Tyrosine ameliorates heat induced delay in event related potential P300 and contingent negative variation Krishna Kishore, Koushik Ray, J.P. Anand, Lalan Thakur, Sanjeev Kumar, Usha Panjwani ⇑ Neurophysiology Division, Defence Institute of Physiology and Allied Sciences, Defence Research and Development Organization, Lucknow Road, Timarpur, Delhi 110054, India article info Article history: Accepted 18 September 2013 Available online 17 October 2013 Keywords: Tyrosine Heat stress P300 CNV Reaction time abstract The efficacy of tyrosine, a catecholamine precursor, as a countermeasure in the reduction of cognitive decline during heat exposure (HE) using event-related potential P300, and contingent negative variation (CNV) was evaluated. Ten healthy males, age 20–30 years participated in the study. Volunteers received placebo or tyrosine (6.5 g) 90 min prior to HE (1.5 h in 45 °C + 30% RH). P300 latency was significantly increased (p < 0.01) during exposure with placebo, which was reduced significantly (p < 0.01) after tyro- sine supplementation. There was an increase in CNV M100 latency (p < 0.05) and reaction time (p < 0.01) and decrease in M100 amplitude (p < 0.01) during HE with placebo, which returns to near normal level with the tyrosine administration. A significantly higher plasma norepinephrine (p < 0.05), dopamine and epinephrine levels were detected in tyrosine supplemented group post heat exposure. HE increases the brain catecholamine activity thereby reduces the plasma norepinephrine and dopamine level leading to a reduction in cognitive performances. Tyrosine supplementation increases the catecholamine level and reduces the impairment of cognitive performance during HE. Ó 2013 Elsevier Inc. All rights reserved. 1. Introduction Environmental conditions above thermally neutral, comfortable zone may produce unwanted effects on humans and degrades mental performance. Brain catecholamine activity increases on exposure to environmental stressors such as cold or heat, altitude and is generally related to decline in cognitive performance (Hoff- man, 2001; Lehnert, Reinstein, Strowbridge, & Wurtman, 1984a; Lieberman, Georgelis, Maher, & Yeghiayan, 2005; Shukitt-Hale, Stillman, & Lieberman, 1996). This reduction in cognitive function may be due to depletion of norepinephrine (Rauch & Lieberman, 1990) and dopamine (Gilbert, 1995; Volkow et al., 1998) which are key neurotransmitters for the maintenance of cognitive and motor skills. Stressful events cause an increase in transmission of noradren- ergic neurons in the frontal cortex, because these neurons are acti- vated by stress (Deijen & Orlebeke, 1994). Exposure to stress activates central and peripheral nervous system and the ability of these neurons to continue to release their neurotransmitter is important in enabling the individual to cope with the stress (Weiss et al., 1980, 1981; Anisman, Pizzino, & Sklar, 1980). Norepineph- rine (NE) depletion is associated with behavioral depression and decreased exploration and motor behavior in animals and lowered attention span in humans. Catecholamines are important for learning and memory processes. Since stress results in increased catecholamine synthesis and depletion, it is likely that the impact of tyrosine supplementation will become more pronounced in this state. Augmenting the availability of the amino acid tyrosine, the pre- cursor for catecholamine synthesis, through dietary supplementa- tion could help maintain brain function by sustaining brain neurotransmitter levels (Wurtman, Hefti, & Melamed, 1981). Liter- ature suggests that its administration specifically accelerates brain catecholamine concentration, turnover and release from physio- logically active catecholamine neurons (Gibson & Wurtman, 1978; Milner & Wurtman, 1986). Being a normal constituent of food, it is rapidly metabolised and therefore, unlikely to have long-term toxicity or side-effects. Earlier studies in humans, suggests that supplementation of 100 mg/kg tyrosine causes a reduction of the number psychomotor impairments and stress symptoms during exposure to cold hypox- ia, compared to a placebo (Banderet & Lieberman, 1989). Adminis- tration of tyrosine, either systemically just prior to initiation of the stress or as a dietary supplement has been shown to protect ani- mals from both neurochemical and behavioral consequences of stress (Brady, Brown, & Thurmond, 1980; Lehnert et al., 1984; Luo, Villmil, Watkins, & Lieberman, 1992). Immobilisation, cold, tail shock has been used as stressors in several studies. Weiss, Bai- ley, & Pohorecky, 1980, have shown a significant linear decline in NE levels as a function of stress duration in several brain areas associated with 60–70% decline in activity. A single intra peritoneal 0278-2626/$ - see front matter Ó 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.bandc.2013.09.005 ⇑ Corresponding author. Fax: +91 11 239 14 790. E-mail address: neurophysiolab_dipas@rediffmail.com (U. Panjwani). Brain and Cognition 83 (2013) 324–329 Contents lists available at ScienceDirect Brain and Cognition journal homepage: www.elsevier.com/locate/b&c