Dietary tyrosine suppresses the rise in plasma corticosterone following acute stress in rats

doi:10.1016/0024-3205(85)90566-1

Life Sciences

Volume 37, Issue 23, 9 December 1985, Pages 2157-2163

https://doi.org/10.1016/0024-3205(85)90566-1 Get rights and content

Abstract

Acute, uncontrollable stress increases norepinephrine (NE) turnover in the rat's brain (depleting NE) and diminishes the animal's subsequent tendency to explore a novel environment. Pretreatment with tyrosine can reverse these adverse effects of stress, presumably by preventing the depletion of NE in the hypothalamus^1,2. Numerous studies suggest that NE inhibits the release of adrenocorticotropic hormone (ACTH) by suppressing corticotropic releasing factor (CRF) secretion in the hypothalamus(3–7). In the present study, we found that pre-treatment with supplemental tyrosine not only prevented the behavioral depression and hypothalamic NE depletion observed after an acute stress, but also suppressed the rise in plasma corticosterone. These results support a role for brain NE in stress-induced corticosterone secretion and demonstrate that supplemental tyrosine can protect against several adverse consequences of such stress.

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Rats given tyrosine before acute tail-shock displayed neither shock induced norepinephrine depletion nor the deficits in exploratory behaviors observed in saline-treated animals (Reinstein et al., 1984). Similarly, pre-treatment with tyrosine not only prevented behavioral depression and norepinephrine depletion after acute restraint stress and intermittent tail-shock but also suppressed the rise in plasma corticosterone (Reinstein et al., 1985). Additionally, we found that dominant hamsters had lower serine concentrations in the BLA/CeA compared to control hamsters.
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The rationale for treatment of depression with tyrosine includes increased production of NA and enhanced resilience against the HPA-mediated stress response. In rats exposed to an acute stressor, pre-treatment with tyrosine prevented NA depletion and behavioral deficits (Reinstein et al., 1984), as well as suppressed the rise in plasma corticosterone levels (Reinstein et al., 1985). Studies on human volunteers demonstrated that tyrosine supplementation alleviated decrements in working memory and psychomotor tasks, adverse moods and performance impairment following the environmental stress of cold exposure (Banderet and Lieberman, 1989; Mahoney et al., 2007; O'Brien et al., 2007; Shurtleff et al., 1994).
Phenelzine, a non-selective irreversible inhibitor of monoamine oxidase (MAO), has been used in the treatment of depression and anxiety disorders for several decades. It is a unique inhibitor of MAO as it is also a substrate for MAO, with one of the metabolites being β-phenylethylidenehydrazine (PEH), and it also inhibits several transaminases (e.g. GABA transaminase) in the brain when administered i.p. to rats. Administration of either phenelzine or PEH to rats has been reported to produce dramatic increases in rat brain levels of GABA and alanine while reducing levels of glutamine; these effects are abolished for phenelzine, but not for PEH, when the animals are pre-treated with another MAO inhibitor, suggesting that they are mediated by the MAO-catalyzed formation of PEH from phenelzine. In the present report, we have found that phenelzine and E- and Z-geometric isomers of PEH significantly increased rat whole brain concentrations of l-tyrosine. In a time-response study, acute administration of phenelzine, E-PEH and Z-PEH (30 mg/kg i.p.) elevated rat whole brain l-tyrosine levels at 3 and 6 h following injection, reaching approximately 265–305% of vehicle-treated controls at 3 h. To determine whether the effect on l-tyrosine is MAO-dependent, animals were pre-treated with the non-selective MAO inhibitor tranylcypromine (1 mg/kg i.p.) prior to administration of phenelzine, racemic PEH or vehicle controls. This pre-treatment reversed the effects of phenelzine, but not of PEH, on brain l-tyrosine levels, suggesting that the tyrosine-elevating property of phenelzine is largely the result of its active metabolite PEH. These results are discussed in relation to possible therapeutic applications of these drugs.
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There was no significant main effect of rearing condition or interaction between rearing condition and diet. Some reports indicate that l-tyrosine ameliorates the changes incognition and behavior caused by acute stress by preventing a reduction of NE in response to acute stress [2,19,29]. However, the effectiveness of l-tyrosine on stress was limited.
