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  1 / 12772 MEDLINE  
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[PMID]:28462392
[Au] Autor:Li WC; Zhu XY; Ritson E
[Ad] Endereço:University of St Andrews, St Andrews, Fife KY16 9JP, Scotland.
[Ti] Título:Mechanosensory Stimulation Evokes Acute Concussion-Like Behavior by Activating GIRKs Coupled to Muscarinic Receptors in a Simple Vertebrate.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Most vertebrates show concussion responses when their heads are hit suddenly by heavy objects. Previous studies have focused on the direct physical injuries to the neural tissue caused by the concussive blow. We study a similar behavior in a simple vertebrate, the tadpole. We find that concussion-like behavior can be reliably induced by the mechanosensory stimulation of the head skin without direct physical impacts on the brain. Head skin stimulation activates a cholinergic pathway which then opens G protein-coupled inward-rectifying potassium channels (GIRKs) via postsynaptic M muscarinic receptors to inhibit brainstem neurons critical for the initiation and maintenance of swimming for up to minutes and can explain many features commonly observed immediately after concussion. We propose that some acute symptoms of concussion in vertebrates can be explained by the opening of GIRKs following mechanosensory stimulation to the head.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/metabolismo
Neurônios/metabolismo
Receptores Muscarínicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Concussão Encefálica/metabolismo
Tronco Encefálico/metabolismo
Seres Humanos
Oócitos/metabolismo
Vertebrados/metabolismo
Xenopus laevis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels); 0 (Receptors, Muscarinic); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  2 / 12772 MEDLINE  
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[PMID]:29311507
[Au] Autor:Sumiyoshi T
[Ad] Endereço:Department of Life Science and Biotechnology, Faculty of Chemistry, Materials and Bioengineering, Kansai University.
[Ti] Título:Foreword.
[So] Source:Chem Pharm Bull (Tokyo);66(1):20, 2018.
[Is] ISSN:1347-5223
[Cp] País de publicação:Japan
[La] Idioma:eng
[Mh] Termos MeSH primário: Peptídeos/farmacologia
Receptores Muscarínicos/metabolismo
[Mh] Termos MeSH secundário: Química Farmacêutica
Descoberta de Drogas
Seres Humanos
Peptídeos/química
[Pt] Tipo de publicação:INTRODUCTORY JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides); 0 (Receptors, Muscarinic)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1248/cpb.c18-ctf6601


  3 / 12772 MEDLINE  
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[PMID]:28470123
[Au] Autor:Dojo K; Yamaguchi Y; Fustin JM; Doi M; Kobayashi M; Okamura H
[Ad] Endereço:Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto, Japan.
[Ti] Título:Carbachol Induces Phase-dependent Phase Shifts of Per1 Transcription Rhythms in Cultured Suprachiasmatic Nucleus Slices.
[So] Source:J Biol Rhythms;32(2):101-108, 2017 Apr.
[Is] ISSN:1552-4531
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Among nonphotic stimulants, a classic cholinergic agonist, carbachol, is known to have a strong and unique phase-resetting effect on the circadian clock: Intracerebroventricular carbachol treatment causes phase delays during the subjective early night and phase advances in the subjective late night, but the effects of this drug on the suprachiasmatic nucleus (SCN) in vivo and in vitro are still controversial. In the present study, we succeeded in reproducing the biphasic phase-shifting effect of carbachol on clock gene expression in organotypic SCN slices prepared from mice carrying a Per1-promoter fused luciferase gene ( Per1-luc). Since this biphasic effect of carbachol in Per1-luc SCN was prevented by atropine but not by mecamylamine, we concluded that these phase shifts were muscarinic receptor-dependent. Next, we analyzed the expression of muscarinic receptors in the SCN by in situ hybridization and found that M3 and M4 subtypes were expressed in SCN cells. These signals appeared neonatally and reached adult levels at postnatal day 10. Together, these findings suggest that carbachol has a phase-dependent phase-shifting effect on the SCN clock through muscarinic receptor subtypes expressed in the SCN.
