scholarly journals Acid-Sensing Ion Channels Mediate Type III Adenylyl Cyclase-Independent Acid-Sensing of Mouse Olfactory Sensory Neurons

2019 ◽  
Author(s):  
Juan Yang ◽  
Liyan Qiu ◽  
Matthew Strobel ◽  
Amanda Kabel ◽  
Xiangming Zha ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Ion Channels ◽  
Adenylyl Cyclase ◽  
Sensory Neurons ◽  
Olfactory System ◽  
Odorant Receptors ◽  
Olfactory Sensory Neurons ◽  
Type Iii ◽  
Camp Pathway ◽  
Acid Sensing Ion Channels

AbstractAcids can disturb the ecosystem of wild animals through altering their olfaction and olfaction-related survival behaviors. It is known that the main olfactory epithelia (MOE) of mammals rely on odorant receptors and type III adenylyl cyclase (AC3) to detect general odorants. However, it is unknown how the olfactory system sense protons or acidic odorants. Here we show that the mouse MOE responded to acidic volatile stimuli in the presence and the absence of AC3. Acetic acid-induced electro-olfactogram (EOG) responses in wild type (WT) MOE can be dissected into two components: one dependent on the AC3-mediated cAMP pathway and the other not. MOE of AC3 knockout (KO) mice retained an acid-evoked EOG response but failed to respond to an odor mix. The acid-evoked responses of the AC3 KO could be blocked by diminazene, an inhibitor of acid-sensing ion channels (ASICs), but not by forskolin/IBMX, which desensitize the cAMP pathway. AC3 KO mice lost their sensitivity to detect pungent odorants but maintained sniffing behavior to acetic acid. Immunofluorescence staining demonstrated that ASIC1 proteins were highly expressed in olfactory sensory neurons (OSNs), mostly enriched in the knobs, dendrites, and somata, but not in olfactory cilia. Moreover, mice exhibited reduced preference to attractive objects when placed in an environment with acidic volatiles. Together, we conclude that the mouse olfactory system has a non-conventional, ASICs-mediated mechanism for acid-sensing. Acid stimulation of ASICs may unselectively depolarize different OSNs and interfere with the anatomical logic for odor perception.

scholarly journals Acid-Sensing Ion Channels Contribute to Type III Adenylyl Cyclase–Independent Acid Sensing of Mouse Olfactory Sensory Neurons

2020 ◽  
Vol 57 (7) ◽  
pp. 3042-3056
Author(s):  
Juan Yang ◽  
Liyan Qiu ◽  
Matthew Strobel ◽  
Amanda Kabel ◽  
Xiang-Ming Zha ◽  
...  
Keyword(s):  
Ion Channels ◽  
Adenylyl Cyclase ◽  
Sensory Neurons ◽  
Olfactory Sensory Neurons ◽  
Type Iii ◽  
Acid Sensing Ion Channels

The type III calcium/calmodulin-sensitive adenylyl cyclase is not specific to olfactory sensory neurons

1992 ◽  
Vol 144 (1-2) ◽  
pp. 169-173 ◽  
Author(s):  
Zhengui Xia ◽  
Eui-Ju Choi ◽  
Fan Wang ◽  
Daniel R. Storm
Keyword(s):  
Adenylyl Cyclase ◽  
Sensory Neurons ◽  
Olfactory Sensory Neurons ◽  
Type Iii

scholarly journals Region-specific amyloid-β accumulation in the olfactory system influences olfactory sensory neuronal dysfunction in 5xFAD mice

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Gowoon Son ◽  
Seung-Jun Yoo ◽  
Shinwoo Kang ◽  
Ameer Rasheed ◽  
Da Hae Jung ◽  
...  
Keyword(s):  
Olfactory Bulb ◽  
Sensory Neurons ◽  
Olfactory System ◽  
Amyloid Β ◽  
Olfactory Sensory Neurons ◽  
Basal Cells ◽  
Irreversible Damage ◽  
5Xfad Mouse ◽  
Peripheral Areas ◽  
5Xfad Mice

Abstract Background Hyposmia in Alzheimer’s disease (AD) is a typical early symptom according to numerous previous clinical studies. Although amyloid-β (Aβ), which is one of the toxic factors upregulated early in AD, has been identified in many studies, even in the peripheral areas of the olfactory system, the pathology involving olfactory sensory neurons (OSNs) remains poorly understood. Methods Here, we focused on peripheral olfactory sensory neurons (OSNs) and delved deeper into the direct relationship between pathophysiological and behavioral results using odorants. We also confirmed histologically the pathological changes in 3-month-old 5xFAD mouse models, which recapitulates AD pathology. We introduced a numeric scale histologically to compare physiological phenomenon and local tissue lesions regardless of the anatomical plane. Results We observed the odorant group that the 5xFAD mice showed reduced responses to odorants. These also did not physiologically activate OSNs that propagate their axons to the ventral olfactory bulb. Interestingly, the amount of accumulated amyloid-β (Aβ) was high in the OSNs located in the olfactory epithelial ectoturbinate and the ventral olfactory bulb glomeruli. We also observed irreversible damage to the ectoturbinate of the olfactory epithelium by measuring the impaired neuronal turnover ratio from the basal cells to the matured OSNs. Conclusions Our results showed that partial and asymmetrical accumulation of Aβ coincided with physiologically and structurally damaged areas in the peripheral olfactory system, which evoked hyporeactivity to some odorants. Taken together, partial olfactory dysfunction closely associated with peripheral OSN’s loss could be a leading cause of AD-related hyposmia, a characteristic of early AD.

