Interactions between the nitrergic and the endocannabinoid system in rats exposed to the elevated T maze

2021 ◽  
pp. 1-14
Author(s):  
L.A Batista ◽  
F.A Moreira ◽  
D.C Aguiar
Keyword(s):  
Nitric Oxide ◽  
Animal Model ◽  
Receptor Agonist ◽  
Wistar Rats ◽  
Endocannabinoid System ◽  
Cb1 Receptor ◽  
Cb1 Receptors ◽  
Male Wistar Rats ◽  
No Signaling ◽  
Cb1 Antagonist

Abstract Objective: the aim of this study was to test the hypothesis that synthesis of nitric oxide (NO) and activation of CB1 receptors have opposite effects in a behavioural animal model of panic and anxiety. Methods: to test the hypothesis male Wistar rats were exposed to the elevated T maze (ETM) model under the following treatments: L-Arginine (L-Arg) was administered before treatment withWIN55,212-2, a CB1 receptor agonist ; AM251, a CB1 antagonist, was administered before treatment with L-Arg. All treatments were by intraperitoneal route. Results: the CB1 receptor agonist, WIN55,212-2 (1 mg/kg), induced an anxiolytic-like effect which was prevented by pretreatment with an ineffective dose of L-Arg (1 mg/kg). Administration of AM251 (1 mg/kg), a CB1 antagonist before treatment with L-Arg (1 mg/kg) did not produce anxiogenic-like responses. Conclusion: altogether, this study suggests that the anxiolytic-like effect of cannabinoids may occur though modulation of NO signaling.

scholarly journals Development of Animal Model for Studying Deep Second-Degree Thermal Burns

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Danielle dos Santos Tavares Pereira ◽  
Maria Helena Madruga Lima-Ribeiro ◽  
Nicodemos Teles de Pontes-Filho ◽  
Ana Maria dos Anjos Carneiro-Leão ◽  
Maria Tereza dos Santos Correia
Keyword(s):  
Animal Model ◽  
Wistar Rats ◽  
Therapeutic Agents ◽  
Collagen Fibers ◽  
Thermal Burns ◽  
Thermal Lesions ◽  
Male Wistar Rats ◽  
Tissue Shrinkage ◽  
Fibroblastic Proliferation ◽  
Second Degree

Thermal lesions were produced in 12 male Wistar rats, positioning a massive aluminum bar 10 mm in diameter (51 g), preheated to 99°C ± 2°C/10 min. on the back of each animal for 15 sec. After 7, 14, 21, and 28 days, animals were euthanized. The edema intensity was mild, with no bubble and formation of a thick and dry crust from the 3rd day. The percentage of tissue shrinkage at 28 days was 66.67 ± 1.66%. There was no sign of infection, bleeding, or secretion. Within 28 days reepithelialization was incomplete, with fibroblastic proliferation and moderate fibrosis and presence of modeled dense collagen fibers. It is concluded that the model established is applicable in obtaining deep second-degree thermal burns in order to evaluate the healing action of therapeutic agents of topical use.

scholarly journals WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges

Epilepsia ◽  
2010 ◽  
Vol 51 (8) ◽  
pp. 1511-1521 ◽  
Author(s):  
Clementina M. Van Rijn ◽  
Silvana Gaetani ◽  
Ines Santolini ◽  
Aleksandra Badura ◽  
Aleksandra Gabova ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Cb1 Receptor ◽  
Cb1 Receptors ◽  
Thalamic Nuclei ◽  
Spike Wave Discharges ◽  
Spike Wave

scholarly journals Evidence for an Interaction between CB1 Cannabinoid and Melanocortin MCR-4 Receptors in Regulating Food Intake