[Mh] Termos MeSH primário: Carbacol/farmacologia
Agonistas Colinérgicos/farmacologia
Ritmo Circadiano/efeitos dos fármacos
Proteínas Circadianas Period/genética
Núcleo Supraquiasmático/efeitos dos fármacos
Núcleo Supraquiasmático/fisiologia
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Atropina/farmacologia
Relógios Circadianos/efeitos dos fármacos
Expressão Gênica
Luciferases/genética
Mecamilamina/farmacologia
Camundongos
Atividade Motora
Antagonistas Muscarínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Técnicas de Cultura de Órgãos
Regiões Promotoras Genéticas
Receptores Muscarínicos/genética
Receptores Muscarínicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agonists); 0 (Muscarinic Antagonists); 0 (Nicotinic Antagonists); 0 (Per1 protein, mouse); 0 (Period Circadian Proteins); 0 (Receptors, Muscarinic); 6EE945D3OK (Mecamylamine); 7C0697DR9I (Atropine); 8Y164V895Y (Carbachol); EC 1.13.12.- (Luciferases)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1177/0748730417691205


  4 / 12772 MEDLINE  
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[PMID]:29283235
[Au] Autor:Silkis IG; Makechiv VA
[Ti] Título:Possible Mechanisms of Influence of Various Concentrations of Acetylcholine on Hippocampal Functioning.
[So] Source:Usp Fiziol Nauk;47(4):57-75, 2016 Oct-Dec.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Analysis of features of influence of acetylcholine on the hippocampal functioning was performed basing on the modulation rules for the efficacy of excitatory and inhibitory synaptic transmission we earlier proposed, and also on the known data about location of pre- and postsynaptic muscarine and nicotinic receptors. According to these rules, activation of postsynaptic muscarine М1/М3 and nicotinic receptors should promote long-term potentiation of excitatory and depressions (LTD) of inhibitory input to a neuron, whereas action on М2/М4 receptors should promote LTD of excitatory input and a decrease in neuromodulator release. If inhibitory input is stronger than excitatory, LTP (LTD) of excitatory input to the interneuron should promote LTD (LTP) of excitatory input to a target cell. It follows from the proposed mechanism that a lowing concentration of acetylcholine in the hippocampus, a decrease in density of М1/ М3 and a4p2 receptors, and augmenting binding of М2 receptors must lead to a depression of responses of pyramidal neurons in СА3 and СА1 fields to signals from the entorhinal cortex. Thereof, interaction of the semantic information, stored in the cortex, with the information of an episode-, stored in the hippocampus must be hindered and this effect can underlie disturbances of recall of stored information at Alzheimer's disease.
[Mh] Termos MeSH primário: Acetilcolina/farmacologia
Doença de Alzheimer/metabolismo
Agonistas Colinérgicos/farmacologia
Hipocampo/efeitos dos fármacos
Potenciação de Longa Duração/efeitos dos fármacos
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Doença de Alzheimer/genética
Doença de Alzheimer/fisiopatologia
Animais
Agonistas Colinérgicos/metabolismo
Córtex Entorrinal/efeitos dos fármacos
Córtex Entorrinal/fisiologia
Regulação da Expressão Gênica
Hipocampo/fisiologia
Seres Humanos
Potenciação de Longa Duração/fisiologia
Depressão Sináptica de Longo Prazo/fisiologia
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Receptores Muscarínicos/genética
Receptores Muscarínicos/metabolismo
Receptores Nicotínicos/genética
Receptores Nicotínicos/metabolismo
Sinapses/efeitos dos fármacos
Sinapses/fisiologia
Transmissão Sináptica/efeitos dos fármacos
Transmissão Sináptica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cholinergic Agonists); 0 (Receptors, Muscarinic); 0 (Receptors, Nicotinic); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE


  5 / 12772 MEDLINE  
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[PMID]:28609709
[Au] Autor:Del Bello F; Bonifazi A; Giorgioni G; Petrelli R; Quaglia W; Altomare A; Falcicchio A; Matucci R; Vistoli G; Piergentili A
[Ad] Endereço:Scuola di Scienze del Farmaco e dei Prodotti della Salute, Università di Camerino, Via S. Agostino 1, 62032 Camerino, Italy.
[Ti] Título:Novel muscarinic acetylcholine receptor hybrid ligands embedding quinuclidine and 1,4-dioxane fragments.
