scholarly journals Large enhancement of canine taste responses to sugars by salts.

1990 ◽  
Vol 95 (5) ◽  
pp. 1007-1018 ◽  
Author(s):  
T Kumazawa ◽  
K Kurihara
Keyword(s):  
Maximal Response ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Glucose Response ◽  
Low Concentrations ◽  
Large Enhancement ◽  
High Concentrations ◽  
Apical Membranes ◽  
The Hill ◽  
Concentration Response Curve

The effects of changed ionic environments on the canine taste responses to sugars were examined by recording the activity of the chorda tympani nerve. a) The responses to various sugars were greatly enhanced by the presence of salts having monovalent cations such as Na+, K+, choline+, or Tris+. The responses to sugars were suppressed by high concentrations of salts. (b) The presence of 100 mM NaCl in fructose solution did not affect the maximal response and changed the Hill constant for the concentration-response relationship from 1.3 to 2.4. (c) CaCl2 greatly enhanced the response to fructose, while MgCl2 exhibited practically no effect. The presence of 20 mM CaCl2 in fructose solution changed the Hill constant from 1.2 to 2.4. (d) CaCl2 suppressed the responses to 0.5 M sugars except for fructose and sucrose and enhanced the responses to all sugars examined at 1 M. In the glucose response, the slope of the concentration-response curve was increased by the presence of CaCl2. Here the curve in the absence of CaCl2 intersected with that in the presence of CaCl2, indicating that CaCl2 suppressed the response to glucose of low concentrations and enhanced that of high concentrations. (e) The enhancement of the sugar responses by salts was not simply explained in terms of ionic permeability at the apical membranes of taste cells. The enhanced and suppressed effects of salts on the sugar responses were interpreted in terms of the cooperativity between receptor molecules for sugars.

Large enhancement of canine taste responses to amino acids by salts

1993 ◽  
Vol 264 (6) ◽  
pp. R1071-R1076 ◽  
Author(s):  
T. Ugawa ◽  
K. Kurihara
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Sodium Potassium ◽  
Calcium Salts ◽  
Receptor Sites ◽  
Large Enhancement ◽  
Magnesium Salts ◽  
High Concentrations

The effects of salts on the canine taste responses to amino acids were examined by recording the activity of the chorda tympani nerve. 1) The tonic responses to most amino acids examined were significantly enhanced by the presence of various salts. 2) The degree of the enhancement varied with the species of amino acid and salt. The responses to most amino acids were enhanced by sodium, potassium, and calcium salts, but not enhanced by magnesium salts. The response to methionine, for example, was enhanced by NaCl, but not by Na phosphate of equimolar Na+. 3) The responses to glycine and alanine were suppressed by high concentrations of NaCl. 4) The presence of salts (NaCl and CaCl2) enhanced the responses to amino acids without affecting the thresholds for the amino acids, suggesting that the presence of the salts did not change the affinity of amino acids to the receptor sites. 5) The enhancing effects of salts on the responses to amino acids could not be explained in terms of permeability of cation and anion of salts. It was speculated that the binding of cation and anion of salts on the receptor membranes induces exposure of the receptor sites for amino acids available for binding of amino acids.

Antagonist actions of bicuculline methiodide and picrotoxin on extrasynaptic γ-aminobutyric acid receptors

1985 ◽  
Vol 63 (11) ◽  
pp. 1465-1470 ◽  
Author(s):  
A. W. Barolet ◽  
A. Li ◽  
S. Liske ◽  
M. E. Morris
Keyword(s):  
Membrane Conductance ◽  
Aminobutyric Acid ◽  
Maximal Response ◽  
Bicuculline Methiodide ◽  
Low Concentrations ◽  
Agonist And Antagonist ◽  
High Concentrations ◽  
The Right ◽  
Transmitter Uptake ◽  
Concentration Response Curve

