Opening a “Wide” Window onto Taste Signal Transmission

Oka, Yuki

doi:10.1016/j.neuron.2018.04.020

Cited by 4 publications

(3 citation statements)

References 10 publications

(17 reference statements)

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“…All of the CALHM genes and previously named FAM26 genes, are present throughout vertebrates and conserved across more than 20 species including mouse, human, and C. elegans. (Ma et al, 2016) Co-expression of CALHM1 with CALHM3, but not with CALHM2, drastically enhances the activation kinetics of currents compared to expression of CALHM1 alone (Oka, 2018;Sclafani and Ackroff, 2018). CALHM1 and CALHM2 may thus form homomeric and heteromeric channels in native smooth muscle cells.…”

Section: Discussionmentioning

confidence: 98%

Upregulation of Calcium Homeostasis Modulators in Contractile-To-Proliferative Phenotypical Transition of Pulmonary Arterial Smooth Muscle Cells

Rodriguez¹,

Chen²,

Jain³

et al. 2021

Front. Physiol.

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Excessive pulmonary artery (PA) smooth muscle cell (PASMC) proliferation and migration are implicated in the development of pathogenic pulmonary vascular remodeling characterized by concentric arterial wall thickening and arteriole muscularization in patients with pulmonary arterial hypertension (PAH). Pulmonary artery smooth muscle cell contractile-to-proliferative phenotypical transition is a process that promotes pulmonary vascular remodeling. A rise in cytosolic Ca2+ concentration [(Ca2+)cyt] in PASMCs is a trigger for pulmonary vasoconstriction and a stimulus for pulmonary vascular remodeling. Here, we report that the calcium homeostasis modulator (CALHM), a Ca2+ (and ATP) channel that is allosterically regulated by voltage and extracellular Ca2+, is upregulated during the PASMC contractile-to-proliferative phenotypical transition. Protein expression of CALHM1/2 in primary cultured PASMCs in media containing serum and growth factors (proliferative PASMC) was significantly greater than in freshly isolated PA (contractile PASMC) from the same rat. Upregulated CALHM1/2 in proliferative PASMCs were associated with an increased ratio of pAKT/AKT and pmTOR/mTOR and an increased expression of the cell proliferation marker PCNA, whereas serum starvation and rapamycin significantly downregulated CALHM1/2. Furthermore, CALHM1/2 were upregulated in freshly isolated PA from rats with monocrotaline (MCT)-induced PH and in primary cultured PASMC from patients with PAH in comparison to normal controls. Intraperitoneal injection of CGP 37157 (0.6 mg/kg, q8H), a non-selective blocker of CALHM channels, partially reversed established experimental PH. These data suggest that CALHM upregulation is involved in PASMC contractile-to-proliferative phenotypical transition. Ca2+ influx through upregulated CALHM1/2 may play an important role in the transition of sustained vasoconstriction to excessive vascular remodeling in PAH or precapillary PH. Calcium homeostasis modulator could potentially be a target to develop novel therapies for PAH.

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Section: Discussionmentioning

confidence: 98%

Upregulation of Calcium Homeostasis Modulators in Contractile-To-Proliferative Phenotypical Transition of Pulmonary Arterial Smooth Muscle Cells

Rodriguez¹,

Chen²,

Jain³

et al. 2021

Front. Physiol.

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“…[ 4–7 ] In a balanced environment, humans encounter complicated situations and neurological reactions, such as a desire to refuse food‐intake after satiety, or to avoid salt after intaking too much of it. These responses are a result of cooperation of separate excitatory and inhibitory neurotransmitters in distinct microdomains within a single axon cooperate, [ 8–10 ] and may require the joint efforts of different sensory nerves. [ 11 ] These variable responses are consequences of synaptic plasticity.…”

Section: Figurementioning

confidence: 99%

Selective Release of Different Neurotransmitters Emulated by a p–i–n Junction Synaptic Transistor for Environment‐Responsive Action Control

Zhang¹,

Guo²,

Sun³

et al. 2021

Advanced Materials

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The design of the first p–i–n junction synaptic transistor (JST) based on n‐type TiO2 film covered with poly(methyl methacrylate) (PMMA) and with a p‐type P3HT/PEO nanowire (NW) on top. Except for basic synaptic functions that can be realized by a single neurotransmitter, the electronic device emulates the multiplexed neurotransmission of different neurotransmissions, i.e., glutamate and acetylcholine, for fast switching between short‐ and long‐term plasticity (STP and LTP). This is realized by the special p–i–n junction with hole transport in the p‐type P3HT NW to form STP, and electron transport in the n‐type TiO2 layer and trapped under the PMMA inversion layer to form LTP. Altering the external input induces changes of the polarity of the charge carriers in the conductive channel, promoting fast switching between STP and LTP modes. When stimulated using two parallel inputs, the response of PMMA/TiO2 emulates the synergistic effect of taste and aroma on the control of food‐intake in the brain. Because of the bipolarity, the p–i–n JST has excellent reconfigurability, which importantly is attributed to simulate the plasticity of synapses and to mimic how distinct types of gustatory receptor neurons respond to different concentrations of salt. The electronic device lays the technical foundation for the realization of the future complex artificial neural networks.

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“…Water is detected only by acid-sensing TRCs (type III cells), whereas support cells are type I cells. Acid-sensing taste bud cells (TBCs) are neuronal cells with visible synaptic vesicles that secrete ATP upon stimulation, as opposed to non-neuronal sweet, umami, and bitter TBCs that release ATP via calcium homeostasis modulator channels (37).…”

Section: Tongue Taste Water Receptors: Acid-sensing Taste Receptor Ce...mentioning

confidence: 99%

Regulation of Thirst and Vasopressin Release

Bichet

2019

Annu. Rev. Physiol.

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Recent experiments using optogenetic tools facilitate the identification and functional analysis of thirst neurons and vasopressin-producing neurons. Four major advances provide a detailed anatomy and physiology of thirst, taste for water, and arginine-vasopressin (AVP) release: ( a) Thirst and AVP release are regulated by the classical homeostatic, interosensory plasma osmolality negative feedback as well as by novel, exterosensory, anticipatory signals. These anticipatory signals for thirst and vasopressin release concentrate on the same homeostatic neurons and circumventricular organs that monitor the composition of blood. ( b) Acid-sensing taste receptor cells (TRCs) expressing otopetrin 1 on type III presynaptic TRCs on the tongue, which were previously suggested as the sour taste sensors, also mediate taste responses to water. ( c) Dehydration is aversive, and median preoptic nucleus (MnPO) neuron activity is proportional to the intensity of this aversive state. ( d) MnPOGLP1R neurons serve as a central detector that discriminates fluid ingestion from solid ingestion, which promotes acute satiation of thirst through the subfornical organ and other downstream targets.

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Opening a “Wide” Window onto Taste Signal Transmission

Abstract: Taste bud cells for sweet, umami, and bitter transmit sensory signals without a synapse. A study by Ma et al. (2018) finds a key ATP-permeable pore-forming subunit required for rapid neurotransmission from the tongue to secondary taste neurons.

Cited by 4 publications

References 10 publications

Upregulation of Calcium Homeostasis Modulators in Contractile-To-Proliferative Phenotypical Transition of Pulmonary Arterial Smooth Muscle Cells

Upregulation of Calcium Homeostasis Modulators in Contractile-To-Proliferative Phenotypical Transition of Pulmonary Arterial Smooth Muscle Cells

Selective Release of Different Neurotransmitters Emulated by a p–i–n Junction Synaptic Transistor for Environment‐Responsive Action Control

Regulation of Thirst and Vasopressin Release

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