[So] Source:Eur J Med Chem;137:327-337, 2017 Sep 08.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:To obtain novel muscarinic acetylcholine receptor (mAChR) antagonists, the enantiomers of the hybrid compounds 3-5, in which the quinuclidin-3-yloxy fragment of solifenacin and the 6,6-diphenyl-1,4-dioxane-2-yl moiety of 2 linked by an ester or ether spacer were embedded in the same chemical entity, were prepared and evaluated for their affinity at the five mAChR subtypes (M -M ). Stereochemistry and the nature of the linker between the quinuclidine moiety and the 1,4-dioxane nucleus play an important role on the affinities of the compounds. The presence of an ether bridge confers higher affinities for all mAChR subtypes to the ligand. Interestingly, the ether enantiomer (R,S)-5 shows the highest affinity at all mAChR subtypes with pK values similar to that of solifenacin at M and higher at the other subtypes. Unlike solifenacin, it shows a preference for M mAChR subtype with respect to the other subtypes. This compound, lacking a permanent positive charge on the nitrogen atom, can be a useful tool for the pharmacological study of mAChRs in the central nervous system.
[Mh] Termos MeSH primário: Dioxanos/farmacologia
Antagonistas Muscarínicos/farmacologia
Quinuclidinas/farmacologia
Receptores Muscarínicos/metabolismo
[Mh] Termos MeSH secundário: Dioxanos/síntese química
Dioxanos/química
Relação Dose-Resposta a Droga
Seres Humanos
Ligantes
Estrutura Molecular
Antagonistas Muscarínicos/síntese química
Antagonistas Muscarínicos/química
Quinuclidinas/síntese química
Quinuclidinas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dioxanes); 0 (Ligands); 0 (Muscarinic Antagonists); 0 (Quinuclidines); 0 (Receptors, Muscarinic); J8A3S10O7S (1,4-dioxane)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE


  6 / 12772 MEDLINE  
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[PMID]:28587876
[Au] Autor:Scarduzio M; Zimmerman CN; Jaunarajs KL; Wang Q; Standaert DG; McMahon LL
[Ad] Endereço:Department of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
[Ti] Título:Strength of cholinergic tone dictates the polarity of dopamine D2 receptor modulation of striatal cholinergic interneuron excitability in DYT1 dystonia.
[So] Source:Exp Neurol;295:162-175, 2017 Sep.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Balance between cholinergic and dopaminergic signaling is central to striatal control of movement and cognition. In dystonia, a common disorder of movement, anticholinergic therapy is often beneficial. This observation suggests there is a pathological increase in cholinergic tone, yet direct confirmation is lacking. In DYT1, an early-onset genetic form of dystonia caused by a mutation in the protein torsinA (TorA), the suspected heightened cholinergic tone is commonly attributed to faulty dopamine D2 receptor (D2R) signaling where D2R agonists cause excitation of striatal cholinergic interneurons (ChIs), rather than the normal inhibition of firing observed in wild-type animals, an effect known as "paradoxical excitation". Here, we provide for the first time direct measurement of elevated striatal extracellular acetylcholine (ACh) in a knock-in mouse model of human DYT1 dystonia (TorA mice), confirming a striatal hypercholinergic state. We hypothesized that this elevated extracellular ACh might cause chronic over-activation of muscarinic acetylcholine receptors (mAChRs) and disrupt normal D2R function due to their shared coupling to G -proteins. We tested this concept in vitro first using a broad-spectrum mAChR antagonist, and then using a M2/M4 mAChR selective antagonist to specifically target mAChRs expressed by ChIs. Remarkably, we found that mAChR inhibition reverses the D2R-mediated paradoxical excitation of ChIs recorded in slices from TorA mice to a typical inhibitory response. Furthermore, we recapitulated the paradoxical D2R excitation of ChIs in striatal slices from wild-type mice within minutes by simply increasing cholinergic tone through pharmacological inhibition of acetylcholinesterase (AChE) or by prolonged agonist activation of mAChRs. Collectively, these results show that enhanced mAChR tone itself is sufficient to rapidly reverse the polarity of D2R regulation of ChI excitability, correcting the previous notion that the D2R mediated paradoxical ChI excitation causes the hypercholinergic state in dystonia. Further, using a combination of genetic and pharmacological approaches, we found evidence that this switch in D2R polarity results from a change in coupling from the preferred G pathway to non-canonical ß-arrestin signaling. These results highlight the need to fully understand how the mutation in TorA leads to pathologically heightened extracellular ACh. Furthermore the discovery of this novel ACh-dopamine interaction and the participation of ß-arrestin in regulation of cholinergic interneurons is likely important for other basal ganglia disorders characterized by perturbation of ACh-dopamine balance, including Parkinson and Huntington diseases, l-DOPA-induced dyskinesia and schizophrenia.
