scholarly journals Neural Input Is Critical for Arcuate Hypothalamic Neurons to Mount Intracellular Signaling Responses to Systemic Insulin and Deoxyglucose Challenges in Male Rats: Implications for Communication Within Feeding and Metabolic Control Networks

Endocrinology ◽  
2014 ◽  
Vol 155 (2) ◽  
pp. 405-416 ◽  
Author(s):  
Arshad M. Khan ◽  
Ellen M. Walker ◽  
Nicole Dominguez ◽  
Alan G. Watts
Keyword(s):  
Feeding Behavior ◽  
Intracellular Signaling ◽  
Male Rats ◽  
Control Networks ◽  
Melanocyte Stimulating Hormone ◽  
Neural Input ◽  
Hypothalamic Arcuate Nucleus ◽  
Metabolic Challenge ◽  
Neuroendocrine Neurons ◽  
Feeding Control

The hypothalamic arcuate nucleus (ARH) controls rat feeding behavior in part through peptidergic neurons projecting to the hypothalamic paraventricular nucleus (PVH). Hindbrain catecholaminergic (CA) neurons innervate both the PVH and ARH, and ablation of CA afferents to PVH neuroendocrine neurons prevents them from mounting cellular responses to systemic metabolic challenges such as insulin or 2-deoxy-d-glucose (2-DG). Here, we asked whether ablating CA afferents also limits their ARH responses to the same challenges or alters ARH connectivity with the PVH. We examined ARH neurons for three features: (1) CA afferents, visualized by dopamine-β-hydroxylase (DBH)– immunoreactivity; (2) activation by systemic metabolic challenge, as measured by increased numbers of neurons immunoreactive (ir) for phosphorylated ERK1/2 (pERK1/2); and (3) density of PVH-targeted axons immunoreactive for the feeding control peptides Agouti-related peptide and α-melanocyte-stimulating hormone (αMSH). Loss of PVH DBH immunoreactivity resulted in concomitant ARH reductions of DBH-ir and pERK1/2-ir neurons in the medial ARH, where AgRP neurons are enriched. In contrast, pERK1/2 immunoreactivity after systemic metabolic challenge was absent in αMSH-ir ARH neurons. Yet surprisingly, axonal αMSH immunoreactivity in the PVH was markedly increased in CA-ablated animals. These results indicate that (1) intrinsic ARH activity is insufficient to recruit pERK1/2-ir ARH neurons during systemic metabolic challenges (rather, hindbrain-originating CA neurons are required); and (2) rats may compensate for a loss of CA innervation to the ARH and PVH by increased expression of αMSH. These findings highlight the existence of a hierarchical dependence for ARH responses to neural and humoral signals that influence feeding behavior and metabolism.

Testosterone modulates the dendritic architecture of arcuate neuroendocrine neurons in adult male rats

2001 ◽  
Vol 890 (1) ◽  
pp. 78-85 ◽  
Author(s):  
Steve C. Danzer ◽  
Nathaniel T. McMullen ◽  
Naomi E. Rance
Keyword(s):  
Adult Male ◽  
Male Rats ◽  
Neuroendocrine Neurons

scholarly journals Age and tissue specific differences in the development of acute insulin resistance following injury

2009 ◽  
Vol 203 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Lidong Zhai ◽  
Joseph L Messina
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Insulin Signaling ◽  
Intracellular Signaling ◽  
Male Rats ◽  
Hepatic Insulin Resistance ◽  
Surgical Trauma ◽  
Induce Insulin Resistance ◽  
Old Rats ◽  
Effect Of Age

Injuries, hemorrhage, sepsis, burn, and critical illnesses all induce insulin resistance, and insulin resistance is strongly associated with advancing age. However, the effect of age on injury induced insulin resistance is not well studied. We performed surgical trauma in male rats of three different ages (3-, 6-, and 10-weeks old). Rats were either hemorrhaged to a mean arterial pressure of 35–40 mmHg and subsequently maintained at that pressure for up to 90 min, or maintained without hemorrhage as controls. Results indicate that insulin-induced intracellular signaling was diminished in liver and skeletal muscle of 6- and 10-week old rats following trauma and hemorrhage. In even younger rats, immediately post-weaning (∼3 weeks of age), insulin signaling was lost in liver, but not in skeletal muscle. Glucocorticoids can play a role in the chronic development of insulin resistance. Our results demonstrate that corticosterone levels were increased in 6- and 10-week old animals following hemorrhage, but little change was measured in 3-week old animals. Blockade of glucocorticoid synthesis prevented the development of insulin resistance in skeletal muscle, but not in liver of 6- and 10-week old rats. Moreover, skeletal muscle glucocorticoid receptor levels increased dramatically between 3 and 6 weeks of age. These results indicate that trauma and hemorrhage-induced hepatic insulin resistance occurs at all ages tested. However, there is no development of insulin resistance following trauma and hemorrhage in skeletal muscle of post-weaning rats. In skeletal muscle of 6- and 10-week old rats, inhibition of glucocorticoid levels prevents the development of insulin resistance.

