• Neuroscience · Sep 2017

    Heat Stress induced Neuroinflammation and Aberration in Monoamine levels in Hypothalamus is associated with Temperature Dysregulation.

    • Chauhan Nishant Ranjan NR Defence Institute of Physiology and Allied Sciences (DIPAS), Defence Research and Development Organisation (DRDO), Lucknow Road, Timarpur, Delhi, Medha Kapoor, Laxmi Prabha Singh, Rajinder Kumar Gupta, Ramesh Chand Meena, Rajkumar Tulsawani, Sarita Nanda, and Bala Singh Shashi S Distinguished Scientist and Director General (Life Sciences), Defence Research and Development Organisation (DRDO), DRDO Bhawan, Rajaji Marg, Delhi 11.
    • Defence Institute of Physiology and Allied Sciences (DIPAS), Defence Research and Development Organisation (DRDO), Lucknow Road, Timarpur, Delhi 110054, India.
    • Neuroscience. 2017 Sep 1; 358: 79-92.

    AbstractHeat Stress (HS) induces diverse pathophysiological changes, which include brain ischemia, oxidative stress and neuronal damage. The present study was undertaken with the objective to ascertain whether neuroinflammation in Hypothalamus (HTH) caused under HS affects monoamine levels and hence, its physiological role in thermoregulation. Rats were exposed to HS in a heat simulation environmental chamber (Ambient temperature, Ta=45±0.5°C and Relative Humidity, RH=30±10%) with real-time measurement of core temperature (Tc) and skin temperature (Ts). Animals were divided into two subgroups: Moderate HS (MHS) (Tc=40°C) and Severe HS (SHS)/Heat stroke (Tc=42°C). Rats with MHS showed an increase in Mean Arterial Pressure (MAP) and Heart Rate (HR) while fall in MAP and rise in HR was observed in rats with SHS. In addition, oxidative stress and an increase in pyknotic neurons were observed in HTH. High levels of Adrenocorticotropic-hormone (ACTH), Epinephrine (EPI), Norepinephrine (NE) and Dopamine (DA) in the systemic circulation and progressive increase in EPI and DA levels in HTH were recorded after the thermal insult. Moreover, a substantial increase in Glutamate (Glu) level was observed in HTH as well as in systemic circulation of heat stroke rats. We found a rise in NE whereas a fall in Serotonin (5-HT) level in HTH at MHS, without perturbing inflammatory mediators. However, rats with SHS exhibited significant elevations in NF-kB, IL-1β, COX2, GFAP and Iba1 protein expression in HTH. In conclusion, the data suggest that SHS induces neuroinflammation in HTH, which is associated with monoamines and Glu imbalances, leading to thermoregulatory disruption.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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