scholarly journals Nitric oxide synthase neurons in the preoptic hypothalamus are sleep-active and contribute to regulating NREM and REM sleep and lowering body temperature.

2021 ◽  
Author(s):  
Edward C Harding ◽  
Wei Ba ◽  
Reesha Zahir ◽  
Xiao Yu ◽  
Raquel Yustos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Rem Sleep ◽  
Active Phase ◽  
Nrem Sleep ◽  
Dark Phase ◽  
Dark Light ◽  
Active Population ◽  
Oxide Synthase

When mice are exposed to external warmth, nitric oxide synthase (NOS1) neurons in the median and medial preoptic (MnPO/MPO) hypothalamus induce sleep and concomitant body cooling. However, how these neurons regulate baseline sleep and body temperature is unknown. Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM active. This is the first instance of a predominantly NREM-active population in the PO area, or to our knowledge, elsewhere in the brain. In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides. We expressed tetanus-toxin light-chain in MnPO/MPO NOS1 cells to reduce vesicular release of transmitters. This induced changes in sleep structure: over 24 hours, mice had less NREM sleep in their dark (active) phase, and more NREM sleep in their light (sleep) phase. REM sleep episodes in the dark phase were longer, and there were fewer REM transitions between other vigilance states. REM sleep had less theta power. Mice with synaptically-blocked MnPO/MPO NOS1 neurons were also warmer. In particular, mice were warmer than control mice at the dark-light transition (ZT0), as well as during the dark phase siesta (ZT16-20), where there is usually a body temperature dip. Also, at this siesta point of cooled body temperature, mice usually have more NREM, but mice with synaptically-blocked MnPO/MPO NOS1 cells showed reduced NREM sleep at this time. Overall, MnPO/MPO NOS1 neurons promote both NREM and REM sleep and contribute to chronically lowering body temperature, particularly at transitions where the mice normally enter NREM sleep.

scholarly journals Nitric Oxide Synthase Neurons in the Preoptic Hypothalamus Are NREM and REM Sleep-Active and Lower Body Temperature

2021 ◽  
Vol 15 ◽  
Author(s):  
Edward C. Harding ◽  
Wei Ba ◽  
Reesha Zahir ◽  
Xiao Yu ◽  
Raquel Yustos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Rem Sleep ◽  
Active Phase ◽  
Nrem Sleep ◽  
Dark Phase ◽  
Dark Light ◽  
Body Cooling ◽  
Oxide Synthase

When mice are exposed to external warmth, nitric oxide synthase (NOS1) neurons in the median and medial preoptic (MnPO/MPO) hypothalamus induce sleep and concomitant body cooling. However, how these neurons regulate baseline sleep and body temperature is unknown. Using calcium photometry, we show that NOS1 neurons in MnPO/MPO are predominantly NREM and REM active, especially at the boundary of wake to NREM transitions, and in the later parts of REM bouts, with lower activity during wakefulness. In addition to releasing nitric oxide, NOS1 neurons in MnPO/MPO can release GABA, glutamate and peptides. We expressed tetanus-toxin light-chain in MnPO/MPO NOS1 cells to reduce vesicular release of transmitters. This induced changes in sleep structure: over 24 h, mice had less NREM sleep in their dark (active) phase, and more NREM sleep in their light (sleep) phase. REM sleep episodes in the dark phase were longer, and there were fewer REM transitions between other vigilance states. REM sleep had less theta power. Mice with synaptically blocked MnPO/MPO NOS1 neurons were also warmer than control mice at the dark-light transition (ZT0), as well as during the dark phase siesta (ZT16-20), where there is usually a body temperature dip. Also, at this siesta point of cooled body temperature, mice usually have more NREM, but mice with synaptically blocked MnPO/MPO NOS1 cells showed reduced NREM sleep at this time. Overall, MnPO/MPO NOS1 neurons promote both NREM and REM sleep and contribute to chronically lowering body temperature, particularly at transitions where the mice normally enter NREM sleep.

REM sleep control during aging in SAM mice: a role for inducible nitric oxide synthase

2005 ◽  
Vol 26 (10) ◽  
pp. 1375-1384 ◽  
Author(s):  
Damien Colas ◽  
Laurent Bezin ◽  
Abdallah Gharib ◽  
Anne Morales ◽  
Raymond Cespuglio ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Rem Sleep ◽  
Oxide Synthase ◽  
Sam Mice ◽  
Sleep Control ◽  
Inducible Nitric Oxide

scholarly journals “Rapid Eye Movement sleep deprivation of rat generates ROS in the hepatocytes and makes them more susceptible to oxidative stress”

2018 ◽  
Author(s):  
Atul Pandey ◽  
Santosh K Kar
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Sleep Deprivation ◽  
Eye Movement ◽  
Rem Sleep ◽  
Rapid Eye Movement Sleep ◽  
Recovery Sleep ◽  
Inos Gene ◽  
Oxide Synthase

