Navegando por Palavras-chave "muscarinic acetylcholine receptors"
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- ItemSomente MetadadadosDeveloping skeletal muscle cells express functional muscarinic acetylcholine receptors coupled to different intracellular signaling systems(Nature Publishing Group, 2005-10-01) Furlan, Ingrid; Godinho, Rosely Oliveira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)1 This study analyzed the expression of muscarinic acetylcholine receptors (mAChRs) in the rat cultured skeletal muscle cells and their coupling to G protein, phospholipase C and adenylyl cyclase (AC).2 Our results showed the presence of a homogeneous population of [H-3]methyl-quinuclidinyl benzilate-binding sites in the membrane fraction from the rat cultured muscle (K-D = 0.4 nM, B-max = 8.9 fmol mg protein(-1)). Specific muscarinic binding sites were also detected in denervated diaphragm muscles from adult rats and in myoblasts isolated from newborn rats.3 Activation of mAChRs with carbachol induced specific [S-35]GTP gamma S binding to cultured muscle membranes and potentiated the forskolin-dependent stimulation of AC. These effects were totally inhibited by 0.1-1 mu M atropine.4 in addition, mAChRs were able to stimulate generation of diacylglycerol (DAG) in response to acetylcholine, carbachol or selective mAChR agonist oxotremorine-M.5 the carbachol-dependent increase in DAG was inhibited in a concentration-dependent manner by mAChR antagonists atropine, pirenzepine and 4-DAMP mustard.6 Finally, activation of these receptors was correlated with increased synthesis of acetylcholinesterase, via a PKC-dependent pathway.7 Taken together, these results indicate that expression of mAChRs, coupled to G protein and distinct intracellular signaling systems, is a characteristic of noninnervated skeletal muscle cells and may be responsible for trophic influences of acetylcholine during formation of the neuromuscular synapse.
- ItemSomente MetadadadosEffect of estrogen on muscarinic acetylcholine receptor expression in rat myometrium(Elsevier B.V., 2004-01-15) Abdalla, FMF; Marostica, E.; Picarelli, Z. P.; Abreu, L. C.; Avellar, MCW; Porto, C. S.; Universidade Federal de São Paulo (UNIFESP); Inst ButantanWe report the effect of acute estrogen treatment in the expression of muscarinic acetylcholine receptors (mAChRs) in myometrium. Strips were obtained from rats in estrus (control) and treated with estrogen, 24 It before the experiments. Reverse transcriptase-polymerase chain reaction (RT-PCR) was performed and m2, m3 and m5 mAChR mRNA subtypes were detected in myometrium from both groups. [H-3]Quinuclidinyl benzilate ([(3)HQNB]) binding studies indicated that estrogen treatment did not change the affinity and density of mAChRs in myometrial membranes. Displacement curves of [(3)HQNB] with different mAChRs antagonists indicated a one-site fit for all antagonists tested. Comparison of pK(i) values indicated a significant correlation to M-2-mAChR subtype. Functional studies, however, showed that estrogen treatment increased myometrium sensitivity to carbachol and the calculated apparent affinity values were significantly correlated to M-3-mAChR. Furthermore, the pharmacological profile of the two populations of mAChR was not affected by estrogen. in conclusion, these results provide evidence for the presence of M-2- and M-3-mAChR, at the mRNA and protein level, in the rat myometrium and indicate that estrogen induces an increase in myometrial responsiveness to mAChR agonists. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
- ItemSomente MetadadadosEffects of estrogen on intracellular signaling pathways linked to activation of muscarinic acetylcholine receptors and on acetylcholinesterase activity in rat hippocampus(Elsevier B.V., 2008-05-01) Santos Pereira, Renato Tavares dos; Porto, Catarina Segreti [UNIFESP]; Godinho, Rosely Oliveira [UNIFESP]; Francis Abdalla, Fernando Mauricio; Inst Butantan; Universidade Federal de São Paulo (UNIFESP)The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [H-3]inositol phosphate ([H-3]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippocampi were obtained from rats in proestrus (PE), ovariectomized for 15 days (C15), ovariectomized for 15 days and then treated with 17 beta-estradiol for 7 days (E7) and ovariectomized and immediately treated with 17 beta-estradiol for 21 days (E21). Ovariectomy did not change the basal level of total [H-3]IP in the hippocampus. 