scholarly journals Changes in taste receptor cell [Ca2+]i modulate chorda tympani responses to salty and sour taste stimuli

2012 ◽  
Vol 108 (12) ◽  
pp. 3206-3220 ◽  
Author(s):  
John A. DeSimone ◽  
ZuoJun Ren ◽  
Tam-Hao T. Phan ◽  
Gerard L. Heck ◽  
Shobha Mummalaneni ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Receptor Cell ◽  
Imaging Techniques ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Taste Receptor Cell ◽  
Atpase Inhibitor ◽  
Acetoxymethyl Ester ◽  
Phasic Response ◽  
Sour Taste

The relationship between taste receptor cell (TRC) Ca2+ concentration ([Ca2+]i) and rat chorda tympani (CT) nerve responses to salty [NaCl and NaCl+benzamil (Bz)] and sour (HCl, CO2, and acetic acid) taste stimuli was investigated before and after lingual application of ionomycin+Ca2+, 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM), U73122 (phospholipase C blocker), and thapsigargin (Ca2+-ATPase inhibitor) under open-circuit or lingual voltage-clamp conditions. An increase in TRC [Ca2+]i attenuated the tonic Bz-sensitive NaCl CT response and the apical membrane Na+ conductance. A decrease in TRC [Ca2+]i enhanced the tonic Bz-sensitive and Bz-insensitive NaCl CT responses and apical membrane Na+ conductance but did not affect CT responses to KCl or NH4Cl. An increase in TRC [Ca2+]i did not alter the phasic response but attenuated the tonic CT response to acidic stimuli. A decrease in [Ca2+]i did not alter the phasic response but attenuated the tonic CT response to acidic stimuli. In a subset of TRCs, a positive relationship between [H+]i and [Ca2+]i was obtained using in vitro imaging techniques. U73122 inhibited the tonic CT responses to NaCl, and thapsigargin inhibited the tonic CT responses to salty and sour stimuli. The results suggest that salty and sour taste qualities are transduced by [Ca2+]i-dependent and [Ca2+]i-independent mechanisms. Changes in TRC [Ca2+]i in a BAPTA-sensitive cytosolic compartment regulate ion channels and cotransporters involved in the salty and sour taste transduction mechanisms and in neural adaptation. Changes in TRC [Ca2+]i in a separate subcompartment, sensitive to inositol trisphosphate and thapsigargin but inaccessible to BAPTA, are associated with neurotransmitter release.

scholarly journals Changes in taste receptor cell [Ca2+]i modulate chorda tympani responses to bitter, sweet, and umami taste stimuli

2012 ◽  
Vol 108 (12) ◽  
pp. 3221-3232 ◽  
Author(s):  
John A. DeSimone ◽  
Tam-Hao T. Phan ◽  
ZuoJun Ren ◽  
Shobha Mummalaneni ◽  
Vijay Lyall
Keyword(s):  
Receptor Cell ◽  
Synergistic Effects ◽  
Monosodium Glutamate ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Taste Receptor Cell ◽  
Acetoxymethyl Ester ◽  
Umami Taste ◽  
Before And After ◽  
Intracellular Ca

The relationship between taste receptor cell (TRC) intracellular Ca2+ ([Ca2+]i) and rat chorda tympani (CT) nerve responses to bitter (quinine and denatonium), sweet (sucrose, glycine, and erythritol), and umami [monosodium glutamate (MSG) and MSG + inosine 5′-monophosphate (IMP)] taste stimuli was investigated before and after lingual application of ionomycin (Ca2+ ionophore) + Ca2+, 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM; Ca2+ chelator), U73122 (phospholipase C blocker), thapsigargin (Ca2+-ATPase blocker), and diC8-PIP2 (synthetic phosphatidylinositol 4,5-bisphosphate). The phasic CT response to quinine was indifferent to changes in [Ca2+]i. However, a decrease in [Ca2+]i inhibited the tonic part of the CT response to quinine. The CT responses to sweet and umami stimuli were indifferent to changes in TRC [Ca2+]i. However, a decrease in [Ca2+]i attenuated the synergistic effects of ethanol on the CT response to sweet stimuli and of IMP on the glutamate CT response. U73122 and thapsigargin inhibited the phasic and tonic CT responses to bitter, sweet, and umami stimuli. Although diC8-PIP2 increased the CT response to bitter and sweet stimuli, it did not alter the CT response to glutamate but did inhibit the synergistic effect of IMP on the glutamate response. The results suggest that bitter, sweet, and umami taste qualities are transduced by [Ca2+]i-dependent and [Ca2+]i-independent mechanisms. Changes in TRC [Ca2+]i in the BAPTA-sensitive cytosolic compartment regulate quality-specific taste receptors and ion channels that are involved in the neural adaptation and mixture interactions. Changes in TRC [Ca2+]i in a separate subcompartment, sensitive to inositol trisphosphate and thapsigargin but inaccessible to BAPTA and ionomycin + Ca2+, are associated with neurotransmitter release.