[Mh] Termos MeSH primário: Distonia/genética
Distonia/fisiopatologia
Interneurônios
Chaperonas Moleculares/genética
Neostriado/fisiopatologia
Sistema Nervoso Parassimpático/fisiopatologia
Receptores de Dopamina D2/metabolismo
[Mh] Termos MeSH secundário: Acetilcolina/metabolismo
Animais
Inibidores da Colinesterase/farmacologia
Técnicas de Introdução de Genes
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Chaperonas Moleculares/metabolismo
Neostriado/metabolismo
Sistema Nervoso Parassimpático/citologia
Receptores Muscarínicos/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinesterase Inhibitors); 0 (DRD2 protein, mouse); 0 (Molecular Chaperones); 0 (Receptors, Dopamine D2); 0 (Receptors, Muscarinic); 0 (TOR1A protein, human); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE


  7 / 12772 MEDLINE  
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[PMID]:28559376
[Au] Autor:Pezze MA; Marshall HJ; Cassaday HJ
[Ad] Endereço:School of Psychology, University of Nottingham, Nottingham NG7 2RD, United Kingdom.
[Ti] Título:Scopolamine Impairs Appetitive But Not Aversive Trace Conditioning: Role of the Medial Prefrontal Cortex.
[So] Source:J Neurosci;37(26):6289-6298, 2017 Jun 28.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The muscarinic acetylcholine receptor is an important modulator of medial prefrontal cortex (mPFC) functions, such as the working memory required to bridge a trace interval in associative leaning. Aversive and appetitive trace conditioning procedures were used to examine the effects of scopolamine (0.1 and 0.5 mg/kg, i.p.) in male rats. Follow-up experiments tested the effects of microinfusion of 0.15 µg of scopolamine (0.075 µg of in 0.5 µl/side) in infralimbic (IL) versus prelimbic regions of rat mPFC, in appetitive trace and locomotor activity (LMA) procedures. Systemic scopolamine was without effect in an aversive trace conditioning procedure, but impaired appetitive conditioning at a 2 s trace interval. This effect was demonstrated as reduced responding during presentations of the conditioned stimulus (CS) and during the interstimulus interval (ISI). There was no such effect on responding during food (unconditioned stimulus, US) responding or in the intertrial interval (ITI). In contrast, systemic scopolamine dose-relatedly increased LMA. Trace conditioning was similarly impaired at the 2 s trace (shown as reduced responding to the CS and during the ISI, but not during US presentations or in the ITI) after infusion in mPFC, whereas LMA was increased (after infusion in IL only). Therefore, our results point to the importance of cholinergic modulation in mPFC for trace conditioning and show that the observed effects cannot be attributed to reduced activity. Events are very often separated in time, in which case working memory is necessary to condition their association in "trace conditioning." The present study used conditioning variants motivated aversively with foot shock and appetitively with food. The drug scopolamine was used to block muscarinic acetylcholine receptors involved in working memory. The results show that reduced cholinergic transmission in medial prefrontal cortex (mPFC) impaired appetitive trace conditioning at a 2 s trace interval. However, scopolamine was without effect in the aversive procedure, revealing the importance of procedural differences to the demonstration of the drug effect. The finding that blockade of muscarinic receptors in mPFC impaired trace conditioning shows that these receptors are critical modulators of short-term working memory.
