scholarly journals CALHM1 Ion Channel Mediates Purinergic Neurotransmission from Taste Buds to Gustatory Nerve Terminals during Sweet and Bitter Perception

2013 ◽  
Vol 104 (2) ◽  
pp. 631a
Author(s):  
Akiyuki Taruno ◽  
Ang Li ◽  
Zhongming Ma ◽  
Philippe Marambaud ◽  
Makoto Ohmoto ◽  
...  
Keyword(s):  
Ion Channel ◽  
Taste Buds ◽  
Nerve Terminals ◽  
Gustatory Nerve ◽  
Purinergic Neurotransmission

scholarly journals Nerve terminals in the taste buds of early postnatal and adult mice.

1985 ◽  
Vol 27 (2) ◽  
pp. 409-416
Author(s):  
Masako Takeda ◽  
Yuko Suzuki ◽  
Yoko Shishido
Keyword(s):  
Taste Buds ◽  
Nerve Terminals ◽  
Adult Mice

Fine structure of degenerating taste buds after denervation

Development ◽  
1969 ◽  
Vol 22 (1) ◽  
pp. 55-68
Author(s):  
Albert I. Farbman
Keyword(s):  
Cell Death ◽  
Fine Structure ◽  
Taste Buds ◽  
Taste Bud ◽  
Nerve Terminals ◽  
Nerve Supply ◽  
Cell Turnover ◽  
Epithelial Surface ◽  
Taste Bud Cells

It is well known that taste buds are dependent on an intact nerve supply, and when experimentally denervated they degenerate and disappear (von Vintschgau & Honigschmied, 1877; von Vintschgau, 1880; Griffini, 1887; Meyer, 1897; Olmsted, 1920a, b, 1921, 1922; May, 1925; Whiteside, 1927; Torrey, 1934, 1936; Wagner, 1953; Guth, 1957, 1958, 1963; Beidler, 1962, 1963). Olmsted (1920b) has suggested that the degenerating taste bud cells are cleared away by macrophages invading the epithelium; Guth (1957, 1958, 1963) has demonstrated sloughing of degenerating taste buds from the epithelial surface, and others believe that taste bud cells dedifferentiate to become lining epithelium (Meyer, 1897; Wagner, 1953). Because of this disagreement and because recent evidence for cell turnover in taste buds has indicated that cell death and replacement is a normal occurrence (Beidler, 1962, 1963; DeLorenzo, 1963; Beidler & Smallman, 1965), it is pertinent to study the fine structure of degenerating taste buds in the hope of elucidating the process by which taste bud cells and nerve terminals degenerate.

scholarly journals CALHM3 Is Essential for Rapid Ion Channel-Mediated Purinergic Neurotransmission of GPCR-Mediated Tastes

Neuron ◽  
2018 ◽  
Vol 98 (3) ◽  
pp. 547-561.e10 ◽  
Author(s):  
Zhongming Ma ◽  
Akiyuki Taruno ◽  
Makoto Ohmoto ◽  
Masafumi Jyotaki ◽  
Jason C. Lim ◽  
...  
Keyword(s):  
Ion Channel ◽  
Purinergic Neurotransmission

scholarly journals Evolutionary origins of taste buds: phylogenetic analysis of purinergic neurotransmission in epithelial chemosensors

Open Biology ◽  
2013 ◽  
Vol 3 (3) ◽  
pp. 130015 ◽  
Author(s):  
Masato Kirino ◽  
Jason Parnes ◽  
Anne Hansen ◽  
Sadao Kiyohara ◽  
Thomas E. Finger
Keyword(s):  
Atpase Activity ◽  
Taste Buds ◽  
Purinergic Signalling ◽  
Nerve Fibres ◽  
Taste System ◽  
Evolutionary Origins ◽  
Gustatory Nerve ◽  
Solitary Chemosensory Cells ◽  
Early Vertebrates ◽  
Chemosensory Systems

Taste buds are gustatory endorgans which use an uncommon purinergic signalling system to transmit information to afferent gustatory nerve fibres. In mammals, ATP is a crucial neurotransmitter released by the taste cells to activate the afferent nerve fibres. Taste buds in mammals display a characteristic, highly specific ecto-ATPase (NTPDase2) activity, suggesting a role in inactivation of the neurotransmitter. The purpose of this study was to test whether the presence of markers of purinergic signalling characterize taste buds in anamniote vertebrates and to test whether similar purinergic systems are employed by other exteroceptive chemosensory systems. The species examined include several teleosts, elasmobranchs, lampreys and hagfish, the last of which lacks vertebrate-type taste buds. For comparison, Schreiner organs of hagfish and solitary chemosensory cells (SCCs) of teleosts, both of which are epidermal chemosensory end organs, were also examined because they might be evolutionarily related to taste buds. Ecto-ATPase activity was evident in elongate cells in all fish taste buds, including teleosts, elasmobranchs and lampreys. Neither SCCs nor Schreiner organs show specific ecto-ATPase activity, suggesting that purinergic signalling is not crucial in those systems as it is for taste buds. These findings suggest that the taste system did not originate from SCCs but arose independently in early vertebrates.

Ion Channels in Presynaptic Nerve Terminals and Control of Transmitter Release

1999 ◽  
Vol 79 (3) ◽  
pp. 1019-1088 ◽  
Author(s):  
Alon Meir ◽  
Simona Ginsburg ◽  
Alexander Butkevich ◽  
Sylvia G. Kachalsky ◽  
Igor Kaiserman ◽  
...  
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Nerve Terminal ◽  
Transmitter Release ◽  
Surface Membrane ◽  
Basic Function ◽  
Fine Tuning ◽  
Nerve Terminals ◽  
Presynaptic Nerve Terminal ◽  
Presynaptic Nerve Terminals

The primary function of the presynaptic nerve terminal is to release transmitter quanta and thus activate the postsynaptic target cell. In almost every step leading to the release of transmitter quanta, there is a substantial involvement of ion channels. In this review, the multitude of ion channels in the presynaptic terminal are surveyed. There are at least 12 different major categories of ion channels representing several tens of different ion channel types; the number of different ion channel molecules at presynaptic nerve terminals is many hundreds. We describe the different ion channel molecules at the surface membrane and inside the nerve terminal in the context of their possible role in the process of transmitter release. Frequently, a number of different ion channel molecules, with the same basic function, are present at the same nerve terminal. This is especially evident in the cases of calcium channels and potassium channels. This abundance of ion channels allows for a physiological and pharmacological fine tuning of the process of transmitter release and thus of synaptic transmission.

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