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3224-3231 ◽  
Author(s):  
A. N. A. Verty ◽  
J. R. McFarlane ◽  
I. S. McGregor ◽  
P. E. Mallet
Keyword(s):  
Locomotor Activity ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Receptor Agonist ◽  
Cannabinoid Receptors ◽  
Cb1 Receptor ◽  
Melanocortin Receptor ◽  
Cb1 Receptors ◽  
Melanocortin System ◽  
Sr 141716

Abstract Melanocortin receptor 4 (MCR4) and CB1 cannabinoid receptors independently modulate food intake. Although an interaction between the cannabinoid and melanocortin systems has been found in recovery from hemorrhagic shock, the interaction between these systems in modulating food intake has not yet been examined. The present study had two primary purposes: 1) to examine whether the cannabinoid and melanocortin systems act independently or synergistically in suppressing food intake; and 2) to determine the relative position of the CB1 receptors in the chain of control of food intake in relation to the melanocortin system. Rats were habituated to the test environment and injection procedure and then received intracerebroventicular injections of various combinations of the MCR4 receptor antagonist JKC-363, the CB1 receptor agonist Δ9-tetrahydrocannabinol, the MCR4 receptor agonist α-MSH, or the cannabinoid CB1 receptor antagonist SR 141716. Food intake and locomotor activity were then recorded for 120 min. When administrated alone, SR 141716 and α-MSH dose-dependently attenuated baseline feeding, whereas sub-anorectic doses of SR 141716 and α-MSH synergistically attenuated baseline feeding when combined. Δ9-Tetrahydrocannabinol-induced feeding was not blocked by α-MSH, whereas SR 141716 dose-dependently attenuated JKC-363-induced feeding. Locomotor activity was not significantly affected by any drug treatment, suggesting that the observed effects on feeding were not due to a nonspecific reduction in motivated behavior. These findings revealed a synergistic interaction between the cannabinoid and melanocortin systems in feeding behavior. These results further suggested that CB1 receptors are located downstream from melanocortin receptors and CB1 receptor signaling is necessary to prevent the melanocortin system from altering food intake.

scholarly journals The role of poly-herbal extract in sodium chloride-induced oxidative stress and hyperlipidemia in male Wistar rats

2021 ◽  
Author(s):  
Olumide Fadahunsi ◽  
Peter Adegbola ◽  
Olayemi Adebola Akintola ◽  
Bamidele Stephen Ajilore ◽  
olubukola sinbad Olorunnisola
Keyword(s):  
Nitric Oxide ◽  
Serum Lipid ◽  
Antioxidant Status ◽  
Wistar Rats ◽  
Density Lipoprotein ◽  
High Salt ◽  
Herbal Extract ◽  
High Salt Diet ◽  
Salt Diet ◽  
Male Wistar Rats

Abstract Consistent consumption of high salt diet (HSD) has been associated with increased cellular generation of free radicals which has been implicated in the derangement of some vital organs and etiology of cardiovascular disorders. This study was designed to investigate the combined effect of some commonly employed medicinal plants on serum lipid profile and antioxidant status of aorta, kidney, and liver of high salt diet-fed animals. Thirty-five male Wistar rats were divided into 5 groups of 7 animals each. Group 1 and 2 animals were fed normal rat and 16 % high salt diet only respectively. Animals in groups 3, 4, and 5 were fed 16% high salt diet with 800, 400, and 200 mg/kg bw poly-herbal extract (PHE) respectively once for 28 consecutive days. Serum low-density lipoprotein (LDL), triacylglycerol (TG), total cholesterol (TC) and high-density lipoprotein (HDL), malondialdehyde, nitric oxide, catalase, superoxide dismutase, glutathione peroxidase, glutathione concentration, and activities were assessed in the aorta, kidney, and liver. PHE (p < 0.05) significantly reduced malondialdehyde and nitric oxide concentration and increased antioxidant enzymes and glutathione activity. Elevated serum TG, TC, LDL, and TC content in HSD-fed animals were significantly (p < 0.05) reduced to normal in PHE-treated rats while HDL was significantly elevated (p < 0.05) in a concentration-dependent manner in PHE treated animals. Feeding with PHE attenuated high salt diet imposed derangement in serum lipid profile and antioxidant status in the organs of the experimental rats.