Apelin and the proopiomelanocortin system: a new regulatory pathway of hypothalamic α-MSH release

2011 ◽  
Vol 301 (5) ◽  
pp. E955-E966 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Laurence Bodineau ◽  
Nadia De Mota ◽  
Lydie Jeandel ◽  
Nicolas Chartrel ◽  
...  
Keyword(s):  
Food Intake ◽  
Neuronal Cell ◽  
Nerve Fibers ◽  
Zucker Rats ◽  
Direct Stimulation ◽  
Melanocyte Stimulating Hormone ◽  
System A ◽  
Neuronal Cell Bodies ◽  
Hypothalamic Arcuate Nucleus ◽  
Apelin Receptor

Neuronal networks originating in the hypothalamic arcuate nucleus (Arc) play a fundamental role in controlling energy balance. In the Arc, neuropeptide Y (NPY)-producing neurons stimulate food intake, whereas neurons releasing the proopiomelanocortin (POMC)-derived peptide α-melanocyte-stimulating hormone (α-MSH) strongly decrease food intake. There is growing evidence to suggest that apelin and its receptor may play a role in the central control of food intake, and both are concentrated in the Arc. We investigated the presence of apelin and its receptor in Arc NPY- and POMC-containing neurons and the effects of apelin on α-MSH release in the hypothalamus. We showed, by immunofluorescence and confocal microscopy, that apelin-immunoreactive (IR) neuronal cell bodies were distributed throughout the rostrocaudal extent of the Arc and that apelin was strongly colocalized with POMC, but weakly colocalized with NPY. However, there were numerous NPY-IR nerve fibers close to the apelin-IR neuronal cell bodies. By combining in situ hybridization with immunohistochemistry, we demonstrated the presence of apelin receptor mRNA in Arc POMC neurons. Moreover, using a perifusion technique for hypothalamic explants, we demonstrated that apelin-17 (K17F) increased α-MSH release, suggesting that apelin released somato-dendritically or axonally from POMC neurons may stimulate α-MSH release in an autocrine manner. Consistent with these data, hypothalamic apelin levels were found to be higher in obese db/db mice and fa/fa Zucker rats than in wild-type animals. These findings support the hypothesis that central apelin is involved in regulating body weight and feeding behavior through the direct stimulation of α-MSH release.

scholarly journals Structural Complexity and Plasticity of Signaling Regulation at the Melanocortin-4 Receptor

2020 ◽  
Vol 21 (16) ◽  
pp. 5728 ◽  
Author(s):  
Gunnar Kleinau ◽  
Nicolas A. Heyder ◽  
Ya-Xiong Tao ◽  
Patrick Scheerer
Keyword(s):  
Intracellular Signaling ◽  
Current Knowledge ◽  
Experimental Studies ◽  
Structural Complexity ◽  
Inactive State ◽  
Signaling Regulation ◽  
Melanocyte Stimulating Hormone ◽  
Agonist Action ◽  
Melanocortin 4 Receptor ◽  
G Protein Coupled

The melanocortin-4 receptor (MC4R) is a class A G protein-coupled receptor (GPCR), essential for regulation of appetite and metabolism. Pathogenic inactivating MC4R mutations are the most frequent cause of monogenic obesity, a growing medical and socioeconomic problem worldwide. The MC4R mediates either ligand-independent or ligand-dependent signaling. Agonists such as α-melanocyte-stimulating hormone (α-MSH) induce anorexigenic effects, in contrast to the endogenous inverse agonist agouti-related peptide (AgRP), which causes orexigenic effects by suppressing high basal signaling activity. Agonist action triggers the binding of different subtypes of G proteins and arrestins, leading to concomitant induction of diverse intracellular signaling cascades. An increasing number of experimental studies have unraveled molecular properties and mechanisms of MC4R signal transduction related to physiological and pathophysiological aspects. In addition, the MC4R crystal structure was recently determined at 2.75 Å resolution in an inactive state bound with a peptide antagonist. Underpinned by structural homology models of MC4R complexes simulating a presumably active-state conformation compared to the structure of the inactive state, we here briefly summarize the current understanding and key players involved in the MC4R switching process between different activity states. Finally, these perspectives highlight the complexity and plasticity in MC4R signaling regulation and identify gaps in our current knowledge.