Effects of osmolarity on taste receptor cell size and function

1999 ◽  
Vol 277 (4) ◽  
pp. C800-C813 ◽  
Author(s):  
Vijay Lyall ◽  
Gerard L. Heck ◽  
John A. DeSimone ◽  
George M. Feldman
Keyword(s):  
Cell Volume ◽  
Receptor Cell ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Taste Receptor Cell ◽  
Salt Taste ◽  
Receptor Cells ◽  
Enhanced Ct ◽  
And Function ◽  
Osmotic Effects

Osmotic effects on salt taste were studied by recording from the rat chorda tympani (CT) nerve and by measuring changes in cell volume of isolated rat fungiform taste receptor cells (TRCs). Mannitol, cellobiose, urea, or DMSO did not induce CT responses. However, the steady-state CT responses to 150 mM NaCl were significantly increased when the stimulus solutions also contained 300 mM mannitol or cellobiose, but not 600 mM urea or DMSO. The enhanced CT responses to NaCl were reversed when the saccharides were removed and were completely blocked by addition of 100 μM amiloride to the stimulus solution. Exposure of TRCs to hyperosmotic solutions of mannitol or cellobiose induced a rapid and sustained decrease in cell volume that was completely reversible, whereas exposure to hypertonic urea or DMSO did not induce sustained reductions in cell volume. These data suggest that the osmolyte-induced increase in the CT response to NaCl involves a sustained decrease in TRC volume and the activation of amiloride-sensitive apical Na+ channels.

Experimentally cross-wired lingual taste nerves can restore normal unconditioned gaping behavior in response to quinine stimulation

2008 ◽  
Vol 294 (3) ◽  
pp. R738-R747 ◽  
Author(s):  
Camille T. King ◽  
Mircea Garcea ◽  
Danielle S. Stolzenberg ◽  
Alan C. Spector
Keyword(s):  
Receptor Cell ◽  
Recovery Of Function ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Gustatory System ◽  
Unresolved Issue ◽  
Taste Receptor Cell ◽  
Receptor Field ◽  
Gustatory Nerve ◽  
Posterior Tongue

Studies examining the effects of transection and regeneration of the glossopharyngeal (GL) and chorda tympani (CT) nerves on various taste-elicited behaviors in rats have demonstrated that the GL (but not the CT) nerve is essential for the maintenance of both an unconditioned protective reflex (gaping) and the neural activity observed in central gustatory structures in response to lingual application of a bitter substance. An unresolved issue, however, is whether recovery depends more on the taste nerve and the central circuits that it supplies and/or on the tongue receptor cell field being innervated. To address this question, we experimentally cross-wired these taste nerves, which, remarkably, can regenerate into parts of the tongue they normally do not innervate. We report that quinine-stimulated gaping behavior was fully restored, and neuronal activity, as assessed by Fos immunohistochemistry in the nucleus of the solitary tract and the parabrachial nucleus, was partially restored only if the posterior tongue (PT) taste receptor cell field was reinnervated; the particular taste nerve supplying the input was inconsequential to the recovery of function. Thus, PT taste receptor cells appear to play a privileged role in triggering unconditioned gaping to bitter tasting stimuli, regardless of which lingual gustatory nerve innervates them. Our findings demonstrate that even when a lingual gustatory nerve (the CT) forms connections with taste cells in a non-native receptor field (the PT), unconditioned taste rejection reflexes to quinine can be maintained. These findings underscore the extraordinary ability of the gustatory system to adapt to peripherally reorganized input for particular behaviors.