Chronic stress induces abnormal mental state and behavior, and can be a risk factor for mental disorders. Although it is reported that l-tyrosine, an amino acid that is a precursor of catecholamine synthesis, alleviated the change of cognition and behavior induced by acute stress, knowledge about its effects on chronic stress is limited. In the present study, the effects of dietary l-tyrosine on behavioral alteration induced by chronic stress were investigated by employing a social isolation stress model in mice. Social isolation stress increased locomotor activity in both the home cage and open field. These increases of locomotor activity were suppressed by dietary l-tyrosine. Moreover, l-tyrosine increased both the concentration and turnover rate of norepinephrine metabolites. These findings partly suggest the availability of dietary l-tyrosine for psychic dysfunctions induced by chronic stress.
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To evaluate plasma amino acid (AA) concentrations in patients affected by fibromyalgia (FM) and to study the relationships between their levels and FM clinical parameters.
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Significant lower plasma taurine, alanine, tyrosine (Tyr), valine, methionine, phenylalanine and threonine concentrations, and the sum of essential AAs were observed in FM patients vs healthy controls (P < 0.05). Tyr CAA' ratio and the sum of AAs competing with tryptophan for brain uptake were significantly reduced in FM (P < 0.05). A significant correlation was found between FM clinical parameters and certain AAs.
Our results suggest probable defects of gut malabsorption of certain AAs in FM patients. Moreover, given the reduced Tyr CAA' ratio in FM patients, a possible impairment of the cathecolaminergic system in the FM syndrome may be suggested.
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The effects of acute cold stress were assessed behaviorally and neurochemically. The norepinephrine (NE) precursor, tyrosine (TYR), the catecholamine-releasing compound, amphetamine (AMPH), and the adrenoceptor agonist, phenylpropanolamine (PPA), were administered systemically either alone or in conjunction with TYR 30 min prior to cold exposure. All three sympathomimetic treatments dose-dependently improved performance in a forced swim test following hypothermia (T_c=30°C). AMPH/TYR or PPA/TYR combinations further improved performance vs. either agent given alone. Microdialysis showed elevated hippocampal NE concentrations in response to hypothermia. TYR further elevated NE concentration in cold/restrained rats vs. saline (SAL)-treated controls. These results suggest that sympathomimetic agents, including the nutrient TYR, which enhance noradrenergic function, improve performance in animals acutely stressed by hypothermia.
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A unique amino acid mixture identical in composition to that of larval saliva of the hornet, referred to as a Vespa amino acid mixture (VAAM) was prepared; the effect of VAAM on the blood biochemical indices and plasma amino acid composition of running rats was studied. Thirty min before running exercise, VAAM, a reference amino acid mixture with a composition identical to that of bovine casein (casein amino acid mixture, CAAM), or distilled water was orally administered to the rats. The blood glucose value in the animals given VAAM did not fall after 45 min of running, the value being significantly higher than that in the rats given CAAM or water (P<0.05). There was no significant change in the blood lactate value for those rats given VAAM, whereas the value in the rats given CAAM or water had significantly increased after 45 min of running (P<0.05). The plasma NEFA value for the VAAM group was significantly higher than that for the CAAM group after 45 min of running (P<0.05). Thirty min after the administration of VAAM or CAAM, the increase in the plasma concentration of amino acids reflected the composition of the amino acid mixture. However, after 45 min of running, the concentration of total plasma amino acid in rats given VAAM was maintained at a higher level than that in the rats given CAAM (3.57±0.30 vs 2.96±0.14 μM/l); the plasma concentrations of Gly, Thr, Tyr and Pro in the rats given VAAM were significantly higher than those in the rats given CAAM. These findings suggest that some amino acids in ingested VAAM were used for gluconeogenesis or as energy sources for muscles during exercise. In addition, a promotive effect of VAAM on the utilization of body fat as an energy source could have been involved in the changes of blood biochemical indices.

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Dietary tyrosine suppresses the rise in plasma corticosterone following acute stress in rats

Abstract

Brain Res.

Life Sci.

Brain Res.

Brain Res.

Regul. Pept.

Neuroscience

Brain Res. Rev.

Neurochem. Intern.

Life Sci.

Physiol. Rev.

The Anterior Pituitary Gland

Ann. N.Y. Acad. Sci.

J. Comp. Neurol.

Ann. Rev. Neurosci.

J. Comp. Neurol.

Neuroendocrinology