scholarly journals Dietary l-tryptophan leaves a lasting impression on the brain and the stress response

2017 ◽  
Vol 117 (10) ◽  
pp. 1351-1357 ◽  
Author(s):  
Erik Höglund ◽  
Øyvind Øverli ◽  
Madelene Å. Andersson ◽  
Patricia Silva ◽  
Danielle Caroline Laursen ◽  
...  

AbstractComparative models suggest that effects of dietary tryptophan (Trp) on brain serotonin (5-hydroxytryptamine; 5-HT) neurochemistry and stress responsiveness are present throughout the vertebrate lineage. Moreover, hypothalamic 5-HT seems to play a central role in control of the neuroendocrine stress axis in all vertebrates. Still, recent fish studies suggest long-term effects of dietary Trp on stress responsiveness, which are independent of hypothalamic 5-HT. Here, we investigated if dietary Trp treatment may result in long-lasting effects on stress responsiveness, including changes in plasma cortisol levels and 5-HT neurochemistry in the telencephalon and hypothalamus of Atlantic salmon. Fish were fed diets containing one, two or three times the Trp content in normal feed for 1 week. Subsequently, fish were reintroduced to control feed and were exposed to acute crowding stress for 1 h, 8 and 21 d post Trp treatment. Generally, acute crowding resulted in lower plasma cortisol levels in fish treated with 3×Trp compared with 1×Trp- and 2×Trp-treated fish. The same general pattern was reflected in telencephalic 5-HTergic turnover, for which 3×Trp-treated fish showed decreased values compared with 2×Trp-treated fish. These long-term effects on post-stress plasma cortisol levels and concomitant 5-HT turnover in the telencephalon lends further support to the fact that the extrahypothalamic control of the neuroendocrine stress response is conserved within the vertebrate lineage. Moreover, they indicate that trophic/structural effects in the brain underlie the effects of dietary Trp treatment on stress reactivity.

2013 ◽  
Vol 47 (4) ◽  
pp. 376-381 ◽  
Author(s):  
Mihaela Jurdana ◽  
Maja Cemazar ◽  
Katarina Pegan ◽  
Tomaz Mars

Abstract Background. Long term effects of different doses of ionizing radiation on human skeletal muscle myoblast proliferation, cytokine signalling and stress response capacity were studied in primary cell cultures. Materials and methods. Human skeletal muscle myoblasts obtained from muscle biopsies were cultured and irradiated with a Darpac 2000 X-ray unit at doses of 4, 6 and 8 Gy. Acute effects of radiation were studied by interleukin - 6 (IL-6) release and stress response detected by the heat shock protein (HSP) level, while long term effects were followed by proliferation capacity and cell death. Results. Compared with non-irradiated control and cells treated with inhibitor of cell proliferation Ara C, myoblast proliferation decreased 72 h post-irradiation, this effect was more pronounced with increasing doses. Post-irradiation myoblast survival determined by measurement of released LDH enzyme activity revealed increased activity after exposure to irradiation. The acute response of myoblasts to lower doses of irradiation (4 and 6 Gy) was decreased secretion of constitutive IL-6. Higher doses of irradiation triggered a stress response in myoblasts, determined by increased levels of stress markers (HSPs 27 and 70). Conclusions. Our results show that myoblasts are sensitive to irradiation in terms of their proliferation capacity and capacity to secret IL-6. Since myoblast proliferation and differentiation are a key stage in muscle regeneration, this effect of irradiation needs to be taken in account, particularly in certain clinical conditions.


1992 ◽  
Vol 70 (1) ◽  
pp. 136-139 ◽  
Author(s):  
Henry J. Harlow ◽  
Frederick G. Lindzey ◽  
Walter D. Van Sickle ◽  
William A. Gern

Five cougars (Felis concolor) were captured and an adrenal response test was administered by injecting synthetic adrenocorticotropic hormone and monitoring plasma cortisol levels at 15-min intervals for 120 min. Three were selected for treatment and chased 5 or 6 more times to simulate the stress they might experience during a pursuit-only season; the other two served as controls and were chased only once more, at recapture. The adrenal response test was administered again at recapture. The cougars in the treatment group had a lowered plasma cortisol profile after the simulated pursuit season, indicating an altered physiological response of the adrenals to the stress of repeated chases.