17 beta-Estradiol replacement (E7 and E21) reduced the basal level of total [H-3]IP. in all experimental groups, carbachol (CCh) caused a concentration -dependent rise in total [H-3]IP. the maximum effect was reached with 10(-4) M CCh. the response to 10(-4) M CCh in the hippocampi from C15 and E7 rats was twofold higher than in hippocampi from PE and E21 animals and was blocked by pirenzepine, but not by methoctramine. Ovariectomy or 17 beta-estradiol treatment for 7 days did not change neither the total acetylcholinesterase (AChE) activity nor the relative amount of mono- and dimeric G(1)/G(2) and tetrameric G(4) globular forms. Conversely, hormonal treatment for 21 days induced an increase in AChE activity of G(1)/G(2) and G(4) forms, indicating that 17 beta-estradiol stimulates both synthesis and assembly of AChE molecular forms. the present results suggest that the duration and/or a critical period with regard to the initiation of estrogen therapy are important to regulate the function of mAChRs and AChE activity in female rat hippocampus. (C) 2008 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosEffects of testosterone on muscarinic acetylcholine receptors in the rat epididymis(Elsevier B.V., 2005-06-24) Marostica, E.; Avellar, MCW; Porto, C. S.; Universidade Federal de São Paulo (UNIFESP)The effect of testosterone on the expression of muscarinic acetylcholine receptor (mAChR) subtypes was studied in the rat epididymis, at mRNA and protein level. the rat androgen status was monitored by measuring plasma testosterone level and caput and cauda epididymis wet weight. Ribonuclease protection assay (RPA) and [(3)H]quinuclidinyl benzilate ([(3)H]QNB) binding assay were performed in the caput and cauda epididymis from control (50-day old), castrated, castrated and treated with testosterone and sexually immature (30-day old) rats. the expression of each mAChR transcript subtype differed depending on the epididymal region analyzed and rat testosterone and/or testicular factors status. in control rats, RPA showed the presence of mRNA for M(1), M(2) and M(3) mAChR in the caput and cauda epididymis. the abundance of m2 and m3 transcripts in the cauda was higher than that in the caput epididymis. Low amount of m1 transcript was observed in both regions. Orchidectomy increased m1 mRNA amount in the caput and cauda epididymis when compared to control rats, an effect slightly modified by testosterone replacement. Although orchidectomy down-regulated the level of m2 transcript in both epididymal regions, castration significantly increased m3 mRNA amount in the caput region. These effects on m2 and m3 transcripts were prevented by testosterone replacement to castrated rats. Similar abundance of m3 transcript, however, was detected in the cauda epididymis of all experimental group tested. [ (3)H]QNB binding studies revealed that orchidectomy down-regulated the number of mAChR detected in both epididymal regions, an effect also prevented by testosterone replacement. Thus, testosterone and/or testicular factors may play a role in the regulation of mAChR expression in the rat epididymis. (c) 2005 Elsevier Inc. All rights reserved.
- ItemAcesso aberto (Open Access)Expression and function of G-protein-coupled receptorsin the male reproductive tract(Academia Brasileira de Ciências, 2009-09-01) Avellar, Maria Christina Werneck [UNIFESP]; Lazari, Maria de Fatima Magalhaes [UNIFESP]; Porto, Catarina Segreti [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)This review focuses on the expression and function of muscarinic acetylcholine receptors (mAChRs), α1-adrenoceptors and relaxin receptors in the male reproductive tract. The localization and differential expression of mAChR and α1-adrenoceptor subtypes in specific compartments of the efferent ductules, epididymis, vas deferens, seminal vesicle and prostate of various species indicate a role for these receptors in the modulation of luminal fluid composition and smooth muscle contraction, including effects on male fertility. Furthermore, the activation of mAChRs induces transactivation of the epidermal growth factor receptor (EGFR) and the Sertoli cell proliferation. The relaxin receptors are present in the testis, RXFP1 in elongated spermatids and Sertoli cells from rat, and RXFP2 in Leydig and germ cells from rat and human, suggesting a role for these receptors in the spermatogenic process. The localization of both receptors in the apical portion of epithelial cells and smooth muscle layers of the vas deferens suggests an involvement of these receptors in the contraction and regulation of secretion.