Stress-induced catecholaminergic function: Transcriptional and post-transcriptional control

Wong, Dona L.; Tank, A. William

doi:10.1080/10253890701393529

Cited by 68 publications

(69 citation statements)

References 85 publications

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“…Our interests focus on the potential role that the stress hormone Epi, which is itself regulated by stress via genetic control of its biosynthetic enzyme, phenylethanolamine N-methyltransferase (PNMT, EC 2.1.1.28) (Wong and Tank 2007;Wong et al 2008Wong et al , 2010, may play in initiating illness. While Epi historically has been associated with short-term stress responsiveness, it has also been linked to many long-term, stress-induced illnesses.…”

Section: Introductionmentioning

confidence: 99%

Epinephrine: A Short- and Long-Term Regulator of Stress and Development of Illness

et al. 2011

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Epinephrine (Epi), which initiates short-term responses to cope with stress, is, in part, stress-regulated via genetic control of its biosynthetic enzyme, phenylethanolamine N-methyltransferase (PNMT). In rats, immobilization (IMMO) stress activates the PNMT gene in the adrenal medulla via Egr-1 and Sp1 induction. Yet, elevated Epi induced by acute and chronic stress is associated with stress induced, chronic illnesses of cardiovascular, immune, cancerous, and behavioral etiologies. Major sources of Epi include the adrenal medulla and brainstem. Although catecholamines do not cross the blood-brain barrier, circulating Epi from the adrenal medulla may communicate with the central nervous system and stress circuitry by activating vagal nerve β-adrenergic receptors to release norepinephrine, which could then stimulate release of the same from the nucleus tractus solitarius and locus coeruleus. In turn, the basal lateral amygdala (BLA) may activate to stimulate afferents to the hypothalamus, neocortex, hippocampus, caudate nucleus, and other brain regions sequentially. Recently, we have shown that repeated IMMO or force swim stress may evoke stress resiliency, as suggested by changes in expression and extinction of fear memory in the fear-potentiated startle paradigm. However, concomitant adrenergic changes seem stressor dependent. Present studies aim to identify stressful conditions that elicit stress resiliency versus stress sensitivity, with the goal of developing a model to investigate the potential role of Epi in stress-associated illness. If chronic Epi over expression does elicit illness, possibilities for alternative therapeutics exist through regulating stress-induced Epi expression, adrenergic receptor function and/or corticosteroid effects on Epi, adrenergic receptors and the stress axis.

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Section: Introductionmentioning

confidence: 99%

Epinephrine: A Short- and Long-Term Regulator of Stress and Development of Illness

et al. 2011

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“…Long-term mechanisms involve induction of TH enzyme protein; these mechanisms are activated during chronic stimulation, such as long-term stress or repeated drug treatment. In adrenal medulla and locus coeruleus, long-term regulation is mediated by mechanisms that modulate TH gene transcription rate and TH mRNA stability (Sabban and Kvetnansky, 2001;Wong and Tank, 2007).…”

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confidence: 99%

Activation of Tyrosine Hydroxylase mRNA Translation by cAMP in Midbrain Dopaminergic Neurons

Chen¹,

Lu²,

Radcliffe³

et al. 2008

Mol Pharmacol

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During prolonged stress or chronic treatment with neurotoxins, robust compensatory mechanisms occur that maintain sufficient levels of catecholamine neurotransmitters in terminal regions. One of these mechanisms is the up-regulation of tyrosine hydroxylase (TH), the enzyme that controls catecholamine biosynthesis. In neurons of the periphery and locus coeruleus, this up-regulation is associated with an initial induction of TH mRNA. In contrast, this induction either does not occur or it is nominal in mesencephalic dopamine neurons. The reasons for this lack of compensatory TH mRNA induction remain obscure, because so little is known about the regulation of TH expression in these neurons. In this study, we test whether activation of the cAMP signaling pathway regulates TH gene expression in two rodent models of midbrain dopamine neurons, ventral midbrain organotypic slice cultures and MN9D cells. Our results demonstrate that elevation of cAMP leads to induction of TH protein and TH activity in both model systems; however, TH mRNA levels are not up-regulated by cAMP. The induction of TH protein is the result of a novel post-transcriptional mechanism that activates TH mRNA translation. This translational activation is mediated by sequences within the 3Ј untranslated region (UTR) of TH mRNA. Our results support a model in which cAMP induces or activates trans-factors that interact with the TH mRNA 3ЈUTR to increase TH protein synthesis. An understanding of this novel regulatory mechanism may help to explain the control of TH gene expression and consequently dopamine biosynthesis in midbrain neurons under different physiological and pathological conditions.

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“…2 Since the introduction of the concept of 'stress' to biomedical research by Hans Selye, stress research has evolved considerably over the last few decades, and cellular and molecular concepts are being forwarded to explain stress responses. 21 Complex neurochemical pathways have been demonstrated to regulate such stress related responses and interactions between varieties of host factors are instrumental in deciding the nature and extent of the impact of such aversive inputs on the biological system. "stress system" is itself a complex system involving the wide array of interactions that occur between CNS, neuroendocrine, immune and visceral systems.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological and biochemical modulation of stress markers by L-NAME and L-Ascorbic acid in chronic restraint model in Wistar rats

Pal

Rohil

Akhtar³

et al. 2017

Asian J Med Sci

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Background: Stress is the psycho-physiologic reaction of the body to diverse stimuli including emotional or physical stimuli that imbalance the homeostasis and is also known to trigger various stress markers. Despite the stressors of different types, chronic stress in particular, is known to influence the physiological milieu and breakdown of adaptive mechanisms consequently aggravating the morbid states. Aims and Objectives: The present study was designed to evaluate the modulatory role of stress marker by N-nitro-L-arginine-methyl ester (L-NAME) and L-Ascorbic acid (L-AA) in experimental model of chronic restraint stress (RSx21) in Wistar rats.Materials and Methods: MDA and GSH levels were determined by the method of Okhawa et al 1979 and Ellman 1959 respectively, the SOD and catalase levels were estimated by the method of Nandi and Chatterjee 1988 and Aebi 1984 respectively.Results: Results from our study reveal the significant enhancement of malondialdehyde (MDA) level while significant attenuation of superoxide dismutase (SOD), reduced glutathione (GSH) and catalase levels in chronic stress group compared with vehicle (non-stress) group. The MDA level was found to be increased by L-NAME (10 and 50 mg/kg) in chronic restraint (RSx21) induced rats as compared to vehicle treated RS group. Antioxidant L-AA (100 and 200 mg/kg) significantly reduced MDA level in chronic stress situation. However, L-NAME and L-Ascorbic Acid were found to cause an increase in level of plasma SOD, GSH and catalase when compared with vehicle treated RS group. On the other hand, L-AA (100 and 200 mg/kg) reversed these RS induced changes in these oxidative parameters.Conclusions: Hence, results from the study underlined the intricate role of antioxidants as evidenced by reversal of oxidative stress markers that command a vital role in the development of morbid condition.Asian Journal of Medical Sciences Vol.8(1) 2017 15-20

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Stress-induced catecholaminergic function: Transcriptional and post-transcriptional control

Cited by 68 publications

References 85 publications

Epinephrine: A Short- and Long-Term Regulator of Stress and Development of Illness

Epinephrine: A Short- and Long-Term Regulator of Stress and Development of Illness

Activation of Tyrosine Hydroxylase mRNA Translation by cAMP in Midbrain Dopaminergic Neurons

Pharmacological and biochemical modulation of stress markers by L-NAME and L-Ascorbic acid in chronic restraint model in Wistar rats

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