimbine had no effect. D‐amphetamine and yohimbine decreased N1 latency and clonidine increased it. D‐amphetamine and yohimbine decreased P3 latency and clonidine increased it but, in each case, only when latency estimates were based on single trials, not on averages. D‐amphetamine's effect on RT, not P3, as measured by the average, is consistent with previous results. Single trial measures appear more sensitive. Speeding of N1 and single‐trial P3 data indicate that noradrenergic durgs affect processing of early (visual) information. D‐amphetamine's speeding of single‐trial P3 estimates was attributed to its noradrenergic actions. Yohimbine's speeding of P3 without changing RT is consistent with neural net (parallel) simulations but not with a serial model. These findings support the assumption that different neurotransmitters modulate specific cognitive processes.