scholarly journals NMDA Receptors and the L-Arginine–Nitric Oxide–Cyclic Guanosine Monophosphate Pathway Are Implicated in the Antidepressant-Like Action of the Ethanolic Extract fromTabebuia avellanedaein Mice

2013 ◽  
Vol 16 (11) ◽  
pp. 1030-1038 ◽  
Author(s):  
Andiara E. Freitas ◽  
Morgana Moretti ◽  
Josiane Budni ◽  
Grasiela O. Balen ◽  
Sinara C. Fernandes ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nmda Receptors ◽  
Ethanolic Extract ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate

Antidepressant-like effect of folic acid: Involvement of NMDA receptors and l-arginine-nitric oxide-cyclic guanosine monophosphate pathway

2008 ◽  
Vol 598 (1-3) ◽  
pp. 37-42 ◽  
Author(s):  
Patrícia de Souza Brocardo ◽  
Josiane Budni ◽  
Kelly Ribas Lobato ◽  
Manuella Pinto Kaster ◽  
Ana Lúcia S. Rodrigues
Keyword(s):  
Nitric Oxide ◽  
Folic Acid ◽  
Nmda Receptors ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate

scholarly journals Cyclic Guanosine Monophosphate Modulates Locomotor Acceleration Induced by Nitric Oxide but not Serotonin in Clione limacina Central Pattern Generator Swim Interneurons

2020 ◽  
Author(s):  
Thomas J Pirtle ◽  
Richard A Satterlie
Keyword(s):  
Nitric Oxide ◽  
Central Pattern Generator ◽  
Guanylyl Cyclase ◽  
Signal Transduction Pathway ◽  
Soluble Guanylyl Cyclase ◽  
Cyclic Guanosine Monophosphate ◽  
Pattern Generator ◽  
Guanosine Monophosphate ◽  
Cellular Changes ◽  
Clione Limacina

Abstract Typically, the marine mollusk, Clione limacina, exhibits a slow, hovering locomotor gait to maintain its position in the water column. However, the animal exhibits behaviorally relevant locomotor swim acceleration during escape response and feeding behavior. Both nitric oxide and serotonin mediate this behavioral swim acceleration. In this study, we examine the role that the second messenger, cGMP, plays in mediating nitric oxide and serotonin-induced swim acceleration. We observed that the application of an analog of cGMP or an activator of soluble guanylyl cyclase increased fictive locomotor speed recorded from Pd-7 interneurons of the animal’s locomotor central pattern generator. Moreover, inhibition of soluble guanylyl cyclase decreased fictive locomotor speed. These results suggest that basal levels of cGMP are important for slow swimming and that increased production of cGMP mediates swim acceleration in Clione. Because nitric oxide has its effect through cGMP signaling and because we show herein that cGMP produces cellular changes in Clione swim interneurons that are consistent with cellular changes produced by serotonin application, we hypothesize that both nitric oxide and serotonin function via a common signal transduction pathway that involves cGMP. Our results show that cGMP mediates nitric oxide-induced but not serotonin-induced swim acceleration in Clione.

The nitric oxide–cGMP signaling pathway plays a significant role in tolerance to the analgesic effect of morphine

2011 ◽  
Vol 89 (2) ◽  
pp. 89-95 ◽  
Author(s):  
Ercan Ozdemir ◽  
Ihsan Bagcivan ◽  
Nedim Durmus ◽  
Ahmet Altun ◽  
Sinan Gursoy
Keyword(s):  
Nitric Oxide ◽  
Analgesic Effect ◽  
Soluble Guanylate Cyclase ◽  
Morphine Tolerance ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Albino Rats ◽  
Tail Flick ◽  
Analgesic Effects ◽  
Cgmp Signaling

Although the phenomenon of opioid tolerance has been widely investigated, neither opioid nor nonopioid mechanisms are completely understood. The aim of the present study was to investigate the role of the nitric oxide (NO)–cyclic guanosine monophosphate (cGMP) pathway in the development of morphine-induced analgesia tolerance. The study was carried out on male Wistar albino rats (weighing 180–210 g; n = 126). To develop morphine tolerance, animals were given morphine (50 mg/kg; s.c.) once daily for 3 days. After the last dose of morphine was injected on day 4, morphine tolerance was evaluated. The analgesic effects of 3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole (YC-1), BAY 41-2272, S-nitroso-N-acetylpenicillamine (SNAP), NG-nitro-l-arginine methyl ester (L-NAME), and morphine were considered at 15 or 30 min intervals (0, 15, 30, 60, 90, and 120 min) by tail-flick and hot-plate analgesia tests (n = 6 in each study group). The results showed that YC-1 and BAY 41-2272, a NO-independent activator of soluble guanylate cyclase (sGC), significantly increased the development and expression of morphine tolerance, and L-NAME, a NO synthase (NOS) inhibitor, significantly decreased the development of morphine tolerance. In conclusion, these data demonstrate that the nitric oxide–cGMP signal pathway plays a pivotal role in developing tolerance to the analgesic effect of morphine.

Nitric Oxide/Cyclic Guanosine Monophosphate Signalling Mediates an Inhibitory Action on Sensory Pathways of the Micturition Reflex in the Rat

2010 ◽  
Vol 58 (4) ◽  
pp. 616-625 ◽  
Author(s):  
Romain Caremel ◽  
Stephanie Oger-Roussel ◽  
Delphine Behr-Roussel ◽  
Philippe Grise ◽  
François A. Giuliano
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Action ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Micturition Reflex ◽  
Sensory Pathways

Distinct regulation of nitric oxide and cyclic guanosine monophosphate production by steroid hormones in the rat uterus

2000 ◽  
Vol 6 (5) ◽  
pp. 404-414 ◽  
Author(s):  
Irina A. Buhimschi ◽  
Chandreskar Yallampalli ◽  
Catalin S. Buhimschi ◽  
George R. Saade ◽  
Robert E. Garfield
Keyword(s):  
Nitric Oxide ◽  
Steroid Hormones ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Rat Uterus
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