Heat stress-induced neuroinflammation and aberration in monoamine levels in hypothalamus are associated with temperature dysregulation

Chauhan, Nishant Ranjan; Kapoor, Medha; Singh, Laxmi Prabha; Gupta, Rajinder K.; Meena, R. C.; Tulsawani, Rajkumar; Nanda, Sarita; Singh, Shashi Bala

doi:10.1016/j.neuroscience.2017.06.023

Cited by 65 publications

(52 citation statements)

References 92 publications

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“…Another possible way is that estradiol and LH might directly affect the DA neurons ( 38 ). Sure there might be interactions between monoamine neurons and hypothalamus ( 46 ). However, our data showed that the LH increase seems to start at the first 7th days, while the DA and 5-HT release decrease tops at the 3rd 7th days, which suggested that LH increase might be the cause for the DA and 5-HT decrease.…”

Section: Discussionmentioning

confidence: 99%

Stress Induced Hormone and Neuromodulator Changes in Menopausal Depressive Rats

Jing

Yang

et al. 2018

Front. Psychiatry

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Objective: Previously, we showed that neuromodulators are important factors involved in depression, here we aim to further investigate the interactions between neuromodulators and sex hormone involved in menopause related depression in rats.Methods: Menopausal depression was made with bilateral ovariectomies in female SD rats followed by chronic mild unpredictable stress treatment for 21 days. Thirty six rats were randomly divided into four groups: sham surgery group, sham/stress group, surgery group, surgery/stress group. Then open-field locomotor scores and sucrose intake were employed to observe behavior changes. The levels of norepinephrine (NE), dopamine (DA), serotonin (5-HT) in the cerebral spinal fluid and serum adrenocorticotropic hormone (ACTH), cortisone were determined with High-performance liquid chromatography (HPLC). Serum estradiol (E2), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were measured with radioimmunoassay.Results: The open-field locomotor scores and sucrose intake were significantly decreased after the surgery and stress treatment (p < 0.01). The Serum E2 level decreased significantly after the surgery (p < 0.01), but serum LH, FSH levels increased significantly in the surgery group than the sham surgery group (p < 0.01). The cortisone levels increased significantly in sham/stress group than that in the sham surgery group during the first 2 weeks at stressful treatment, but decrease afterwards. The monoamine levels in the surgery/stress group were much lower than those in the sham surgery group (p < 0.01). The correlation analysis found that LH and FSH are related more to the neurotransmitter release than E2.Conclusion: Ovary removal rats showed depression-like behaviors, with LH and FSH increase and monoamine decrease, and the levels of these monoamines in the stress treated groups changed only after the stressful treatment. The LH, FSH hormone increasing might be the reason for the lower monoamine release, which in turn might be the reason for depressed syndromes in the menopause. The cortisone and ACTH in the serum in the surgery/stress group were much higher than that in the sham surgery group.

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Section: Discussionmentioning

confidence: 99%

Stress Induced Hormone and Neuromodulator Changes in Menopausal Depressive Rats

Jing

Yang

et al. 2018

Front. Psychiatry

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“…Over 32°C, systemic injection of apomorphine fails to elicit any significant fall in core temperatures . Furthermore, rats exposed to heat stress (ambient temperature = 45 ± 0.5°C) demonstrate a significant increase of dopamine and glutamate in the systemic circulation and hypothalamus, along with signs of hypothalamic inflammation . Moreover, abnormal thermoregulation, which is part of the spectrum of dysautonomia in PD, might trigger DHS, further enhancing the effect of high ambient temperature on dopaminergic receptors.…”

Section: Discussionmentioning

confidence: 99%

Dyskinesia‐Hyperpyrexia Syndrome in Parkinson's Disease: A Heat Shock–Related Emergency?

