Estradiol replacement enhances sleep deprivation-induced c-Fos immunoreactivity in forebrain arousal regions of ovariectomized rats

2008 ◽  
Vol 295 (4) ◽  
pp. R1328-R1340 ◽  
Author(s):  
S. Deurveilher ◽  
E. M. Cumyn ◽  
T. Peers ◽  
B. Rusak ◽  
K. Semba
Keyword(s):  
Sleep Deprivation ◽  
Body Weight Gain ◽  
Ovariectomized Rats ◽  
Adult Rats ◽  
Limbic Forebrain ◽  
Bed Nucleus ◽  
Tuberomammillary Nucleus ◽  
Female Sex Hormones ◽  
Ventrolateral Preoptic Nucleus ◽  
Oil Injection

To understand how female sex hormones influence homeostatic mechanisms of sleep, we studied the effects of estradiol (E2) replacement on c-Fos immunoreactivity in sleep/wake-regulatory brain areas after sleep deprivation (SD) in ovariectomized rats. Adult rats were ovariectomized and implanted subcutaneously with capsules containing 17β-E2 (10.5 μg; to mimic diestrous E2 levels) or oil. After 2 wk, animals with E2 capsules received a single subcutaneous injection of 17β-E2 (10 μg/kg; to achieve proestrous E2 levels) or oil; control animals with oil capsules received an oil injection. Twenty-four hours later, animals were either left undisturbed or sleep deprived by “gentle handling” for 6 h during the early light phase, and killed. E2 treatment increased serum E2 levels and uterus weights dose dependently, while attenuating body weight gain. Regardless of hormonal conditions, SD increased c-Fos immunoreactivity in all four arousal-promoting areas and four limbic and neuroendocrine nuclei studied, whereas it decreased c-Fos labeling in the sleep-promoting ventrolateral preoptic nucleus (VLPO). Low and high E2 treatments enhanced the SD-induced c-Fos immunoreactivity in the laterodorsal subnucleus of the bed nucleus of stria terminalis and the tuberomammillary nucleus, and in orexin-containing hypothalamic neurons, with no effect on the basal forebrain and locus coeruleus. The high E2 treatment decreased c-Fos labeling in the VLPO under nondeprived conditions. These results indicate that E2 replacement modulates SD-induced or spontaneous c-Fos expression in sleep/wake-regulatory and limbic forebrain nuclei. These modulatory effects of E2 replacement on neuronal activity may be, in part, responsible for E2's influence on sleep/wake behavior.

scholarly journals Identification of the Active Ingredient and Beneficial Effects of Vitex rotundifolia Fruits on Menopausal Symptoms in Ovariectomized Rats

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1033
Author(s):  
Ji Hwan Lee ◽  
Sullim Lee ◽  
Quynh Nhu Nguyen ◽  
Hung Manh Phung ◽  
Myoung-Sook Shin ◽  
...  
Keyword(s):  
Weight Gain ◽  
Body Weight Gain ◽  
Animal Experiments ◽  
Ovariectomized Rats ◽  
Biological Functions ◽  
Menopausal Syndrome ◽  
Active Constituents ◽  
Mcf 7

Estrogen replacement therapy is a treatment to relieve the symptoms of menopause. Many studies suggest that natural bioactive ingredients from plants resemble estrogen in structure and biological functions and can relieve symptoms of menopause. The fruit of V. rotundifolia, called “Man HyungJa” in Korean, is a traditional medicine used to treat headache, migraine, eye pain, neuralgia, and premenstrual syndrome in Korea and China. The aim of the present study was to confirm that V. rotundifolia fruit extract (VFE) exerts biological functions similar to those of estrogen in menopausal syndrome. We investigated its in vitro effects on MCF-7 cells and in vivo estrogen-like effects on weight gain and uterine contraction in ovariectomized rats. Using the polar extract, the active constituents of VFE (artemetin, vitexicarpin, hesperidin, luteolin, vitexin, and vanillic acid) with estrogen-like activity were identified in MCF-7 cells. In animal experiments, the efficacy of VFE in ameliorating body weight gain was similar to that of estrogen, as evidenced from improvements in uterine atrophy. Vitexin and vitexicarpin are suggested as the active constituents of V. rotundifolia fruits.

