Behaviour and cardiac response to stress in signal crayfish exposed to environmental concentrations of tramadol

2019 ◽  
Vol 213 ◽  
pp. 105217 ◽  
Author(s):  
F. Ložek ◽  
I. Kuklina ◽  
K. Grabicová ◽  
J. Kubec ◽  
M. Buřič ◽  
...  
Keyword(s):  
Cardiac Response ◽  
Signal Crayfish ◽  
Environmental Concentrations ◽  
Response To Stress

scholarly journals Cardiac and Locomotor Responses to Acute Stress in Signal Crayfish Pacifastacus leniusculus Exposed to Methamphetamine at an Environmentally Relevant Concentration

2020 ◽  
Vol 17 (6) ◽  
pp. 2084
Author(s):  
Filip Ložek ◽  
Iryna Kuklina ◽  
Kateřina Grabicová ◽  
Jan Kubec ◽  
Miloš Buřič ◽  
...  
Keyword(s):  
Surface Waters ◽  
Acute Stress ◽  
Concentration Level ◽  
Pacifastacus Leniusculus ◽  
Cardiac Response ◽  
Signal Crayfish ◽  
Nontarget Organisms ◽  
Central Nervous System Stimulant ◽  
Response To Stress

Methamphetamine (METH), a central nervous system stimulant used as a recreational drug, is frequently found in surface waters at potentially harmful concentrations. To determine effects of long-term exposure to environmentally relevant levels on nontarget organisms, we analysed cardiac and locomotor responses of signal crayfish Pacifastacus leniusculus to acute stress during a 21-day exposure to METH at 1 μg L−1 followed by 14 days depuration. Heart rate and locomotion were recorded over a period of 30 min before and 30 min after exposure to haemolymph of an injured conspecific four times during METH exposure and four times during the depuration phase. Methamphetamine-exposed crayfish showed a weaker cardiac response to stress than was observed in controls during both exposure and depuration phases. Similarly, methamphetamine-exposed crayfish, during METH exposure, showed lower locomotor reaction poststressor application in contrast to controls. Results indicate biological alterations in crayfish exposed to METH at low concentration level, potentially resulting in a shift in interactions among organisms in natural environment.

Sympathetic contribution to the cardiac response to stress in hypertension.

Hypertension ◽  
1983 ◽  
Vol 5 (1) ◽  
pp. 147-154 ◽  
Author(s):  
C Alicandri ◽  
F M Fouad ◽  
R C Tarazi ◽  
E L Bravo ◽  
R L Greenstreet
Keyword(s):  
Cardiac Response ◽  
Response To Stress

scholarly journals Common genetic factors for depression and cardiovascular disease

2007 ◽  
Vol 9 (1) ◽  
pp. 19-28 ◽  
Keyword(s):  
Cardiovascular Disease ◽  
Candidate Genes ◽  
Psychiatric Symptoms ◽  
Renin Angiotensin System ◽  
Developed Countries ◽  
Cardiac Response ◽  
Response To Stress ◽  
S Allele ◽  
Or Gene ◽  
The Impact

There is increasing knowledge regarding the considerable comorbidity between depression and cardiovascular disease, which are two of the most common disorders in developed countries. The associated vulnerability is not unidirectional, as the presence of cardiovascular disease can also influence mood states. Although this may be the result of psychological factors, common biological mechanisms, including genetic ones, are thought to be responsible for this interaction; we can thus question whether variations in genes could be predisposing factors. Regarding the multiple interactions in the mechanisms between depression and cardiovascular system disorders, e.g., dysfunctions in the hypothalamic-pituitary-adrenocortical and sympathoadrenal axis and the response to stress, the importance of the serotonergic and immune systems, or the impact on the renin-angiotensin system, several candidate genes are being investigated. However, despite the interest in unraveling the potential susceptibility genes for both disorders, most available studies have so far dealt with the impact of polymorphisms in relation to either depression or cardiovascular disease. A few recent studies have now examined the effects of gene-gene or gene-environment interactions, and are investigating the impact of "depression-related" variants on cardiac response to stress. The first promising results were obtained with the serotonin transporter, and it may be hypothesized that this polymorphism interacts via the impact of the S allele on depression and via the effect of the L allele on platelet activation. However, the role played by various other candidate genes remains to be determined, especially regarding the question as to whether they are indicative of common pathophysiological mechanisms, or for identifying a subgroup of patients with somatic disorders that are more closely related to psychiatric symptoms.