AbstractBackgroundRapid Eye Movement sleep deprivation (REMSD) of rats causes inflammation of the liver and apoptotic cell death of neurons and hepatocytes. Studies also suggest that REMSD are involved with muscle injury, cardiac injury and neurodegerative diseases.Objective and methodsThe aim of this research was to determine whether REMSD of rats would generate reactive oxygen species (ROS) and create oxidative stress in the hepatocytes. We selectively deprived the rats from REM sleep using the standard flower pot method.ResultsWe observed that when rats were subjected to REMSD, the levels of ROS in the hepatocytes increased with the increase in the number of days of REMSD by ∼265%, but it returned towards normal levels after recovery sleep for 5 days (∼36%) compared to controls. Nitric oxide synthase (iNOS) gene and protein was found elevated in hepatocytes in response to REM sleep loss as confirmed by real time PCR and western blot analysis compared to controls. The level of nitric oxide (NO) also increased by ∼ 675% in the hepatocytes of REMSD rats as compared to that of control group of animals.DiscussionWe have analyzed the oxidative stress generated and potentiation of hepatocytes against oxidative stress in response to REMSD. Since, REM sleep is known to play an important role for survival of most animals and has important role in maintenance of body physiology. Hence, our findings that loss of REM sleep in hepatocytes of rats can affect the ROS levels and induce iNOS & NO circulation, while making them more susceptible to oxidative stress assumes significance.Highlights of the studyWe observed elevated levels of ROS in the hepatocytes of REM sleep deprived rats.The hepatocytes of REMSD group of rats were found more susceptible to oxidative stress than that of control groups.We found increased expression of iNOS gene and nitric oxide synthase protein in the hepatocytes of REMSD rats.We observed that nitric oxide levels in the hepatocytes of REM sleep deprived rats increased positively with days of REMSD, but returned to its normal levels after 5 days of recovery sleep.

Inhibitors of nitric oxide synthesis block cold-induced thermogenesis in rats

2003 ◽  
Vol 81 (8) ◽  
pp. 834-838 ◽  
Author(s):  
Peter R Kamerman ◽  
Helen P Laburn ◽  
Duncan Mitchell
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Metabolic Rate ◽  
Water Loss ◽  
T Test ◽  
Evaporative Water Loss ◽  
Evaporative Water ◽  
Oxide Synthase

N-nitro-L-arginine methyl ester (L-NAME), an unspecific nitric oxide synthase inhibitor, was administered to individually caged Sprague–Dawley rats exposed to cold (18°C) and thermoneutral (30°C) environmental temperatures during the active phase of the animals' circadian cycle. Unrestrained rats were administered intraperitoneal injections of 100 mg·kg–1 L-NAME or 1 mL·kg–1 saline. Telemetry was used to measure abdominal temperature. On a separate occasion, metabolic rate and evaporative water loss were measured using indirect calorimetery, before and after the injection of 100 mg·kg–1 L-NAME, in rats exposed to the two environments. Injection of L-NAME had no significant effect on body temperature, metabolic rate, or evaporative water loss in rats exposed to the 30°C environment. In the 18°C environment, L-NAME injection caused a prolonged fall in body temperature (F(1,12) = 17.43, P = 0.001) and a significant decrease in metabolic rate (Student's t test, P = 0.001) and evaporative water loss (one-sample t test, P = 0.04). Therefore, the effects that systemic injection of L-NAME has on body temperature are dependent on environmental temperature, with nitric oxide synthase inhibition seemingly preventing the metabolic component of cold defence.Key words: N-nitro-L-arginine methyl ester, thermoregulation, telemetry, oxygen consumption.

scholarly journals Acute thermal stress promotes morphological and molecular changes in the heart of broiler chickens

2020 ◽  
Vol 9 (8) ◽  
pp. e63985059
Author(s):  
Kariny Ferreira Moreira ◽  
Camila Quaglio Neves ◽  
Stephanie Carvalho Borges ◽  
Ana Paula Del Vesco ◽  
Maria Ida Bonini Ravanelli Speziali ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Thermal Stress ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Angiotensin Converting Enzyme ◽  
Converting Enzyme ◽  
Molecular Changes ◽  
Transfer Protein ◽  
Aortic Artery ◽  
Oxide Synthase

