scholarly journals Acid-Sensing Ion Channels in Zebrafish

Animals ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 2471
Author(s):  
Giuseppe Montalbano ◽  
Maria Levanti ◽  
Kamel Mhalhel ◽  
Francesco Abbate ◽  
Rosaria Laurà ◽  
...  
Keyword(s):  
Nervous System ◽  
Ion Channels ◽  
Molecular Biology ◽  
Inner Ear ◽  
Peripheral Nervous System ◽  
Lateral Line ◽  
Experimental Models ◽  
Acid Sensing Ion Channels ◽  
Physiological Values ◽  
Olfactory Rosette

The ASICs, in mammals as in fish, control deviations from the physiological values of extracellular pH, and are involved in mechanoreception, nociception, or taste receptions. They are widely expressed in the central and peripheral nervous system. In this review, we summarized the data about the presence and localization of ASICs in different organs of zebrafish that represent one of the most used experimental models for the study of several diseases. In particular, we analyzed the data obtained by immunohistochemical and molecular biology techniques concerning the presence and expression of ASICs in the sensory organs, such as the olfactory rosette, lateral line, inner ear, taste buds, and in the gut and brain of zebrafish.

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.

Acid-Sensing Ion Channels

2020 ◽  
Author(s):  
Stefan Gründer
Keyword(s):  
Nervous System ◽  
Ion Channels ◽  
Excitatory Synapses ◽  
Detailed Characterization ◽  
High Affinity ◽  
Acid Sensing Ion Channels ◽  
Long Time ◽  
Pathological Pain

Acid-sensing ion channels (ASICs) are proton-gated Na+ channels. Being almost ubiquitously present in neurons of the vertebrate nervous system, their precise function remained obscure for a long time. Various animal toxins that bind to ASICs with high affinity and specificity have been tremendously helpful in uncovering the role of ASICs. We now know that they contribute to synaptic transmission at excitatory synapses as well as to sensing metabolic acidosis and nociception. Moreover, detailed characterization of mouse models uncovered an unanticipated role of ASICs in disorders of the nervous system like stroke, multiple sclerosis, and pathological pain. This review provides an overview on the expression, structure, and pharmacology of ASICs plus a summary of what is known and what is still unknown about their physiological functions and their roles in diseases.

scholarly journals The Rotenone Models Reproducing Central and Peripheral Features of Parkinson’s Disease

NeuroSci ◽  
2020 ◽  
Vol 1 (1) ◽  
pp. 1-14
Author(s):  
Ikuko Miyazaki ◽  
Masato Asanuma
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Peripheral Nervous System ◽  
Neurodegenerative Disorder ◽  
Rem Sleep Behavior Disorder ◽  
Experimental Models ◽  
Motor Symptoms ◽  
Sleep Behavior ◽  
Disease Modifying Drugs

Parkinson’s disease (PD) is a complex, multi-system, neurodegenerative disorder; PD patients exhibit motor symptoms (such as akinesia/bradykinesia, tremor, rigidity, and postural instability) due to a loss of nigrostriatal dopaminergic neurons, and non-motor symptoms such as hyposmia, autonomic disturbance, depression, and REM sleep behavior disorder (RBD), which precedes motor symptoms. Pathologically, α-synuclein deposition is observed in the central and peripheral nervous system of sporadic PD patients. To clarify the mechanism of neurodegeneration in PD and to develop treatment to slow or stop PD progression, there is a great need for experimental models which reproduce neurological features of PD. Animal models exposed to rotenone, a commonly used pesticide, have received most attention since Greenamyre and his colleagues reported that chronic exposure to rotenone could reproduce the anatomical, neurochemical, behavioral, and neuropathological features of PD. In addition, recent studies demonstrated that rotenone induced neuropathological change not only in the central nervous system but also in the peripheral nervous system in animals. In this article, we review rotenone models especially focused on reproducibility of central and peripheral multiple features of PD. This review also highlights utility of rotenone models for investigation of PD pathogenesis and development of disease-modifying drugs for PD in future.

scholarly journals Physiopathological Role of Neuroactive Steroids in the Peripheral Nervous System

2020 ◽  
Vol 21 (23) ◽  
pp. 9000
Author(s):  
Eva Falvo ◽  
Silvia Diviccaro ◽  
Roberto Cosimo Melcangi ◽  
Silvia Giatti
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Experimental Models ◽  
Neuroactive Steroids ◽  
Physiological Status ◽  
Sexually Dimorphic ◽  
Protective Effects ◽  
Traumatic Injuries ◽  
High Prevalence

