TYROSINE REVERSES A COLD-INDUCED WORKING-MEMORY DEFICIT IN HUMANS

Acute exposure to cold stress has been shown to impair short-term, or working, memory, which may be related to reduction in, or disruption of, sustained release of brain catecholamines. Administering a supplemental dose of the catecholamine precursor tyrosine may alleviate cold stress-induced memory impairments by preventing cold-induced deficits in brain catecholamine levels. The present experiment determined whether administration of tyrosine would prevent a cold-induced working memory deficit, using a computer-based delayed matching-to-sample (DMTS) memory task. Eight male volunteers performed the DMTS task for 30 min at an ambient temperature of either 4 degrees C (cold) or 22 degrees C following a 30-min preexposure period and 2 h after ingesting 150 mg/kg of L-tyrosine or placebo. Subjects demonstrated a decline in matching accuracy on the DMTS task as delay interval increased, such that matching accuracy following a 16-s delay between sample and comparison stimuli was lower than that following a delay of 2 or 8 s. Consistent with previous research, and relative to 22 degrees C exposure sessions, matching accuracy during 4 degrees C exposure sessions was reduced significantly following placebo administration, which is attributed to the effect of cold exposure on short-term, or working, memory. Administration of tyrosine significantly improved matching accuracy at the longest delay interval most affected by cold exposure, such that matching accuracy in the cold following tyrosine was at the same level as matching accuracy following placebo or tyrosine administration at 22 degrees C. Tyrosine administered prior to 22 degrees C exposure had no effect on DMTS performance. Plasma norepinephrine levels and diastolic and systolic blood pressure were significantly elevated just prior to performing the DMTS task and following 30 min of acute cold exposure, indicating that the cold exposure produced a typical stress response. Tyrosine was effective in protecting against the effects of cold stress on DMTS performance, possibly by preventing cold stress-induced reduction in brain catecholamine levels.