Abstract 401: The γ2-AMPK Regulates Glucose and Glycogen Metabolism in the Heart by Modulating Cytosolic Hexokinase II Level

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Maengjo Kim ◽  
Lorena Garcia-Menendez ◽  
Yong Seon Choi ◽  
Birthe Roos ◽  
Mirjam M Wamelink ◽  
...  
Keyword(s):  
Glycogen Content ◽  
Glycogen Metabolism ◽  
Glycogen Storage ◽  
Cardiac Response ◽  
Neonatal Rat ◽  
Hexokinase Ii ◽  
Response To Stress ◽  
Ampk Activity ◽  
Rat Ventricle ◽  
Specific Deletion

Mutations in the γ2-subunit of AMPK (encoded by PRKAG2 gene) cause glycogen storage cardiomyopathy. We generated a mouse model with cardiac specific deletion of γ2-AMPK (cKO) to define its function in the heart. The cKO mice were born normal and remained indistinguishable from control mice under baseline conditions but developed greater cardiac hypertrophy and dysfunction after transverse aortic constriction (TAC). The total AMPK activity was normal in cKO hearts and it increased after TAC to the same extent as that of the controls. However, the γ2-AMPK activity was abolished in the cKO and the overall AMPK activity was maintained by a compensatory increase in the γ1-AMPK activity. The lack of γ2-AMPK selectively reduced hexokinase II in the cytosol resulting in decreases in glycogen content and NADPH levels. Knock-down of γ2-AMPK subunit in neonatal rat ventricle cardiomyocytes resulted in increased oxidative stress and exacerbated response to phenylephrine and H 2 O 2 , both were rescued by HKII overexpression. Taken together, these data identify isoform-specific functions of γ2-AMPK in regulating glucose and glycogen metabolism that are critical for cardiac response to stress. The results also indicate that the specific activation of γ2-AMPK is responsible for the glycogen storage cardiomyopathy associated with PRKAG2 mutations.

scholarly journals New Insights into the Role of Mitochondrial Dynamics and Autophagy during Oxidative Stress and Aging in the Heart

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Yoshiyuki Ikeda ◽  
Sebastiano Sciarretta ◽  
Narayani Nagarajan ◽  
Speranza Rubattu ◽  
Massimo Volpe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aging Process ◽  
Protein Quality ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
The Elderly ◽  
Cardiac Response ◽  
Highly Sensitive ◽  
Close Relationship ◽  
Response To Stress

The heart is highly sensitive to the aging process. In the elderly, the heart tends to become hypertrophic and fibrotic. Stiffness increases with ensuing systolic and diastolic dysfunction. Aging also affects the cardiac response to stress. At the molecular level, the aging process is associated with accumulation of damaged proteins and organelles, partially due to defects in protein quality control systems. The accumulation of dysfunctional and abnormal mitochondria is an important pathophysiological feature of the aging process, which is associated with excessive production of reactive oxygen species. Mitochondrial fusion and fission and mitochondrial autophagy are crucial mechanisms for maintaining mitochondrial function and preserving energy production. In particular, mitochondrial fission allows for selective segregation of damaged mitochondria, which are afterward eliminated by autophagy. Unfortunately, recent evidence indicates that mitochondrial dynamics and autophagy are progressively impaired over time, contributing to the aging process. This suggests that restoration of these mechanisms could delay organ senescence and prevent age-associated cardiac diseases. Here, we discuss the current understanding of the close relationship between mitochondrial dynamics, mitophagy, oxidative stress, and aging, with a particular focus on the heart.

scholarly journals mTORC2 Regulates Cardiac Response to Stress by Inhibiting MST1

Cell Reports ◽  
2015 ◽  
Vol 11 (1) ◽  
pp. 125-136 ◽  
Author(s):  
Sebastiano Sciarretta ◽  
Peiyong Zhai ◽  
Yasuhiro Maejima ◽  
Dominic P. Del Re ◽  
Narayani Nagarajan ◽  
...  
Keyword(s):  
Cardiac Response ◽  
Response To Stress

Aerodynamic and Acoustic Voice Measures Before and After an Acute Public Speaking Stressor

2020 ◽  
Vol 63 (10) ◽  
pp. 3311-3325
Author(s):  
Brittany L. Perrine ◽  
Ronald C. Scherer
Keyword(s):  
Fundamental Frequency ◽  
Salivary Cortisol ◽  
Public Speaking ◽  
Stress System ◽  
Before And After ◽  
Subglottal Pressure ◽  
Response To Stress ◽  
System Activation ◽  
Speaking Fundamental Frequency ◽  
Pituitary Adrenal Axis

Purpose The goal of this study was to determine if differences in stress system activation lead to changes in speaking fundamental frequency, average oral airflow, and estimated subglottal pressure before and after an acute, psychosocial stressor. Method Eighteen vocally healthy adult females experienced the Trier Social Stress Test (TSST) to activate the hypothalamic–pituitary–adrenal axis. The TSST includes public speaking and performing mental arithmetic in front of an audience. At seven time points, three before the stressor and four after the stressor, the participants produced /pa/ repetitions, read the Rainbow Passage, and provided a saliva sample. Measures included (a) salivary cortisol level, (b) oral airflow, (c) estimated subglottal pressure, and (d) speaking fundamental frequency from the second sentence of the Rainbow Passage. Results Ten of the 18 participants experienced a hypothalamic–pituitary–adrenal axis response to stress as indicated by a 2.5-nmol/L increase in salivary cortisol from before the TSST to after the TSST. Those who experienced a response to stress had a significantly higher speaking fundamental frequency before and immediately after the stressor than later after the stressor. No other variable varied significantly due to the stressor. Conclusions This study suggests that the idiosyncratic and inconsistent voice changes reported in the literature may be explained by differences in stress system activation. In addition, laryngeal aerodynamic measures appear resilient to changes due to acute stress. Further work is needed to examine the influence of other stress systems and if these findings hold for dysphonic individuals.

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