Estrogens and antiestrogens: actions and interactions with fluphenazine on food intake and body weight in rats

1993 ◽  
Vol 264 (6) ◽  
pp. R1214-R1218 ◽  
Author(s):  
J. M. Gray ◽  
S. Schrock ◽  
M. Bishop
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Ethinyl Estradiol ◽  
Body Weight Gain ◽  
Fatty Acid Synthetase ◽  
Ovariectomized Rats ◽  
Synthetase Activity ◽  
Concurrent Administration

Treatment of ovariectomized rats for 3 days with 2 micrograms estradiol benzoate (E2B), 6 micrograms ethinyl estradiol, or 1-2 mg of either of the antiestrogens nafoxidine or tamoxifen led to similar decreases in food intake, body weight gain, adipose tissue lipoprotein lipase activity, and hepatic fatty acid synthetase activity, despite their different effects on uterine growth and induction of progestin receptors in pituitary and adipose tissue. Longer-term (2 wk) treatment with tamoxifen resulted in similar transient changes in food intake and body weight gain, as did treatment with E2B. Daily administration of 50 micrograms fluphenazine (FLU) led to significant decreases in body weight, although there was no change in food intake. Concurrent administration of FLU with either E2B or tamoxifen led to additive effects on body weight and food intake change. None of the treatments had any effect on in vitro binding of [3H]tamoxifen to antiestrogen binding sites in pooled hypothalamic-preoptic area samples.

Nutritional and metabolic adaptations to prolonged sleep deprivation in the rat

1993 ◽  
Vol 264 (2) ◽  
pp. R376-R387 ◽  
Author(s):  
C. A. Everson ◽  
T. A. Wehr
Keyword(s):  
Body Weight ◽  
Sleep Deprivation ◽  
Food Consumption ◽  
Time Course ◽  
Body Weight Gain ◽  
Clinical Chemistry ◽  
Plasma Cholesterol ◽  
Skin Lesions ◽  
Weight Regulation ◽  
Body Weight Regulation

To understand how and why sleep deprivation is physically harmful, we explored the possible causal relationship between its two main effects, 1) negative energy balance and 2) a composite of symptoms that resemble protein malnutrition, both of which occur despite increased food consumption. We provided balanced diets augmented with either protein or calories (by increased fat content) to freely moving rats. Interactions between sleep deprivation symptoms and energy and protein supplies were assessed from measurements of body weight regulation, consumption of macronutrients, clinical chemistry and hematology profiles, and physical appearance. The results indicate that sleep deprivation causes malnutrition, which is secondary to increased energy expenditure. Even though food consumption remained normal in sleep-deprived rats fed a diet of high protein-to-calorie ratio, body weight loss was more than 16% of baseline, development of skin lesions was hastened, and longevity was shortened by 40% compared with sleep-deprived rats fed the calorie-augmented diet. Food consumption of the calorie-fed rats was lower during baseline than that of the protein-fed group but during sleep deprivation increased to amounts 250% of normal without net body weight gain. Despite a fat-laden diet the calorie-fed hyperphagic group did not have abnormal levels of plasma cholesterol, triglycerides, or glucose, indicating accelerated turnover of nutrients. As would be consistent with calorie malnutrition, pronounced clinical chemistry or hematological abnormalities were not found in any group. Beneficial effects of the calorie-augmented diet are attributed to 1) caloric density of fat, 2) induction of hyperphagia, and 3) efficiency of utilization of fat. We conclude that diet composition interacts strongly with sleep deprivation, affecting the time course and development of pathologies, whereas it exerted negligible influence on body weight regulation under normal conditions.

Sleep Deprivation Impairs Ca2+ Expression in the Hippocampus: Ionic Imaging Analysis for Cognitive Deficiency with TOF-SIMS

2012 ◽  
Vol 18 (3) ◽  
pp. 425-435 ◽  
Author(s):  
Hung-Ming Chang ◽  
Wen-Chieh Liao ◽  
Ji-Nan Sheu ◽  
Chun-Chao Chang ◽  
Chyn-Tair Lan ◽  
...  
Keyword(s):  
Sleep Deprivation ◽  
Neuronal Plasticity ◽  
Molecular Mechanisms ◽  
Secondary Ion Mass Spectrometry ◽  
Maze Learning ◽  
Behavioral Testing ◽  
Adult Rats ◽  
Cognitive Deficiency ◽  
Learning Test ◽  
Oxide Synthase