This study aimed to understand the possible effects of acute thermal stress (32ºC, 12 hours) on body temperature using two measurement methods (via probe and rectal), on the morphometric aspects of the heart and aortic artery, on gene expression (superoxide dismutase, glutathione peroxidase-3, nitric oxide synthase, angiotensin-converting enzyme and esterified cholesterol transfer protein), inflammatory parameters (myeloperoxidase and N-acetylglycosaminidase), oxidative stress parameters and nitrite levels in broilers (Cobb 500) at 42 days of age.  36 broilers with 42 days of age were used, distributed in a 2x2 factorial scheme: two thermal environments (comfort at 18ºC and stress at 32ºC) and two methods of measuring body temperature (via probe and rectal). Thermal stress triggered an increase in body temperature regardless of the measurement method. There was a significant effect on the thickness of the aortic artery wall and on the lateral lateral and posterior antero diameters (P <0.05). Likewise, there was a difference in the dosages of lipid hydroperoxides, in the quantification of reactive oxygen species and in the dosage of nitrite (P <0.05). The quantification of the mRNA of the induced nitric oxide synthase, angiotensin-converting enzyme and esterified cholesterol transfer protein genes were significantly higher in animals subjected to heat stress. Thus, it can be concluded that acute thermal stress was able to promote several morphological and molecular changes in the heart and aorta artery of broilers.

scholarly journals Role of biologically active molecules in uterine contractile activity

2019 ◽  
Vol 68 (1) ◽  
pp. 21-27
Author(s):  
Tatyana U. Kuzminykh ◽  
Vera Yu. Borisova ◽  
Igor P. Nikolayenkov ◽  
Georgy R. Kozonov ◽  
Gulrukhsor Kh. Tolibova
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Adhesion Molecules ◽  
Connexin 43 ◽  
Contractile Activity ◽  
Active Phase ◽  
Uterine Contractile ◽  
Uterine Inertia ◽  
Oxide Synthase

Hypothesis/aims of study. Myometrial relaxation and contraction require synchronous cellular interactions. At present, it has been established that the coordination of myometrial contractile activity is carried out by a conduction system constructed from gap junctions with intercellular channels. There are no clinical data on inhibiting (nitric oxide synthase) and activating (connexin-43) factors of uterine contractile activity in the myometrium during pregnancy and parturition in the published literature. This study was undertaken to measure the expression levels of nitric oxide synthase, adhesion molecules CD51, CD61, and connexin-43 in the myometrium during pregnancy and parturition; and to assess the role of inhibitory and activating factors in the development of uterine contractile activity. Study design, materials and methods. An immunohistochemical study of myometrial biopsy specimens obtained from the lower uterus segment during cesarean section was performed in eight women with a full-term physiological pregnancy, in another eight individuals in the active phase of uncomplicated parturition, and in eight patients with uterine inertia. Integrins (CD51 and CD61 proteins) were used as markers of cell adhesion. Localization and the number of intercellular contacts were assessed by measuring the expression level of connexin-43, with the intensity of oxidative processes assessed by nitric oxide synthase activity. Results. In the myometrium, in the active phase of physiological parturition, a three-fold increase in the expression of activating (CD51, CD61, and connexin-43) factors of uterine contractile activity and a five-fold decrease in that of inhibitory (nitric oxide synthase) ones occur compared to those in full-term physiological pregnancy. Conclusion. In the pathogenesis of uterine inertia and resistance to labor induction, an important role is played by the decreased expression of adhesion molecules (CD51, CD61) and connexin-43 and the increased expression of nitric oxide synthase in the myometrium.

Role of neuronal nitric oxide synthase in hypoxia-induced anapyrexia in rats

2000 ◽  
Vol 89 (3) ◽  
pp. 1131-1136 ◽  
Author(s):  
Alexandre A. Steiner ◽  
Evelin C. Carnio ◽  
Luiz G. S. Branco
Keyword(s):  
Nitric Oxide ◽  
Body Temperature ◽  
Nitric Oxide Synthase ◽  
Intraperitoneal Injection ◽  
Neuronal Nitric Oxide Synthase ◽  
Body Core Temperature ◽  
Body Core ◽  
Significant Attenuation ◽  
Oxide Synthase

Anapyrexia (a regulated decrease in body temperature) is a response to hypoxia that occurs in organisms ranging from protozoans to mammals, but very little is known about the mechanisms involved. Recently, it has been shown that the NO pathway plays a major role in hypoxia-induced anapyrexia. However, very little is known about which of the three different nitric oxide synthase isoforms (neuronal, endothelial, or inducible) is involved. The present study was designed to test the hypothesis that neuronal nitric oxide synthase (nNOS) plays a role in hypoxia-induced anapyrexia. Body core temperature (Tc) of awake, unrestrained rats was measured continuously using biotelemetry. Rats were submitted to hypoxia, 7-nitroindazole (7-NI; a selective nNOS inhibitor) injection, or both treatments together. Control animals received vehicle injections of the same volume. We observed a significant ( P < 0.05) reduction in Tc of ∼2.8°C after hypoxia (7% inspired O2), whereas intraperitoneal injection of 7-NI at 25 mg/kg caused no significant change in Tc. 7-NI at 30 mg/kg elicited a reduction in Tc and was abandoned in further experiments. When the two treatments were combined (25 mg/kg of 7-NI and 7% inspired O2), we observed a significant attenuation of hypoxia-induced anapyrexia. The data indicate that nNOS plays a role in hypoxia-induced anapyrexia.

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