[Mh] Termos MeSH primário: Apetite/fisiologia
Condicionamento Clássico/fisiologia
Memória de Curto Prazo/fisiologia
Córtex Pré-Frontal/fisiologia
Receptores Muscarínicos/metabolismo
Hidrobrometo de Escopolamina/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Apetite/efeitos dos fármacos
Condicionamento Clássico/efeitos dos fármacos
Relação Dose-Resposta a Droga
Extinção Psicológica
Masculino
Memória de Curto Prazo/efeitos dos fármacos
Antagonistas Muscarínicos/administração & dosagem
Rede Nervosa/efeitos dos fármacos
Rede Nervosa/fisiologia
Córtex Pré-Frontal/efeitos dos fármacos
Ratos
Ratos Wistar
Retenção (Psicologia)
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Muscarinic Antagonists); 0 (Receptors, Muscarinic); 451IFR0GXB (Scopolamine Hydrobromide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3308-16.2017


  8 / 12772 MEDLINE  
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[PMID]:28472649
[Au] Autor:Foster DJ; Conn PJ
[Ad] Endereço:Department of Pharmacology, Vanderbilt University, Nashville, TN 37232, USA; Vanderbilt Center for Neuroscience Drug Discovery, Vanderbilt University, Nashville, TN 37232, USA.
[Ti] Título:Allosteric Modulation of GPCRs: New Insights and Potential Utility for Treatment of Schizophrenia and Other CNS Disorders.
[So] Source:Neuron;94(3):431-446, 2017 May 03.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:G-protein-coupled receptors (GPCRs) play critical roles in regulating brain function. Recent advances have greatly expanded our understanding of these receptors as complex signaling machines that can adopt numerous conformations and modulate multiple downstream signaling pathways. While agonists and antagonists have traditionally been pursued to target GPCRs, allosteric modulators provide several mechanistic advantages, including the ability to distinguish between closely related receptor subtypes. Recently, the discovery of allosteric ligands that confer bias and modulate some, but not all, of a given receptor's downstream signaling pathways can provide pharmacological modulation of brain circuitry with remarkable precision. In addition, allosteric modulators with unprecedented specificity have been developed that can differentiate between subpopulations of a given receptor subtype based on the receptor's dimerization state. These advances are not only providing insight into the biological roles of specific receptor populations, but hold great promise for treating numerous CNS disorders.
[Mh] Termos MeSH primário: Regulação Alostérica/efeitos dos fármacos
Antipsicóticos/farmacologia
Receptores Dopaminérgicos/efeitos dos fármacos
Receptores de Glutamato Metabotrópico/efeitos dos fármacos
Receptores Muscarínicos/efeitos dos fármacos
Esquizofrenia/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antipsicóticos/uso terapêutico
Doenças do Sistema Nervoso Central/tratamento farmacológico
Cognição/efeitos dos fármacos
Seres Humanos
Córtex Pré-Frontal/efeitos dos fármacos
Receptor de Glutamato Metabotrópico 5/efeitos dos fármacos
Receptor Muscarínico M4/efeitos dos fármacos
Receptores Acoplados a Proteínas-G/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (Receptor, Metabotropic Glutamate 5); 0 (Receptor, Muscarinic M4); 0 (Receptors, Dopamine); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Metabotropic Glutamate); 0 (Receptors, Muscarinic); 0 (metabotropic glutamate receptor type 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  9 / 12772 MEDLINE  
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[PMID]:28436626
[Au] Autor:Wang Y; Wang Y; Chen Z
[Ad] Endereço:College of Pharmaceutial Science, Zhejiang University, Hangzhou 310058, China.
[Ti] Título:[The role of central cholinergic system in epilepsy].
[So] Source:Zhejiang Da Xue Xue Bao Yi Xue Ban;46(1):15-21, 2017 Jan 25.
[Is] ISSN:1008-9292
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Epilepsy is a chronic neurological disorder, which is not only related to the imbalance between excitatory glutamic neurons and inhibitory GABAergic neurons, but also related to abnormal central cholinergic regulation. This article summarizes the scientific background and experimental data about cholinergic dysfunction in epilepsy from both cellular and network levels, further discusses the exact role of cholinergic system in epilepsy. In the cellular level, several types of epilepsy are believed to be associated with aberrant metabotropic muscarinic receptors in several different brain areas, while the mutations of ionotropic nicotinic receptors have been reported to result in a specific type of epilepsy-autosomal dominant nocturnal frontal lobe epilepsy. In the network level, cholinergic projection neurons as well as their interaction with other neurons may regulate the development of epilepsy, especially the cholinergic circuit from basal forebrain to hippocampus, while cholinergic local interneurons have not been reported to be associated with epilepsy. With the development of optogenetics and other techniques, dissect and regulate cholinergic related epilepsy circuit has become a hotspot of epilepsy research.