AbstractSleep deprivation causes cognitive dysfunction in which impaired neuronal plasticity in hippocampus may underlie the molecular mechanisms of this deficiency. Considering calcium-mediated NMDA receptor subunit 1 (NMDAR1) and neuronal nitric oxide synthase (nNOS) activation plays an important role in the regulation of neuronal plasticity, the present study is aimed to determine whether total sleep deprivation (TSD) would impair calcium expression, together with injury of the neuronal plasticity in hippocampus. Adult rats subjected to TSD were processed for time-of-flight secondary ion mass spectrometry, NMDAR1 immunohistochemistry, nNOS biochemical assay, cytochrome oxidase histochemistry, and the Morris water maze learning test to detect ionic, neurochemical, bioenergetic as well as behavioral changes of neuronal plasticity, respectively. Results indicated that in normal rats, strong calcium signaling along with intense NMDAR1/nNOS expression were observed in hippocampal regions. Enhanced calcium imaging and neurochemical expressions corresponded well with strong bioenergetic activity and good performance of behavioral testing. However, following TSD, both calcium intensity and NMDAR1/nNOS expressions were significantly decreased. Behavioral testing also showed poor responses after TSD. As proper calcium expression is essential for maintaining hippocampal neuronal plasticity, impaired calcium expression would depress downstream NMDAR1-mediated nNOS activation, which might contribute to the initiation or development of TSD-related cognitive deficiency.

scholarly journals Suppressor of cytokine signaling 3 knockdown in the mediobasal hypothalamus: counterintuitive effects on energy balance

2010 ◽  
Vol 45 (5) ◽  
pp. 341-353 ◽  
Author(s):  
M W A de Backer ◽  
M A D Brans ◽  
A J van Rozen ◽  
E M van der Zwaal ◽  
M C M Luijendijk ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Energy Balance ◽  
Viral Vectors ◽  
Body Weight Gain ◽  
Cytokine Signaling ◽  
Dark Phase ◽  
Mrna Levels ◽  
Mediobasal Hypothalamus ◽  
Suppressor Of Cytokine Signaling ◽  
Adult Rats

An increase in brain suppressor of cytokine signaling 3 (SOCS3) has been implicated in the development of both leptin and insulin resistance. Socs3 mRNA is localized throughout the brain, and it remains unclear which brain areas are involved in the effect of SOCS3 levels on energy balance. We investigated the role of SOCS3 expressed in the mediobasal hypothalamus (MBH) in the development of diet-induced obesity in adult rats. Socs3 mRNA was down-regulated by local injection of adeno-associated viral vectors expressing a short hairpin directed against Socs3, after which we determined the response to high-fat high-sucrose choice diet. In contrast to neuronal Socs3 knockout mice, rats with SOCS3 knockdown limited to the MBH showed increased body weight gain, larger amounts of white adipose tissue, and higher leptin concentrations at the end of the experiment. These effects were partly due to the decrease in locomotor activity, as 24 h food intake was comparable with controls. In addition, rats with Socs3 knockdown in the MBH showed alterations in their meal patterns: average meal size in the light period was increased and was accompanied by a compensatory decrease in meal frequency in the dark phase. In addition, neuropeptide Y (Npy) mRNA levels were significantly increased in the arcuate nucleus of Socs3 knockdown rats. Since leptin is known to stimulate Npy transcription in the absence of Socs3, these data suggest that knockdown of Socs3 mRNA limited to the MBH increases Npy mRNA levels, which subsequently decreases locomotor activity and alters feeding patterns.

scholarly journals The Anteroventral Bed Nucleus of the Stria Terminalis Differentially Regulates Hypothalamic-Pituitary-Adrenocortical Axis Responses to Acute and Chronic Stress

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 818-826 ◽  
Author(s):  
Dennis C. Choi ◽  
Nathan K. Evanson ◽  
Amy R. Furay ◽  
Yvonne M. Ulrich-Lai ◽  
Michelle M. Ostrander ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Hpa Axis ◽  
Paraventricular Nucleus ◽  
Restraint Stress ◽  
Body Weight Gain ◽  
Stria Terminalis ◽  
Thymic Involution ◽  
Bed Nucleus ◽  
Acute And Chronic Stress