Sarchioto

Ricchi

Melis

et al. 2018

Movement Disord Clin Pract

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“…TH is the current therapy of choice for HS because no pharmacologic agent is currently available [13][14][15]. Although the true mechanisms underlying the beneficial effect of TH on HS reactions remain unclear, evidence has accumulated to indicate that TH may improve outcomes of HS via reducing cardiac dysfunction [16,17]. Indeed, our previous findings showed that after the onset of HS, animals displayed hypotension and altered cardiac protein profiles, which could be reversed by TH.…”

Section: Ivyspringmentioning

confidence: 98%

Therapeutic Hypothermia Protects Against Heat Stroke-Induced Arterial Hypotension via Promoting Left Ventricular Performance in Rats

Ko¹,

Lin²,

Lee³

et al. 2020

Int. J. Med. Sci.

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We aimed to ascertain whether therapeutic hypothermia (TH) acts as cardioprotective management for heat stroke (HS). Adult male rats under general anesthesia were exposed to whole-body heating (43°C for 70 min) to induce HS. Rats with HS displayed hyperthermia (core body temperature 42°C vs. 36°C); hypotension (30 mmHg vs. 90 mmHg mean arterial blood pressure); suppressed left ventricular (LV) performance (stroke volume 52 µl/min vs. 125 µl/min), ejection fraction (0.29% vs. 0.69%), relaxation factor (72 ms vs. 12 ms), and arterial elastance (0.31 mmHg/ µl vs. 10 mmHg/ µl); increased myocardial injury markers (e.g., creatine kinase-MB: 86 U/L vs. 24 U/L, cardiac troponin I: 3.08 ng/ml vs. 0.57 ng/ml); increased myocardial oxidative stress markers (e.g., malondialdehyde: 6.52 nmol/mg vs. 1.06 nmol/mg, thiobarbituric acid-reactive substances: 29 nmol/g vs. 2 nmol/g); decreased myocardial antioxidants (e.g., superoxide dismutase: 6 unit/mg vs. 17 unit/mg, reduced glutathione: 0.64 nmol/mg vs. 2.53 nmol/mg); increased myocardial proinflammatory cytokines (e.g., tumor necrosis factor-α 3200 pg/ml vs. 1000 pg/ml, interleukin-6: 668 pg/ml vs. 102 pg/ml); and increased cardiac damage scores (2.2 vs. 0.3). TH therapy significantly reversed the following conditions: HS-induced hyperthermia (37.5°C core body temperature), hypotension (71 mmHg), suppressed LV performance (stroke volume: 97 µl/min, ejection fraction: 0.65%, relaxation factor: 39 ms, and arterial elastance: 0.99 mmHg/µl), increased myocardial injury markers (e.g., creatine kinase-MB: 37 U/L, cardiac troponin I: 1.06 ng/ml), increased myocardial oxidative stress markers (e.g., malondialdehyde: 2.68 nmol/mg, thiobarbituric acid-reactive substances: 12.3 nmol/g), decreased myocardial antioxidants (e.g., superoxide dismutase: 13.3 unit/mg, reduced glutathione: 2.71 mmol/mg), increased myocardial proinflammatory cytokines (e.g., tumor necrosis factor-α 1500 pg/ml, interleukin-6: 108 ng/ml); and increased cardiac damage scores (0.9). We thus conclude that TH protects against HS-induced arterial hypotension by promoting LV performance in rats. These results add to the literature regarding the use of TH as cardioprotective management for HS.

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Heat stress-induced neuroinflammation and aberration in monoamine levels in hypothalamus are associated with temperature dysregulation

Cited by 65 publications

References 92 publications

Stress Induced Hormone and Neuromodulator Changes in Menopausal Depressive Rats

Stress Induced Hormone and Neuromodulator Changes in Menopausal Depressive Rats

Dyskinesia‐Hyperpyrexia Syndrome in Parkinson's Disease: A Heat Shock–Related Emergency?

Therapeutic Hypothermia Protects Against Heat Stroke-Induced Arterial Hypotension via Promoting Left Ventricular Performance in Rats

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