EFFECT OF α-MELANOCYTE-STIMULATING HORMONE AND OVARIAN STEROIDS ON PREPUTIAL GLAND FUNCTION IN THE FEMALE RAT

1981 ◽  
Vol 90 (1) ◽  
pp. 53-58 ◽  
Author(s):  
S. M. DONOHOE ◽  
A. J. THODY ◽  
S. SHUSTER
Keyword(s):  
Pituitary Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Female Rat ◽  
Preputial Gland ◽  
Melanocyte Stimulating Hormone ◽  
Experienced Male ◽  
Hypophysectomized Rats ◽  
Gland Function ◽  
Preputial Glands

Sexually experienced male rats were used to test the attractiveness of preputial gland odours of female rats. The male rats showed a clear preference for the preputial gland odours of hypophysectomized females given oestradiol benzoate (OB) for 3 or 8 days to those of control rats. Progesterone treatment had no effect on the attractiveness of the preputial gland odours of OB-treated hypophysectomized female rats. Administration of α-MSH for either 3 or 8 days, on the other hand, increased the attractiveness to male rats of preputial gland odours of OB-treated hypophysectomized females and the presence of progesterone produced no further change. When administered alone α-MSH had no effect on the attractiveness of the preputial gland odours. Other pituitary hormones, such as ACTH and prolactin, had no effect on the attractiveness of preputial gland odours of OB-treated hypophysectomized rats when administered for 3[unk]days. An increase in preputial gland size was only seen when OB, progesterone and α-MSH were administered together. It would appear that no relationship exists between the size of the preputial glands and their ability to attract male rats. It is concluded that, while α-MSH and progesterone may be important in controlling growth of the preputial glands, an interaction between α-MSH and oestrogen is more important for regulating the production of sex attractants by the preputial glands.

Degenerative changes of the Medial arcuate hypothalamic nucleus neurons in the male hypogonadism model

2015 ◽  
Vol 6 (3) ◽  
pp. 62-68
Author(s):  
Yulia Nikolaevna Khodulaeva ◽  
Zakhar Petrovich Asaulenko ◽  
Alekber Azizovoch Baymarov ◽  
Irina Leorovna Nikitina ◽  
Andreiy Vsevolodovich Droblenkov
Keyword(s):  
Hormonal Regulation ◽  
Structural Changes ◽  
Arcuate Nucleus ◽  
Male Rats ◽  
Hypothalamic Nucleus ◽  
Control Group ◽  
Male Hypogonadism ◽  
Testosterone Therapy ◽  
Reactive Changes ◽  
Hypothalamic Arcuate Nucleus

The study of patterns of hormonal regulation of sexual development of adolescents including mechanisms of physiological and pathological changes in the rate of maturation of the hypothalamic-pituitary-gonadal axis remains the subject of active research interest. The study of reactive changes of the medial arcuate nucleus of cells in experimental hypogonadism and degree of correction of these changes after testosterone therapy is necessary for a better understanding of the mechanisms of endocrine interaction gonads and gonadoliberin centers during puberty. The aim of this article was to determine the quantitative, structural changes of neurons, glio-neuronal and interneuronal relationships in the medial arcuate nucleus in experimental hypogonadism and the degree of correction of these changes after testosterone therapy. In male Wistar rats induced hypogonadism (model created by the removal of one gonad on postnatal day 2-3), and histological sections were examined medial hypothalamic arcuate nucleus puberty animals (2 months) and the absence of treatment with testosterone after correction. The control group consisted of intact animals puberty. It was found that after the experimental inhibition of testosterone production in newborn male rats in the medial hypothalamic arcuate nucleus of rat puberty develop degenerative (degenerative, atrophic) and compensatory-adaptive changes. First expressed in the reduction of the share and the decrease in the normochromic neurons area, wrinkling, the growth of the share of shadowly neurons. The latter expressed signs of activation glio-neuronal and interneuronal relations. Many reactive changes in the cells exposed to compensatory adjustment in the period of puberty.