Meditation refers to a state of mind of relaxation and concentration, where generally the mind and body is at rest. The process of meditation reflects the state of the brain which is distinct from sleep or typical wakeful states of consciousness. Meditative practices usually involve regulation of emotions and monitoring of attention. Over the past decade there has been a tremendous increase in an interest to study the neural mechanisms involved in meditative practices. It could also be beneficial to explore if the effect of meditation is altered by the number of years of meditation practice. Functional Magnetic Resonance Imaging (fMRI) is a very useful imaging technique which can be used to perform this analysis due to its inherent benefits, mainly it being a non-invasive technique. Functional activation and connectivity analysis can be performed on the fMRI data to find the active regions and the connectivity in the brain regions. Functional connectivity is defined as a simple temporal correlation between anatomically separate, active neural regions. Functional connectivity gives the statistical dependencies between regional time series. It is a statistical concept and is quantified using metrics like Correlation. In this study, a comparison is made between functional connectivity in the brain regions of long term meditation practitioners (LTP) and short-term meditation practitioners (STP) to see the differences and similarities in the connectivity patterns. From the analysis, it is evident that in fact there is a difference in connectivity between long term and short term practitioners and hence continuous practice of meditation can have long term effects.


2013 ◽  
Vol 43 (1) ◽  
pp. 79
Author(s):  
R. Ghalamghash ◽  
H.Z. Mammedov ◽  
H. Ashayeri ◽  
A. Hosseini

Author(s):  
Angela Duckworth ◽  

For more than a century, scientists have known that acute stress activates the fight-or-flight response. When your life is on the line, your body reacts instantly: your heart races, your breath quickens, and a cascade of hormones sets off physiological changes that collectively improve your odds of survival. More recently, scientists have come to understand that the fight-or-flight response takes a toll on the brain and the body—particularly when stress is chronic rather than acute. Systems designed to handle transient threats also react to stress that occurs again and again, for weeks, months, or years. It turns out that poverty, abuse, and other forms of adversity repeatedly activate the fight-or-flight response, leading to long-term effects on the immune system and brain, which in turn increase the risk for an array of illnesses, including asthma, diabetes, arthritis, depression, and cardiovascular disease. Pioneering neuroscientist Bruce McEwen called this burden of chronic stress “allostatic load.”


Toxins ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 314 ◽  
Author(s):  
Nicole Blanshan ◽  
Hollis Krug

Chronic osteoarthritis pain is an increasing worldwide problem. Treatment for osteoarthritis pain is generally inadequate or fraught with potential toxicities. Botulinum toxins (BoNTs) are potent inhibitors of neuropeptide release. Paralytic toxicity is due to inhibition at the neuromuscular junction, and this effect has been utilized for treatments of painful dystonias. Pain relief following BoNT muscle injection has been noted to be more significant than muscle weakness and hypothesized to occur because of the inhibition of peripheral neuropeptide release and reduction of peripheral sensitization. Because of this observation, BoNT has been studied as an intra-articular (IA) analgesic for chronic joint pain. In clinical trials, BoNT appears to be effective for nociceptive joint pain. No toxicity has been reported. In preclinical models of joint pain, BoNT is similarly effective. Examination of the dorsal root ganglion (DRG) and the central nervous system has shown that catalytically active BoNT is retrogradely transported by neurons and then transcytosed to afferent synapses in the brain. This suggests that pain relief may also be due to the central effects of the drug. In summary, BoNT appears to be safe and effective for the treatment of chronic joint pain. The long-term effects of IA BoNT are still being determined.


2019 ◽  
Vol 46 (3) ◽  
pp. 484-495 ◽  
Author(s):  
Federico E Turkheimer ◽  
Pierluigi Selvaggi ◽  
Mitul A Mehta ◽  
Mattia Veronese ◽  
Fernando Zelaya ◽  
...  

Abstract The use of antipsychotic medication to manage psychosis, principally in those with a diagnosis of schizophrenia or bipolar disorder, is well established. Antipsychotics are effective in normalizing positive symptoms of psychosis in the short term (delusions, hallucinations and disordered thought). Their long-term use is, however, associated with side effects, including several types of movement (extrapyramidal syndrome, dyskinesia, akathisia), metabolic and cardiac disorders. Furthermore, higher lifetime antipsychotic dose-years may be associated with poorer cognitive performance and blunted affect, although the mechanisms driving the latter associations are not well understood. In this article, we propose a novel model of the long-term effects of antipsychotic administration focusing on the changes in brain metabolic homeostasis induced by the medication. We propose here that the brain metabolic normalization, that occurs in parallel to the normalization of psychotic symptoms following antipsychotic treatment, may not ultimately be sustainable by the cerebral tissue of some patients; these patients may be characterized by already reduced oxidative metabolic capacity and this may push the brain into an unsustainable metabolic envelope resulting in tissue remodeling. To support this perspective, we will review the existing data on the brain metabolic trajectories of patients with a diagnosis of schizophrenia as indexed using available neuroimaging tools before and after use of medication. We will also consider data from pre-clinical studies to provide mechanistic support for our model.


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