Peripheral analgesia involves cannabinoid receptors

2018 ◽  
Author(s):  
Julie Desroches
Keyword(s):  
Cannabinoid Receptors ◽  
Receptor Gene ◽  
Endocannabinoid System ◽  
Cb1 Receptor ◽  
Pain Modulation ◽  
Cb1 Receptors ◽  
Gene Encoding ◽  
Cannabinoid Type 1 Receptor ◽  
Peripheral Analgesia

This landmark paper by Agarwal and colleagues was published in 2007, when the exact contribution of the activation of the cannabinoid type 1 receptor (CB1) receptors expressed on the peripheral terminals of nociceptors in pain modulation was still uncertain. At that time, while it was clearly demonstrated that the central nervous system (CNS) was involved in the antinociceptive effects induced by the activation of the CB1 receptor, many strains of mice in which the gene encoding the CB1 receptor was deleted by conditional mutagenesis were used to study the specific role of these receptors in pain. Creating an ingenious model of genetically modified mice with a conditional deletion of the CB1 receptor gene exclusively in the peripheral nociceptors, Agarwal and colleagues were the first to unequivocally demonstrate the major role of this receptor in the control of pain at the peripheral level. In fact, these mutant mice lacking CB1 receptors only in sensory neurons (those expressing the sodium channel Nav1.8) have been designed to highlight that CB1 receptors on nociceptors, and not those within the CNS, constitute an important target for mediating local or systemic (but not intrathecal) cannabinoid analgesia. Overall, they have clarified the anatomical locus of cannabinoid-induced analgesia, highlighted the potential significance of peripheral CB1-mediated cannabinoid analgesia, and revealed important insights into how the peripheral endocannabinoid system works in controlling both inflammatory pain and neuropathic pain.

Abstract 16884: Involvement of Hydrogen Sulfide (H2S) in Dexamethasone (DEX) Induced Hypertension in Rat

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Erminia Donnarumma ◽  
Emma Mitidieri ◽  
Teresa Tramontano ◽  
Vincenzo Brancaleone ◽  
Mariarosaria Bucci ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Shear Stress ◽  
Carotid Artery ◽  
Wistar Rats ◽  
Colorimetric Assay ◽  
Induced Hypertension ◽  
Effect Curve ◽  
Male Wistar Rats ◽  
H2s Production

Introduction: Glucocorticoid (GC) excess is related to hypertension. The deletion of endothelial GC-receptors abrogates the blood pressure increase, suggesting GC-induced hypertension is endothelium-dependent. In response to shear stress endothelium releases nitric oxide, endothelial derived hyperpolarizing factor (EDHF) and prostacyclin. Recently H2S has been proposed as a candidate for EDHF. H2S is mainly produced by the enzymes cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) from L-cysteine. The aim of this study was to investigate the EDHF/H2S signaling in GC-hypertension. Methods: Male Wistar rats were treated with DEX (1.5 mg/kg/sc) or vehicle (VEH) for 8 days. Systolic blood pressure (SBP) was monitored every 2 days. EDHF was evaluated in mesenteric plexus and carotid artery performing a concentration-effect curve of acetylcholine in presence of indomethacin (INDO) and nitro-L-arginine methyl ester (L-NAME). Apamin (APA) plus charibdotoxin (CTX), SKCa and BKCa inhibitors, or propargylglycine (PAG), CSE inhibitor, were used. CBS and CSE levels were analyzed by immunoblot. H2S levels were measured by a colorimetric assay. Results: DEX treatment significantly increased SBP compared to VEH (*p<0.05, **p<0.01, ***p<0.001 at days 2-4, 6, 8 respectively). EDHF-mediated relaxation of mesenteric bed or carotid artery was markedly reduced in DEX group compared to VEH (***p<0.001). APA and CTX as well as PAG abolished EDHF-mediated relaxation in DEX or VEH group (***,°°°p<0.001 respectively). CBS and CSE levels were significantly reduced in mesenteric plexus and carotid artery in DEX group (*p<0.05). The H2S production was markedly reduced in mesenteric plexus and carotid artery (*p<0.05, **p<0.01 respectively) as well as plasmatic H2S levels (*p<0.05) in DEX rats compared to VEH. Conclusions: Our data demonstrate that GC-excess induces an impairment of H2S/EDHF signaling indicating an additional cause of GC-mediated hypertension.