The anteroventral region of the bed nucleus of the stria terminalis (BST) stimulates hypothalamic-pituitary-adrenocortical (HPA) axis responses to acute stress. However, the role of the anterior BST nuclei in chronic drive of the HPA axis has yet to be established. Therefore, this study tests the role of the anteroventral BST in physiological responses to chronic drive, using a chronic variable stress (CVS) model. Male Sprague-Dawley rats received either bilateral ibotenate lesions, targeting the anteroventral BST, or vehicle injection into the same region. Half of the lesion and control rats were exposed to a 14-d CVS paradigm consisting of twice-daily exposure to unpredictable, alternating stressors. The remaining rats were nonhandled control animals that remained in home cages. On the morning after the end of CVS exposure, all rats were exposed to a novel restraint stress challenge. CVS induced attenuated body weight gain, adrenal hypertrophy, thymic involution, and enhanced CRH mRNA in hypophysiotrophic neurons of the hypothalamic paraventricular nucleus, none of which were affected by anteroventral BST lesions. In the absence of CVS, lesions attenuated the plasma corticosterone and paraventricular nucleus c-fos mRNA responses to the acute restraint stress. In contrast, lesions of the anteroventral BST elevated plasma ACTH and corticosterone responses to novel restraint in the rats previously exposed to CVS. These data suggest that the anterior BST plays very different roles in integrating acute stimulation and chronic drive of the HPA axis, perhaps mediated by chronic stress-induced recruitment of distinct BST cell groups or functional reorganization of stress-integrative circuits.

Role of the organum vasculosum laminae terminalis in the control of gonadotrophin secretion in rats

1982 ◽  
Vol 93 (3) ◽  
pp. 355-NP ◽  
Author(s):  
F. Piva ◽  
P. Limonta ◽  
L. Martini
Keyword(s):  
Ovariectomized Rats ◽  
Adult Rats ◽  
Organum Vasculosum Laminae Terminalis ◽  
Serum Lh ◽  
Parallel Increase ◽  
Gonadotrophin Secretion ◽  
Radiofrequency Lesions ◽  
Organum Vasculosum

The organum vasculosum laminae terminalis (OVLT) was destroyed by radiofrequency lesions in regularly cycling and in long-term ovariectomized adult rats. After OVLT lesion practically all cyclic females (16 out of 22) became dioestrous, as indicated by vaginal smears. At the time of killing these animals (8 days after the lesion) serum LH levels were undetectable, while serum FSH was as low as in cyclic animals in dioestrus. In the few OVLT-lesioned animals which exhibited some sort of oestrous cyclicity, serum LH showed a small subphysiological increase at pro-oestrus: this was not accompanied by a parallel increase in serum FSH and in these animals a delayed peak of FSH occurred on the day of oestrus. Ovariectomized rats bearing OVLT lesions had serum titres of LH and FSH as high as those of ovariectomized control rats. It is suggested that the OVLT may play a role in the control of the cyclic release of gonadotrophins but is not involved in the tonic regulation of gonadotrophin secretion.

Sleep Deprivation Impairs Long-Term Potentiation in Rat Hippocampal Slices

2002 ◽  
Vol 88 (2) ◽  
pp. 1073-1076 ◽  
Author(s):  
I. G. Campbell ◽  
M. J. Guinan ◽  
J. M. Horowitz
Keyword(s):  
Sleep Deprivation ◽  
Neural Plasticity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Adult Rats ◽  
Cellular Processes ◽  
Term Potentiation ◽  
Population Spike Amplitude ◽  
Specific Factors

To determine if 12-h sleep deprivation disrupts neural plasticity, we compared long-term potentiation (LTP) in five sleep-deprived and five control rats. Thirty minutes after tetanus population spike amplitude increased 101 ± 15% in 16 slices from sleep deprived rats and 139 ± 14% in 14 slices from control rats. This significant ( P < 0.05) reduction of LTP, the first demonstration that the sleep deprivation protocol impairs plasticity in adult rats, may be due to several factors. Reduced LTP may indicate that sleep provides a period of recuperation for cellular processes underlying neural plasticity. Alternatively, the stress of sleep deprivation, as indicated by elevated blood corticosterone levels, or other non-sleep-specific factors of deprivation may contribute to the LTP reduction.

Sign in / Sign up

Export Citation Format

Share Document