[Mh] Termos MeSH primário: Neurônios Colinérgicos/química
Neurônios Colinérgicos/patologia
Neurônios Colinérgicos/fisiologia
Epilepsia/genética
Epilepsia/patologia
Epilepsia/fisiopatologia
Sistema Colinérgico não Neuronal/fisiologia
[Mh] Termos MeSH secundário: Acetilcolina/fisiologia
Prosencéfalo Basal/patologia
Química Encefálica/genética
Química Encefálica/fisiologia
Neurônios Colinérgicos/classificação
Epilepsia do Lobo Frontal/genética
Neurônios GABAérgicos/fisiologia
Hipocampo/patologia
Seres Humanos
Mutação/genética
Mutação/fisiologia
Neurônios
Sistema Colinérgico não Neuronal/genética
Receptores Muscarínicos/genética
Receptores Muscarínicos/fisiologia
Receptores Nicotínicos/genética
Receptores Nicotínicos/fisiologia
Transmissão Sináptica/genética
Transmissão Sináptica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Muscarinic); 0 (Receptors, Nicotinic); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE


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[PMID]:28432022
[Au] Autor:Pelissier-Rota M; Chartier NT; Bonaz B; Jacquier-Sarlin MR
[Ad] Endereço:Université Grenoble Alpes, Grenoble Institut des Neurosciences, GIN, F-38000 Grenoble, France; INSERM U1216, F-38000 Grenoble, France.
[Ti] Título:A crosstalk between muscarinic and CRF2 receptors regulates cellular adhesion properties of human colon cancer cells.
[So] Source:Biochim Biophys Acta;1864(7):1246-1259, 2017 07.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Patients with inflammatory bowel disease often suffer from chronic and relapsing intestinal inflammation that favor the development of colitis associated cancer. An alteration of the epithelial intestinal barrier function observed in IBD is supposed to be a consequence of stress. It has been proposed that corticotrophin-releasing factor receptor (CRF2), one of the two receptors of CRF, the principal neuromediator of stress, acts on cholinergic nerves to induce stress-mediated epithelial barrier dysfunction. Non-neuronal acetylcholine (Ach) and muscarinic receptors (mAchR) also contribute to alterations of epithelial cell functions. In this study, we investigated the mechanisms through which stress and Ach modulate epithelial cell adhesive properties. We show that Ach-induced activation of mAchR in HT-29 cells results in cell dissociation together with changes in cell-matrix contacts, which correlates with the acquisition of invasive potential consistent with a matrix metalloproteinase (MMP) mode of invasion. These processes result from mAchR subsequent stimulation of the cascade of src/Erk and FAK activation. Ach-induced secretion of laminin 332 leads to α3ß1 integrin activation and RhoA-dependent reorganization of the actin cytoskeleton. We show that Ach-mediated effects on cell adhesion are blocked by astressin 2b, a CRF2 antagonist, suggesting that Ach action depends partly on CRF2 signaling. This is reinforced by the fact that Ach-mediated activation of mAchR stimulates both the synthesis and the release of CRF2 ligands in HT-29 cells (effects blocked by atropine). In summary, our data provides evidence for a novel intracellular circuit involving mAchR acting on CRF2-signaling that could mediate colonic mucosal barrier dysfunction and exacerbate mucosal inflammation.
[Mh] Termos MeSH primário: Adesão Celular
Receptores de Hormônio Liberador da Corticotropina/metabolismo
Receptores Muscarínicos/metabolismo
[Mh] Termos MeSH secundário: Hormônio Liberador da Corticotropina/farmacologia
Enterócitos/efeitos dos fármacos
Enterócitos/metabolismo
Células HT29
Seres Humanos
Integrina alfa3beta1/metabolismo
Laminina/metabolismo
Antagonistas Muscarínicos/farmacologia
Fragmentos de Peptídeos/farmacologia
Receptores de Hormônio Liberador da Corticotropina/antagonistas & inibidores
Transdução de Sinais
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CRF receptor type 2); 0 (Integrin alpha3beta1); 0 (Laminin); 0 (Muscarinic Antagonists); 0 (Peptide Fragments); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (Receptors, Muscarinic); 170809-51-5 (astressin); 9015-71-8 (Corticotropin-Releasing Hormone); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE



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