Distribution of acid-sensing ion channel 3 in the rat hypothalamus

Meng, Qing‐Yuan; Wang, W.; Chen, X.-N.; Xu, Tian‐Le; Zhou, Jiang‐Ning

doi:10.1016/j.neuroscience.2009.01.069

Cited by 54 publications

(38 citation statements)

References 44 publications

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“…ASICs are expressed in the CNS in multiple locations including hippocampus, hypothalamus, midbrain, and cerebellum (6,215,274,307). While not all of these locations are involved in pain sensing, it is likely that ASICs identified in neurons of the dorsal horn are responsible for integrating peripheral pain signals before transmission to the cortex (32).…”

Section: Asics and Painmentioning

confidence: 99%

ENaCs and ASICs as therapeutic targets

Qadri

Rooj

Fuller

2012

American Journal of Physiology-Cell Physiology

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The epithelial Na+channel (ENaC) and acid-sensitive ion channel (ASIC) branches of the ENaC/degenerin superfamily of cation channels have drawn increasing attention as potential therapeutic targets in a variety of diseases and conditions. Originally thought to be solely expressed in fluid absorptive epithelia and in neurons, it has become apparent that members of this family exhibit nearly ubiquitous expression. Therapeutic opportunities range from hypertension, due to the role of ENaC in maintaining whole body salt and water homeostasis, to anxiety disorders and pain associated with ASIC activity. As a physiologist intrigued by the fundamental mechanics of salt and water transport, it was natural that Dale Benos, to whom this series of reviews is dedicated, should have been at the forefront of research into the amiloride-sensitive sodium channel. The cloning of ENaC and subsequently the ASIC channels has revealed a far wider role for this channel family than was previously imagined. In this review, we will discuss the known and potential roles of ENaC and ASIC subunits in the wide variety of pathologies in which these channels have been implicated. Some of these, such as the role of ENaC in Liddle's syndrome are well established, others less so; however, all are related in that the fundamental defect is due to inappropriate channel activity.

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Section: Asics and Painmentioning

confidence: 99%

ENaCs and ASICs as therapeutic targets

Qadri

Rooj

Fuller

2012

American Journal of Physiology-Cell Physiology

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“…Inactivation of ASIC3 enhanced visual transduction at the age of 2 to 3 months but induced late-onset rod photoreceptor death in mice, suggesting an important role of ASIC3 in maintaining retinal integrity (85). ASIC3 was also reported to be expressed in the rat vestibular endorgans and ganglia (86), hypothalamus (87), and suprachiasmatic nucleus (88), in which the roles of ASIC3 have not been explored.…”

Section: Participation In Other Sensory Modalitiesmentioning

confidence: 99%

ASIC3 Channels in Multimodal Sensory Perception

2010

ACS Chem. Neurosci.

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Acid-sensing ion channels (ASICs), which are members of the sodium-selective cation channels belonging to the epithelial sodium channel/degenerin (ENaC/ DEG) family, act as membrane-bound receptors for extracellular protons as well as nonproton ligands. At least five ASIC subunits have been identified in mammalian neurons, which form both homotrimeric and heterotrimeric channels. The highly proton sensitive ASIC3 channels are predominantly distributed in peripheral sensory neurons, correlating with their roles in multimodal sensory perception, including nociception, mechanosensation, and chemosensation. Different from other ASIC subunit composing ion channels, ASIC3 channels can mediate a sustained window current in response to mild extracellular acidosis (pH 7.3-6.7), which often occurs accompanied by many sensory stimuli. Furthermore, recent evidence indicates that the sustained component of ASIC3 currents can be enhanced by nonproton ligands including the endogenous metabolite agmatine. In this review, we first summarize the growing body of evidence for the involvement of ASIC3 channels in multimodal sensory perception and then discuss the potential mechanisms underlying ASIC3 activation and mediation of sensory perception, with a special emphasis on its role in nociception. We conclude that ASIC3 activation and modulation by diverse sensory stimuli represent a new avenue for understanding the role of ASIC3 channels in sensory perception. Furthermore, the emerging implications of ASIC3 channels in multiple sensory dysfunctions including nociception allow the development of new pharmacotherapy.

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“…DM, receiving dense efferents from SCN via Spa, is now noted for the critical role in the central regulation of the brown adipose tissues (BAT) for energy homeostasis in mammals (Kataoka et al, 2014;Nakamura and Morrison, 2011), particularly via central leptin signaling (Enriori et al, 2011;Rezai-Zadeh et al, 2014). The DTM, a classical subnucleus of histaminergic neurons, is noted for an important role in the regulation of arousal (Castillo-Ruiz et al, 2013) through signal transduction of the acid-sensing ion channels (ASICs) for brain chemosensation (Meng et al, 2009), melanin-concentration hormone (MCH) for memory formation (Casatti et al, 2002), and neuropeptide S for wakefulness (Zhao et al, 2012). In summary, E4 appears to be predominantly involved in the regulation of circadian rhythms of energy metabolism in strong association with diurnal control of the SCN-DM-BAT sympathetic pathway.…”

Section: Discussionmentioning

confidence: 99%

Distribution of histaminergic neuronal cluster in the rat and mouse hypothalamus

Moriwaki

Chiba

Wei

et al. 2015

Journal of Chemical Neuroanatomy

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Histidine decarboxylase (HDC) catalyzes the biosynthesis of histamine from L-histidine and is expressed throughout the mammalian nervous system by histaminergic neurons. Histaminergic neurons arise in the posterior mesencephalon during the early embryonic period and gradually develop into two histaminergic substreams around the lateral area of the posterior hypothalamus and the more anterior peri-cerebral aqueduct area before finally forming an adult-like pattern comprising five neuronal clusters, E1, E2, E3, E4, and E5, at the postnatal stage. This distribution of histaminergic neuronal clusters in the rat hypothalamus appears to be a consequence of neuronal development and reflects the functional differentiation within each neuronal cluster. However, the close linkage between the locations of histaminergic neuronal clusters and their physiological functions has yet to be fully elucidated because of the sparse information regarding the location and orientation of each histaminergic neuronal clusters in the hypothalamus of rats and mice. To clarify the distribution of the five-histaminergic neuronal clusters more clearly, we performed an immunohistochemical study using the anti-HDC antibody on serial sections of the rat hypothalamus according to the brain maps of rat and mouse. Our results confirmed that the HDC-immunoreactive (HDCi) neuronal clusters in the hypothalamus of rats and mice are observed in the ventrolateral part of the most posterior hypothalamus (E1), ventrolateral part of the posterior hypothalamus (E2), ventromedial part from the medial to the posterior hypothalamus (E3), periventricular part from the anterior to the medial hypothalamus (E4), and diffusely extended part of the more dorsal and almost entire hypothalamus (E5). The stereological estimation of the total number of HDCi neurons of each clusters revealed the larger amount of the rat than the mouse. The characterization of histaminergic neuronal clusters in the hypothalamus of rats and mice may provide useful information for further investigations.

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Distribution of acid-sensing ion channel 3 in the rat hypothalamus

Cited by 54 publications

References 44 publications

ENaCs and ASICs as therapeutic targets

ENaCs and ASICs as therapeutic targets

ASIC3 Channels in Multimodal Sensory Perception

Distribution of histaminergic neuronal cluster in the rat and mouse hypothalamus

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