Peripheral neuropathy (PN) refers to many conditions involving damage to the peripheral nervous system (PNS). Usually, PN causes weakness, numbness and pain and is the result of traumatic injuries, infections, metabolic problems, inherited causes, or exposure to chemicals. Despite the high prevalence of PN, available treatments are still unsatisfactory. Neuroactive steroids (i.e., steroid hormones synthesized by peripheral glands as well as steroids directly synthesized in the nervous system) represent important physiological regulators of PNS functionality. Data obtained so far and here discussed, indeed show that in several experimental models of PN the levels of neuroactive steroids are affected by the pathology and that treatment with these molecules is able to exert protective effects on several PN features, including neuropathic pain. Of note, the observations that neuroactive steroid levels are sexually dimorphic not only in physiological status but also in PN, associated with the finding that PN show sex dimorphic manifestations, may suggest the possibility of a sex specific therapy based on neuroactive steroids.

scholarly journals Taste Receptors in the Gastrointestinal Tract. V. Acid sensing in the gastrointestinal tract

2007 ◽  
Vol 292 (3) ◽  
pp. G699-G705 ◽  
Author(s):  
Peter Holzer
Keyword(s):  
Gastrointestinal Tract ◽  
Ion Channels ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Extracellular Ph ◽  
Taste Receptors ◽  
Acid Sensing Ion Channels ◽  
Transient Receptor ◽  
Physiological Values ◽  
Pore Domain

Luminal acidity is a physiological challenge in the foregut, and acidosis can occur throughout the gastrointestinal tract as a result of inflammation or ischemia. These conditions are surveyed by an elaborate network of acid-governed mechanisms to maintain homeostasis. Deviations from physiological values of extracellular pH are monitored by multiple acid sensors expressed by epithelial cells and sensory neurons. Acid-sensing ion channels are activated by moderate acidification, whereas transient receptor potential ion channels of the vanilloid subtype are gated by severe acidosis. Some ionotropic purinoceptor ion channels and two-pore domain background K+ channels are also sensitive to alterations of extracellular pH.

scholarly journals Meis2 Is Required for Inner Ear Formation and Proper Morphogenesis of the Cochlea

2021 ◽  
Vol 9 ◽  
Author(s):  
María Beatriz Durán Alonso ◽  
Victor Vendrell ◽  
Iris López-Hernández ◽  
María Teresa Alonso ◽  
Donna M. Martin ◽  
...  
Keyword(s):  
Nervous System ◽  
Inner Ear ◽  
Cell Line ◽  
Peripheral Nervous System ◽  
Target Genes ◽  
Otic Vesicle ◽  
Vesicle Formation ◽  
Tissue Specific ◽  
Cochlear Duct ◽  
Candidate Target

Meis genes have been shown to control essential processes during development of the central and peripheral nervous system. Here we have explored the roles of the Meis2 gene during vertebrate inner ear induction and the formation of the cochlea. Meis2 is expressed in several tissues required for inner ear induction and in non-sensory tissue of the cochlear duct. Global inactivation of Meis2 in the mouse leads to a severely reduced size of the otic vesicle. Tissue-specific knock outs of Meis2 reveal that its expression in the hindbrain is essential for otic vesicle formation. Inactivation of Meis2 in the inner ear itself leads to an aberrant coiling of the cochlear duct. By analyzing transcriptomes obtained from Meis2 mutants and ChIPseq analysis of an otic cell line, we define candidate target genes for Meis2 which may be directly or indirectly involved in cochlear morphogenesis. Taken together, these data show that Meis2 is essential for inner ear formation and provide an entry point to unveil the network underlying proper coiling of the cochlear duct.

scholarly journals Acid-sensing ion channels emerged over 600 Mya and are conserved throughout the deuterostomes

2018 ◽  
Vol 115 (33) ◽  
pp. 8430-8435 ◽  
Author(s):  
Timothy Lynagh ◽  
Yana Mikhaleva ◽  
Janne M. Colding ◽  
Joel C. Glover ◽  
Stephan A. Pless
Keyword(s):  
Nervous System ◽  
Ion Channels ◽  
Sodium Current ◽  
Oikopleura Dioica ◽  
Acid Sensing Ion Channels ◽  
Mammalian Lineage ◽  
Molecular Determinants ◽  
Animal Phyla ◽  
The Central Nervous System ◽  
Functionally Diverse

