Muscarinic receptor-mediated excitation of rat intracardiac ganglion neurons

Hirayama, Masayuki; Ogata, Masao; Kawamata, Tomoyuki; Ishibashi, Hiroyuki

doi:10.1016/j.neuropharm.2015.04.014

Cited by 7 publications

(2 citation statements)

References 59 publications

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“…To study the effect of intracellular Ca 2+ levels on the nanoscale organization and first-order phase transition of endogenous SAP97/hDLG, we relied on a pharmacological approach to modulate cytosolic Ca 2+ levels. We incubated the cells with Thapsigargin (Tg) (1 µM) 42 – 44 for elevating intracellular Ca 2+ and with the membrane-permeable BAPTA-AM (Bapta) (50 µM) 45 to chelate the soluble Ca 2+ present in the cell. To confirm differential sensitivity of SAP97/hDLG to [Ca 2+ .CaM], we inhibited the Ca 2+ sensing ability of CaM using w7 (25 µM) 46 , 47 .…”

Section: Resultsmentioning

confidence: 99%

Nanoscale regulation of Ca2+ dependent phase transitions and real-time dynamics of SAP97/hDLG

et al. 2022

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Synapse associated protein-97/Human Disk Large (SAP97/hDLG) is a conserved, alternatively spliced, modular, scaffolding protein critical in regulating the molecular organization of cell-cell junctions in vertebrates. We confirm that the molecular determinants of first order phase transition of SAP97/hDLG is controlled by morpho-functional changes in its nanoscale organization. Furthermore, the nanoscale molecular signatures of these signalling islands and phase transitions are altered in response to changes in cytosolic Ca2+. Additionally, exchange kinetics of alternatively spliced isoforms of the intrinsically disordered region in SAP97/hDLG C-terminus shows differential sensitivities to Ca2+ bound Calmodulin, affirming that the molecular signatures of local phase transitions of SAP97/hDLG depends on their nanoscale heterogeneity and compositionality of isoforms.

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Section: Resultsmentioning

confidence: 99%

Nanoscale regulation of Ca2+ dependent phase transitions and real-time dynamics of SAP97/hDLG

et al. 2022

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“…The genes give rise to five, functionally divided subtypes, M1‐M5. M1, M3 and M5 receptors are G q/11 coupled and stimulated by the phospholipase Cβ (PLC) and inositol trisphosphate (IP3) signal transduction pathways to increase cytosolic calcium levels . M2 and M4 receptors, in contrast, are G i/o coupled and inhibit the cAMP‐dependent pathway via inhibition of adenylyl cyclase (AC) …”

Section: Muscarinic Acetylcholine Receptorsmentioning

confidence: 99%

Muscarinic receptors in energy homeostasis: Physiology and pharmacology

Falk

Lund

Clemmensen

2019

Basic Clin Pharma Tox

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Despite increased awareness and intensified biomedical research efforts, the prevalence of obesity continues to rise worldwide. This is alarming, because obesity accelerates the progression of several chronic disorders, including type 2 diabetes, cancer and cardiovascular disease. Individuals who experience significant weight loss must combat powerful counter-regulatory energy homeostatic processes, and, typically, most individuals regain the lost weight. Therefore, decoding the neural mechanisms underlying the regulation of energy homeostasis is necessary for developing breakthroughs in obesity management. It has been known for decades that cholinergic neurotransmission both directly and indirectly modulates energy homeostasis and metabolic health. Despite this insight, the molecular details underlying the modulation remain ill-defined, and the potential for targeting cholinergic muscarinic receptors for treating metabolic disease is largely uncharted. In this MiniReview, we scrutinize the literature that has formed our knowledge of muscarinic acetylcholine receptors (mAChRs) in energy homeostasis. The role of mAChRs in canonical appetite-regulating circuits will be discussed as will the more indirect regulation of energy homoeostasis via neurocircuits linked to motivated behaviours and emotional states. Finally, we discuss the therapeutic prospects of targeting mAChRs for the treatment of obesity and type 2 diabetes. K E Y W O R D Sacetylcholine, energy metabolism, GPCR, muscarinic, obesity, pharmacology, type 2 diabetes | 67 FALK et AL.

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