Effects of α-Melanocyte-Stimulating Hormone on Magnocellular Oxytocin Neurones and their Activation at Intromission in Male Rats

2006 ◽  
Vol 18 (9) ◽  
pp. 685-691 ◽  
Author(s):  
C. Caquineau ◽  
G. Leng ◽  
X. M. M. Guan ◽  
M. Jiang ◽  
L. Van der Ploeg ◽  
...  
Keyword(s):  
Male Rats ◽  
Melanocyte Stimulating Hormone ◽  
Oxytocin Neurones ◽  
Stimulating Hormone

Effect of moderate and high-intensity endurance and resistance training on serum concentrations of MSTN and IGF-1 in old male Wistar rats

2019 ◽  
Vol 38 (2) ◽  
Author(s):  
Zohreh Shanazari ◽  
Mohammad Faramarzi ◽  
Ebrahim Banitalebi ◽  
Roohullah Hemmati
Keyword(s):  
Resistance Training ◽  
Endurance Training ◽  
High Intensity ◽  
Intracellular Signaling ◽  
Male Rats ◽  
Moderate Intensity ◽  
Exercise Session ◽  
Control Group ◽  
Significance Level ◽  
Significant Difference

Abstract Background Skeletal muscle is very sensitive to extracellular and intracellular signaling evoked by contractions from endurance and resistance exercise. The aim of this study was to compare the effects of moderate- and high-intensity endurance and resistance training on the serum myostatin (MSTN) and insulin-like growth factor (IGF-1) levels in older rats. Materials and methods Fifty old Wistar male rats (23 months old) were randomly divided into four experimental and one control groups, including moderate-endurance training (MET) (n = 10), high-intensity endurance training (EHT) (n = 10), moderate-intensity resistance training (MRT) (n = 10), high-intensity resistance training (HRT) (n = 10), and control group (C) (n = 10). Seventy-two hours after the last exercise session, euthanasia of the rats were rendered unconscious and direct blood samples were collected. Serum IGF-1 and MSTN concentration were measured using the enzyme-linked immuno sorbent assay (ELISA) method. The statistical analysis was performed using one-way analysis of variance (ANOVA) test with a significance level of p ≤ 0.05. Results There was a significant reduction in MSTN and an increase in IGF-1 concentrations was observed between IGF-I levels in high and moderate resistance and endurance training. However, no significant difference was observed in MSTN levels between groups. Discussion Therefore, it appears that resistance training, especially HRT, is effective to increase growth mediators among older rats.

mTOR signaling response to resistance exercise is altered by chronic resistance training and detraining in skeletal muscle

2013 ◽  
Vol 114 (7) ◽  
pp. 934-940 ◽  
Author(s):  
Riki Ogasawara ◽  
Koji Kobayashi ◽  
Arata Tsutaki ◽  
Kihyuk Lee ◽  
Takashi Abe ◽  
...  
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Intracellular Signaling ◽  
Gastrocnemius Muscle ◽  
Male Rats ◽  
Exercise Session ◽  
Signaling Proteins ◽  
Signaling Mechanisms ◽  
Exercise Induced ◽  
Training And Detraining

Resistance training-induced muscle anabolism and subsequent hypertrophy occur most rapidly during the early phase of training and become progressively slower over time. Currently, little is known about the intracellular signaling mechanisms underlying changes in the sensitivity of muscles to training stimuli. We investigated the changes in the exercise-induced phosphorylation of hypertrophic signaling proteins during chronic resistance training and subsequent detraining. Male rats were divided into four groups: 1 bout (1B), 12 bouts (12B), 18 bouts (18B), and detraining (DT). In the DT group, rats were subjected to 12 exercise sessions, detrained for 12 days, and then were subjected to 1 exercise session before being killed. Isometric training consisted of maximum isometric contraction, which was produced by percutaneous electrical stimulation of the gastrocnemius muscle every other day. Muscles were removed 24 h after the final exercise session. Levels of total and phosphorylated p70S6K, 4E-BP1, rpS6, and p90RSK levels were measured, and phosphorylation of p70S6K, rpS6, and p90RSK was elevated in the 1B group compared with control muscle (CON) after acute resistance exercise, whereas repeated bouts of exercise suppressed those phosphorylation in both 12B and 18B groups. Interestingly, these phosphorylation levels were restored after 12 days of detraining in the DT group. On the contrary, phosphorylation of 4E-BP1 was not altered with chronic training and detraining, indicating that, with chronic resistance training, anabolic signaling becomes less sensitive to resistance exercise stimuli but is restored after a short detraining period.

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