Myotoxic effects of clenbuterol in the rat heart and soleus muscle

2002 ◽  
Vol 93 (5) ◽  
pp. 1824-1832 ◽  
Author(s):  
Jatin G. Burniston ◽  
Yeelan Ng ◽  
William A. Clark ◽  
John Colyer ◽  
Lip-Bun Tan ◽  
...  
Keyword(s):  
Soleus Muscle ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Wistar Rats ◽  
Sampling Time ◽  
Irreversible Damage ◽  
Single Subcutaneous Injection ◽  
Male Wistar Rats ◽  
Adrenergic Receptor Agonist

Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic β2-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 ± 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 ± 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.

Insulin sensitivity is mediated by the activation of the ACh/NO/cGMP pathway in rat liver

2004 ◽  
Vol 287 (3) ◽  
pp. G527-G532 ◽  
Author(s):  
Maria P. Guarino ◽  
Nina C. Correia ◽  
W. Wayne Lautt ◽  
M. Paula Macedo
Keyword(s):  
Nitric Oxide ◽  
Insulin Sensitivity ◽  
Muscarinic Receptors ◽  
Wistar Rats ◽  
No Donor ◽  
Parasympathetic Nerves ◽  
Cgmp Pathway ◽  
Male Wistar Rats ◽  
Oxide Synthase

The hepatic parasympathetic nerves and hepatic nitric oxide synthase (NOS) are involved in the secretion of a hepatic insulin sensitizing substance (HISS), which mediates peripheral insulin sensitivity. We tested whether binding of ACh to hepatic muscarinic receptors is an upstream event to the synthesis of nitric oxide (NO), which, along with the activation of hepatic guanylate cyclase (GC), permits HISS release. Male Wistar rats (8–9 wk) were anesthetized with pentobarbital sodium (65 mg/kg). Insulin sensitivity was assessed using a euglycemic clamp [the rapid insulin sensitivity test (RIST)]. HISS inhibition was induced by antagonism of muscarinic receptors (atropine, 3 mg/kg iv) or by blockade of NOS [ NG-nitro-l-arginine methyl ester (l-NAME), 1 mg/kg intraportally (ipv)]. After the blockade, HISS action was tentatively restored using a NO donor [3-morpholynosydnonimine (SIN-1), 5–10 mg/kg ipv] or ACh (2.5–5 μg·kg−1·min−1 ipv). SIN-1 (10 mg/kg) reversed the inhibition caused by atropine (RIST postatropine 137.7 ± 8.3 mg glucose/kg; reversed to 288.3 ± 15.5 mg glucose/kg, n = 6) and by l-NAME (RIST post-l-NAME 152.2 ± 21.3 mg glucose/kg; reversed to 321.7 ± 44.7 mg glucose/kg, n = 5). ACh did not reverse HISS inhibition induced by l-NAME. The role of GC in HISS release was assessed using 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 5 nmol/kg ipv), a GC inhibitor that decreased HISS action (control RIST 237.6 ± 18.6 mg glucose/kg; RIST post-ODQ 111.7 ± 6.2 mg glucose/kg, n = 5). We propose that hepatic parasympathetic nerves release ACh, leading to hepatic NO synthesis, which activates GC, triggering HISS action.

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