Acid-sensing ion channels (ASICs) are proton-gated ion channels broadly expressed in the vertebrate nervous system, converting decreased extracellular pH into excitatory sodium current. ASICs were previously thought to be a vertebrate-specific branch of the DEG/ENaC family, a broadly conserved but functionally diverse family of channels. Here, we provide phylogenetic and experimental evidence that ASICs are conserved throughout deuterostome animals, showing that ASICs evolved over 600 million years ago. We also provide evidence of ASIC expression in the central nervous system of the tunicate, Oikopleura dioica. Furthermore, by comparing broadly related ASICs, we identify key molecular determinants of proton sensitivity and establish that proton sensitivity of the ASIC4 isoform was lost in the mammalian lineage. Taken together, these results suggest that contributions of ASICs to neuronal function may also be conserved broadly in numerous animal phyla.

scholarly journals Acid-Sensing Ion Channels as Potential Therapeutic Targets in Neurodegeneration and Neuroinflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Audrey Ortega-Ramírez ◽  
Rosario Vega ◽  
Enrique Soto
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
Nervous System ◽  
Ion Channels ◽  
Neurodegenerative Diseases ◽  
Therapeutic Targets ◽  
Recent Advances ◽  
Acid Sensing Ion Channels ◽  
Inflammatory Processes

Acid-sensing ion channels (ASICs) are a family of proton-sensing channels that are voltage insensitive, cation selective (mostly permeable to Na+), and nonspecifically blocked by amiloride. Derived from 5 genes (ACCN1–5), 7 subunits have been identified, 1a, 1b, 2a, 2b, 3, 4, and 5, that are widely expressed in the peripheral and central nervous system as well as other tissues. Over the years, different studies have shown that activation of these channels is linked to various physiological and pathological processes, such as memory, learning, fear, anxiety, ischemia, and multiple sclerosis to name a few, so their potential as therapeutic targets is increasing. This review focuses on recent advances that have helped us to better understand the role played by ASICs in different pathologies related to neurodegenerative diseases, inflammatory processes, and pain.

Acid-Sensing Ion Channels Structural Aspects, Pathophysiological Importance and Experimental Mutational Data Available Across Various Species to Target Human ASIC1

2018 ◽  
Vol 20 (1) ◽  
pp. 111-121 ◽  
Author(s):  
Anurag Singh Chauhan ◽  
Ganesh Chandra Sahoo ◽  
Manas Ranjan Dikhit ◽  
Pradeep Das
Keyword(s):  
Nervous System ◽  
Ion Channels ◽  
Pain Perception ◽  
Neuronal Degeneration ◽  
Sodium Cation ◽  
Neuronal System ◽  
Acid Sensing Ion Channels ◽  
Extracellular Environment ◽  
Structural Aspects ◽  
Ischemic Neuronal Injury

The H+-gated (proton) currents are widely present in brain sensory neuronal system and various studies identified the structural units and deciphered the physiological and pathological function of ion channels. The normal neuron requires an optimal pH to carry out its functions. In acidosis, the ASICs (Acid-sensing Ion Channels) are activated in both the CNS (central nervous system) and PNS (peripheral nervous system). ASICs are related to degenerin channels (DEGs), epithelial sodium cation channels (ENaCs), and FMRF-amide (Phe-Met-Arg-Phe-NH2)-gated channels (FaNaC). Its activation leads physiologically to pain perception, synaptic plasticity, learning and memory, fear, ischemic neuronal injury, seizure termination, neuronal degeneration, and mechanosensation. It detects the level of acid fluctuation in the extracellular environment and responds to acidic pH by increasing the rate of membrane depolarization. It conducts cations like Na+ (Sodium) and Ca2+ (Calcium) ions across the membrane upon protonation. The ASICs subtypes are characterized by differing biophysical properties and pH sensitivities. The subtype ASIC1 is involved in various CNS diseases and therefore focusing on its specific functional properties will guide in drug design methods. The review highlights the cASIC1 (Chicken ASIC1) crystal structures, involvement in physiological environment and limitations of currently available inhibitors. In addition, it details the mutational data available to design an inhibitor against hASIC1 (Human ASIC1).

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