Auditory Sensory Receptor Cell, Model

2015 ◽  
pp. 278-278
Keyword(s):  
Receptor Cell ◽  
Cell Model ◽  
Sensory Receptor

Sensory Transduction

2019 ◽  
Author(s):  
Gordon L. Fain
Keyword(s):  
Ion Channels ◽  
Receptor Cell ◽  
Electrical Response ◽  
Second Messengers ◽  
Sensory Transduction ◽  
Sensory Receptor ◽  
Signal Pathways ◽  
Sense Organs ◽  
Sensory Physiology ◽  
Effector Molecules

Sensory Transduction provides a thorough and easily accessible introduction to the mechanisms that each of the different kinds of sensory receptor cell uses to convert a sensory stimulus into an electrical response. Beginning with an introduction to methods of experimentation, sensory specializations, ion channels, and G-protein cascades, it provides up-to-date reviews of all of the major senses, including touch, hearing, olfaction, taste, photoreception, and the “extra” senses of thermoreception, electroreception, and magnetoreception. By bringing mechanisms of all of the senses together into a coherent treatment, it facilitates comparison of ion channels, metabotropic effector molecules, second messengers, and other components of signal pathways that are common themes in the physiology of the different sense organs. With its many clear illustrations and easily assimilated exposition, it provides an ideal introduction to current research for the professional in neuroscience, as well as a text for an advanced undergraduate or graduate-level course on sensory physiology.

scholarly journals The odontoblast as a sensory receptor cell? The expression of TRPV1 (VR-1) channels

2005 ◽  
Vol 68 (4) ◽  
pp. 251-257 ◽  
Author(s):  
Reijiro Okumura ◽  
Kaori Shima ◽  
Takashi Muramatsu ◽  
Kan-ichi Nakagawa ◽  
Masaki Shimono ◽  
...  
Keyword(s):  
Receptor Cell ◽  
Sensory Receptor

A colonic mineralocorticoid receptor cell model expressing epithelial Na+ channels

2009 ◽  
Vol 382 (2) ◽  
pp. 280-285 ◽  
Author(s):  
Theresa Bergann ◽  
Svenja Plöger ◽  
Anja Fromm ◽  
Sebastian Zeissig ◽  
Steffen A. Borden ◽  
...  
Keyword(s):  
Mineralocorticoid Receptor ◽  
Receptor Cell ◽  
Cell Model ◽  
Na Channels ◽  
Epithelial Na Channels

Receptor cell habituation in the A1 auditory receptor of four noctuoid moths.

1998 ◽  
Vol 201 (20) ◽  
pp. 2879-2890 ◽  
Author(s):  
F Coro ◽  
M Pérez ◽  
E Mora ◽  
D Boada ◽  
WE Conner ◽  
...  
Keyword(s):  
Duty Cycle ◽  
Repetition Rate ◽  
Receptor Cell ◽  
Response Duration ◽  
Sensory Receptor ◽  
Stimulus Repetition ◽  
Constant Intensity ◽  
Acoustic Stimuli ◽  
Cell Responses ◽  
Stimulus Repetition Rate

Moths of both sexes of Empyreuma affinis (=pugione) and Syntomeida epilais (Arctiidae, Ctenuchinae), Maenas jussiae (Arctiidae, Arctiinae) and Spodoptera frugiperda (Noctuidae, Amphipyrinae) were studied. Spike activity in the A1 cell was recorded using a stainless-steel hook electrode from the tympanic nerve in the mesothorax. Acoustic stimuli consisting of 25 and 100 ms pulses at the best frequency for the species and at intensities that evoke A1 cell saturation response were used at repetition rates of 0.5 and 5 Hz for 100 ms stimuli, and between 2 and 20 Hz for 25 ms stimuli. Stimuli at a repetition rate corresponding to a duty cycle of 5 % (25 ms at 2 Hz and 100 ms at 0.5 Hz) did not evoke monotonic changes in the responses of the A1 cell. With 25 ms pulses, rates above 5 Hz evoked an exponential decrease in the number of spikes and an increase in the latency of the responses of all the 37 specimens tested. The response duration showed no apparent change with stimulus repetition rates even at the highest duty cycle used (50 %), i.e. 25 ms at 20 Hz and 100 ms at 5 Hz. The higher the rate of stimulus repetition, the more marked were the changes in the A1 cell responses. In 16 of 17 preparations from two species, habituation had no effect on the adaptation rate in each response, while in seven of eight specimens of another species, the adaptation rate decreased with stimulus repetition. These results, and those from another mechanoreceptor cell, indicate that receptor cell adaptation (changes evoked in the response by a stimulus of constant intensity) and habituation (changes in the responses due to stimulus repetition rate) are two distinctive phenomena. The A1 cell in its habituated state showed an increase in its response to incremental increases in stimulus intensity of 10 dB. This result supports the idea that receptor cell habituation does not seem to be due to fatigue, i.e. to a temporary loss of the ability to respond to stimulation induced in a sensory receptor by continued stimulation.

Ultrastructural aspects of olfactory signal transduction and its development

1994 ◽  
Vol 52 ◽  
pp. 142-143
Author(s):  
Bert Ph. M. Menco
Keyword(s):  
Signal Transduction ◽  
Olfactory Receptor ◽  
Receptor Cell ◽  
Freeze Substitution ◽  
Luminal Surface ◽  
Tissue Sections ◽  
Olfactory Receptor Cells ◽  
Receptor Cells ◽  
Olfactory Signal ◽  
Odor Molecule

Vertebrate olfactory receptor cells are specialized neurons that have numerous long tapering cilia. The distal parts of these cilia line the interface between the external odorous environment and the luminal surface of the olfactory epithelium. The length and number of these cilia results in a large surface area that presumably increases the chance that an odor molecule will meet a receptor cell. Advanced methods of cryoprepration and immuno-gold labeling were particularly useful to preserve the delicate ultrastructural and immunocytochemical features of olfactory cilia required for localization of molecules involved in olfactory signal-transduction. We subjected olfactory tissues to freeze-substitution in acetone (unfixed tissues) or methanol (fixed tissues) followed by low temperature embedding in Lowicryl K11M for that purpose. Tissue sections were immunoreacted with several antibodies against proteins that are presumably important in olfactory signal-transduction.

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

Sign in / Sign up

Export Citation Format

Share Document