Muscarinic Receptor Activation (muscarinic + receptor_activation)

Distribution by Scientific Domains


Selected Abstracts


Switching between "On" and "Off" states of persistent activity in lateral entorhinal layer III neurons,

HIPPOCAMPUS, Issue 4 2007
Babak Tahvildari
Abstract Persistent neural spiking maintains information during a working memory task when a stimulus is no longer present. During retention, this activity needs to be stable to distractors. More importantly, when retention is no longer relevant, cessation of the activity is necessary to enable processing and retention of subsequent information. Here, by means of intracellular recording with sharp microelectrode in in vitro rat brain slices, we demonstrate that single principal layer III neurons of the lateral entorhinal cortex (EC) generate persistent spiking activity with a novel ability to reliably toggle between spiking activity and a silent state. Our data indicates that in the presence of muscarinic receptor activation, persistent activity following an excitatory input may be induced and that a subsequent excitatory input can terminate this activity and cause the neuron to return to a silent state. Moreover, application of inhibitory hyperpolarizing stimuli is neither able to decrease the frequency of the persistent activity nor terminate it. The persistent activity can also be initiated and terminated by synchronized synaptic stimuli of layer II/III of the perirhinal cortex. The neuronal ability to switch "On" and "Off" persistent activity may facilitate the concurrent representation of temporally segregated information arriving in the EC and being directed toward the hippocampus. © 2007 Wiley-Liss, Inc. [source]


Role of muscarinic receptor activation in regulating immune cell activity in nasal mucosa

ALLERGY, Issue 8 2010
T. Liu
To cite this article: Liu T, Xie C, Chen X, Zhao F, Liu A-M, Cho D-B, Chong J, Yang P-C. Role of muscarinic receptor activation in regulating immune cell activity in nasal mucosa. Allergy 2010; 65: 969,977. Abstract Background:, The prevalence of airway inflammatory disorders keeps rising; its pathogenic mechanism is still not fully understood. Objective:, The present study aimed to investigate the role of muscarinic receptor (M receptor) in regulating the immune cell activity in nasal mucosa by using surgical removed nasal mucosa from patients with nasal polyposis (NP) as a study platform. Methods:, Human nasal mucosal sample was collected from inferior turbinectomy of 86 patients with NP or/and allergic rhinitis. Expression of tumor necrosis factor alpha (TNF-alpha), M receptor, OX40 ligand was measured in nasal mucosa by enzyme-linked immunosorbent assay, flow cytometry, and Western blotting assay. Results:, When compared with non-NP (nNP) nasal mucosa, contents of TNF-alpha and TNF-alpha(+) cells markedly increased in NP nasal mucosa; immune staining colocalized M3 receptor(+) and TNF-alpha(+) cells in NP nasal mucosa; exposure of isolated CD4(+) T cells to methacholine induced the release of TNF-alpha. We also found CD11c(+)/M3 receptor(+) cells in NP nasal mucosa. Methacholine increased the expression of OX40L in dendritic cells. Staphylococcal (S) aureus and S. enterotoxin B (SEB) were detected in NP nasal mucosa. Exposure of dendritic cells or naïve CD4(+) T cells to SEB initiated the expression of M3 receptor at mRNA and protein levels. Conclusions:, The present data demonstrate that parasympathetic activity has the capacity to activate dendritic cells to release OX40 ligand, the latter induces CD4(+) T cells to produce IL-4 and TNF-alpha that may further contribute to the pathogenesis of NP. [source]


Clinical and experimental aspects of Adreno-muscarinic synergy in the bladder base and prostate,,

NEUROUROLOGY AND URODYNAMICS, Issue 8 2009
Alexander Roosen
Abstract Recent clinical trials have shown that combination therapy using an alpha-receptor antagonist and an antimuscarinic is more effective than either agent alone in improving quality of life and objective urodynamic variables in men with bladder outflow obstruction. There appear to be no negative effects on bladder function. The mode of action of this combination is unknown but presumed to be an antimuscarinic reduction in detrusor overactivity and the alpha-receptor antagonist reduced outflow tract resistance. We have shown with in vitro experiments that in smooth muscles influencing outflow tract resistance (prostate, trigone) there is a profound contractile synergy between adrenergic and muscarinic pathways. We propose the hypothesis that both arms of the combination therapy reduce contractile tone of the outflow tract and that their simultaneous attenuation has a disproportionately large effect on outflow tract resistance. Our data from trigone muscle suggest that adrenergic and muscarinic receptor activation increase the intracellular [Ca2+] but the adrenergic pathway also operates through Ca2+ -sensitisation of the contractile apparatus, primarily through a PKC-dependent pathway. Neurourol. Urodynam. 28:938,943, 2009. © 2009 Wiley-Liss, Inc. [source]


SPATIAL AND TEMPORAL ASPECTS OF cAMP SIGNALLING IN CARDIAC MYOCYTES

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2008
Radu V Iancu
SUMMARY 1,1 -Adrenoceptor and M2 muscarinic receptor regulation of cAMP production plays a pivotal role in autonomic regulation of cardiac myocyte function. However, not all responses are easily explained by a uniform increase or decrease in cAMP activity throughout the entire cell. 2Adenovirus expression of fluorescence resonance energy transfer (FRET)-based biosensors can be used to monitor cAMP activity in protein kinase A (PKA) signalling domains, as well as the bulk cytoplasmic domain of intact adult cardiac myocytes. 3Data obtained using FRET-based biosensors expressed in different cellular microdomains have been used to develop a computational model of compartmentalized cAMP signalling. 4A systems biology approach that uses quantitative computational modelling together with experimental data obtained using FRET-based biosensors has been used to provide evidence for the idea that compartmentation of cAMP signalling is necessary to explain the stimulatory responses to ,1 -adrenoceptor activation as well as the complex temporal responses to M2 muscarinic receptor activation. [source]