scholarly journals G protein-coupled odorant receptors underlie mechanosensitivity in mammalian olfactory sensory neurons

2014 ◽  
Vol 112 (2) ◽  
pp. 590-595 ◽  
Author(s):  
Timothy Connelly ◽  
Yiqun Yu ◽  
Xavier Grosmaitre ◽  
Jue Wang ◽  
Lindsey C. Santarelli ◽  
...  
Keyword(s):  
G Protein ◽  
Sensory Neurons ◽  
Ectopic Expression ◽  
Host Cells ◽  
Odorant Receptors ◽  
Olfactory Sensory Neurons ◽  
Mechanical Stimuli ◽  
Genetic Ablation ◽  
Mechanical Responses ◽  
G Protein Coupled

Mechanosensitive cells are essential for organisms to sense the external and internal environments, and a variety of molecules have been implicated as mechanical sensors. Here we report that odorant receptors (ORs), a large family of G protein-coupled receptors, underlie the responses to both chemical and mechanical stimuli in mouse olfactory sensory neurons (OSNs). Genetic ablation of key signaling proteins in odor transduction or disruption of OR–G protein coupling eliminates mechanical responses. Curiously, OSNs expressing different OR types display significantly different responses to mechanical stimuli. Genetic swap of putatively mechanosensitive ORs abolishes or reduces mechanical responses of OSNs. Furthermore, ectopic expression of an OR restores mechanosensitivity in loss-of-function OSNs. Lastly, heterologous expression of an OR confers mechanosensitivity to its host cells. These results indicate that certain ORs are both necessary and sufficient to cause mechanical responses, revealing a previously unidentified mechanism for mechanotransduction.

scholarly journals Expression Patterns of Odorant Receptors and Response Properties of Olfactory Sensory Neurons in Aged Mice

2009 ◽  
Vol 34 (8) ◽  
pp. 695-703 ◽  
Author(s):  
Anderson C. Lee ◽  
Huikai Tian ◽  
Xavier Grosmaitre ◽  
Minghong Ma
Keyword(s):  
Sensory Neurons ◽  
Expression Patterns ◽  
Odorant Receptors ◽  
Olfactory Sensory Neurons ◽  
Response Properties ◽  
Aged Mice

scholarly journals Acid-sensing ion channels in sensory signaling

2020 ◽  
Vol 318 (3) ◽  
pp. F531-F543 ◽  
Author(s):  
Marcelo D. Carattino ◽  
Nicolas Montalbetti
Keyword(s):  
Nervous System ◽  
Ion Channels ◽  
Peripheral Nervous System ◽  
Sensory Neurons ◽  
Genetically Modified ◽  
Physiological Processes ◽  
Acid Sensing Ion Channels ◽  
Genetically Modified Mice ◽  
Sensory Processes

Acid-sensing ion channels (ASICs) are cation-permeable channels that in the periphery are primarily expressed in sensory neurons that innervate tissues and organs. Soon after the cloning of the ASIC subunits, almost 20 yr ago, investigators began to use genetically modified mice to assess the role of these channels in physiological processes. These studies provide critical insights about the participation of ASICs in sensory processes, including mechanotransduction, chemoreception, and nociception. Here, we provide an extensive assessment of these findings and discuss the current gaps in knowledge with regard to the functions of ASICs in the peripheral nervous system.

scholarly journals Oxytocin inhibits the activity of acid-sensing ion channels through the vasopressin, V1Areceptor in primary sensory neurons

2014 ◽  
Vol 171 (12) ◽  
pp. 3065-3076 ◽  
Author(s):  
Fang Qiu ◽  
Chun-Yu Qiu ◽  
Huilan Cai ◽  
Ting-Ting Liu ◽  
Zu-Wei Qu ◽  
...  
Keyword(s):  
Ion Channels ◽  
Sensory Neurons ◽  
Primary Sensory Neurons ◽  
Acid Sensing Ion Channels

scholarly journals Heart failure induces changes in acid-sensing ion channels in sensory neurons innervating skeletal muscle

2015 ◽  
Vol 593 (20) ◽  
pp. 4575-4587 ◽  
Author(s):  
David D. Gibbons ◽  
William J. Kutschke ◽  
Robert M. Weiss ◽  
Christopher J. Benson
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Ion Channels ◽  
Sensory Neurons ◽  
Acid Sensing Ion Channels

Odorant Receptors in the Formation of the Olfactory Bulb Circuitry

Physiology ◽  
2012 ◽  
Vol 27 (4) ◽  
pp. 200-212 ◽  
Author(s):  
Claudia Lodovichi ◽  
Leonardo Belluscio
Keyword(s):  
Olfactory Bulb ◽  
Axon Guidance ◽  
Sensory Neurons ◽  
Odorant Receptors ◽  
Olfactory Sensory Neurons ◽  
Neural Connectivity ◽  
Axon Terminals ◽  
Primary Function

In mammals, smell is mediated by odorant receptors expressed by sensory neurons in the nose. These specialized receptors are found both on olfactory sensory neurons' cilia and axon terminals. Although the primary function of ciliary odorant receptors is to detect odorants, their axonal role remains unclear but is thought to involve axon guidance. This review discusses findings that show axonal odorant receptors are indeed functional and capable of modulating neural connectivity.

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