A Novel Pharmacological Probe Links the Amiloride-Insensitive NaCl, KCl, and NH4Cl Chorda Tympani Taste Responses

2001 ◽  
Vol 86 (5) ◽  
pp. 2638-2641 ◽  
Author(s):  
John A. DeSimone ◽  
Vijay Lyall ◽  
Gerard L. Heck ◽  
Tam-Hao T. Phan ◽  
Rammy I. Alam ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Apical Membrane ◽  
Cetylpyridinium Chloride ◽  
Taste Receptor ◽  
Chorda Tympani ◽  
Intracellular Acidification ◽  
Cellular Origin ◽  
Receptor Cells ◽  
Nacl Concentration

Chorda tympani taste nerve responses to NaCl can be dissected pharmacologically into amiloride-sensitive and -insensitive components. It is now established that the amiloride-sensitive, epithelial sodium channel acts as a sodium-specific ion detector in taste receptor cells (TRCs). Much less is known regarding the cellular origin of the amiloride-insensitive component, but its anion dependence indicates an important role for paracellular shunts in the determination of its magnitude. However, this has not precluded the possibility that undetected apical membrane ion pathways in TRCs may also contribute to its origin. Progress toward making such a determination has suffered from lack of a pharmacological probe for an apical amiloride-insensitive taste pathway. We present data here showing that, depending on the concentration used, cetylpyridinium chloride (CPC) can either enhance or inhibit the amiloride-insensitive response to NaCl. The CPC concentration giving maximal enhancement was 250 μM. At 2 mM, CPC inhibited the entire amiloride-insensitive part of the NaCl response. The NaCl response is, therefore, composed entirely of amiloride- and CPC-sensitive components. The magnitude of the maximally enhanced CPC-sensitive component varied with the NaCl concentration and was half-maximal at [NaCl] = 62 ± 11 (SE) mM. This was significantly less than the corresponding parameter for the amiloride-sensitive component (268 ± 71 mM). CPC had similiar effects on KCl and NH4Cl responses except that in these cases, after inhibition with 2 mM CPC, a significant CPC-insensitive response remained. CPC (2 mM) inhibited intracellular acidification of TRCs due to apically presented NH4Cl, suggesting that CPC acts on an apical membrane nonselective cation pathway.

scholarly journals Taste Receptor Cells in Mice Express Receptors for the Hormone Adiponectin

2018 ◽  
Author(s):  
Sean M. Crosson ◽  
Andrew Marques ◽  
Peter Dib ◽  
Cedrick D. Dotson ◽  
Steven D. Munger ◽  
...  
Keyword(s):  
Cell Function ◽  
Receptor Cell ◽  
Taste Receptor ◽  
Acid Oxidation ◽  
Taste Receptor Cell ◽  
Umami Taste ◽  
Receptor Cells ◽  
Taste Receptor Cells ◽  
Immunohistochemical Studies ◽  
Adipocyte Development

AbstractThe metabolic hormone adiponectin is secreted into the circulation by adipocytes, and mediates key biological functions including insulin sensitivity, adipocyte development, and fatty acid oxidation. Adiponectin is also abundant in saliva, where its functions are poorly understood. Here we report that murine taste receptor cells express adiponectin receptors, and may be a target for salivary adiponectin. Analysis of a transcriptome dataset obtained by RNA-seq analysis of purified circumvallate taste buds, revealed high expression levels for three adiponectin receptor types. Immunohistochemical studies showed that two of these receptors, AdipoR1 and T-cadherin, are localized to subsets of taste receptor cells. Immunofluorescence for T-cadherin was primarily co-localized with the Type 2 taste receptor cell marker phospholipase β2, suggesting that adiponectin signaling could impact sweet, bitter, or umami taste signaling. However, adiponectin null mice showed no differences in taste responsiveness compared to wildtype controls in brief-access taste testing. AAV-mediated overexpression of adiponectin in the salivary glands of adiponectin null mice did result in a small but significant increase in behavioral taste responsiveness to the fat emulsion Intralipid. Together, these results suggest that salivary adiponectin can effect taste receptor cell function, though its impact on taste responsiveness and peripheral taste coding remains unclear.

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