The effects of picrotoxin and bicuculline methiodide to block depolarizing responses of extrasynaptic receptors for γ-aminobutyric acid (GABA) are compared using excitability testing of myelinated axons in amphibian peripheral nerve. The actions of the antagonists appear both complex and dissimilar. Picrotoxin (10–1000 μM) produces large reversible depressions of the maximal response to GABA (0.01–10 mM) and increases the EC50 from 0.33 to 12.6 mM. With high concentrations of agonist and antagonist an insensitive component is apparent. The action of picrotoxin is not classically noncompetitive: it may represent a mixed antagonism (competitive and noncompetitive) or a noncompetitive one, masked by the presence of receptor reserve and (or) secondary depolarizing influences (e.g., GABA-evoked [K+]o accumulation). Bicuculline methiodide (10–200 μM) shifts the GABA concentration–response curve to the right; maximal responses persist and are even enhanced. The impression that bicuculline methiodide has a competitive action is supported by analysis of its inhibition of responses to low concentrations of the agonist. It is suggested that the enhancement of GABA responses by bicuculline methiodide and their apparent resistance to block by picrotoxin may be due to a common secondary effect of the antagonists such as a decrease in membrane conductance to K+ and (or) block of transmitter uptake.

scholarly journals Effect of Pseudomonas moorei KB4 Cells’ Immobilisation on Their Degradation Potential and Tolerance towards Paracetamol

Molecules ◽  
2021 ◽  
Vol 26 (4) ◽  
pp. 820
Author(s):  
Robert Surma ◽  
Danuta Wojcieszyńska ◽  
Jagna Karcz ◽  
Urszula Guzik
Keyword(s):  
Protective Effect ◽  
Kinetic Parameters ◽  
Toxicity Assessment ◽  
Bacterial Cells ◽  
Low Concentrations ◽  
Toxicity Analysis ◽  
Immobilised Cells ◽  
Degradation Activity ◽  
High Concentrations ◽  
The Hill

Pseudomonas moorei KB4 is capable of degrading paracetamol, but high concentrations of this drug may cause an accumulation of toxic metabolites. It is known that immobilisation can have a protective effect on bacterial cells; therefore, the toxicity and degradation rate of paracetamol by the immobilised strain KB4 were assessed. Strain KB4 was immobilised on a plant sponge. A toxicity assessment was performed by measuring the concentration of ATP using the colony-forming unit (CFU) method. The kinetic parameters of paracetamol degradation were estimated using the Hill equation. Toxicity analysis showed a protective effect of the carrier at low concentrations of paracetamol. Moreover, a pronounced phenomenon of hormesis was observed in the immobilised systems. The obtained kinetic parameters and the course of the kinetic curves clearly indicate a decrease in the degradation activity of cells after their immobilisation. There was a delay in degradation in the systems with free cells without glucose and immobilised cells with glucose. However, it was demonstrated that the immobilised systems can degrade at least ten succeeding cycles of 20 mg/L paracetamol degradation. The obtained results indicate that the immobilised strain may become a useful tool in the process of paracetamol degradation.

Loss of sensitivity to low concentrations of NaCl following bilateral chorda tympani nerve sections in rats

1994 ◽  
Vol 19 (2) ◽  
pp. 169-184 ◽  
Author(s):  
Gwen B. O'Keefe ◽  
Juliann Schumm ◽  
James C. Smith
Keyword(s):  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Low Concentrations

scholarly journals Development of Rat Chorda Tympani Sodium Responses: Evidence for Age-Dependent Changes in Global Amiloride-Sensitive Na+Channel Kinetics

2000 ◽  
Vol 84 (3) ◽  
pp. 1531-1544 ◽  
Author(s):  
Susan J. Hendricks ◽  
Robert E. Stewart ◽  
Gerard L. Heck ◽  
John A. DeSimone ◽  
David L. Hill
Keyword(s):  
Kinetic Model ◽  
Maximum Rate ◽  
Taste Receptor ◽  
Taste Bud ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Channel Density ◽  
Age Dependent ◽  
Response Increase ◽  
Apical Membranes

In rat, chorda tympani nerve taste responses to Na+ salts increase between roughly 10 and 45 days of age to reach stable, mature magnitudes. Previous evidence from in vitro preparations and from taste nerve responses using Na+ channel blockers suggests that the physiological basis for this developmental increase in gustatory Na+ sensitivity is the progressive addition of functional, Na+ transduction elements (i.e., amiloride-sensitive Na+ channels) to the apical membranes of fungiform papilla taste receptor cells. To avoid potential confounding effects of pharmacological interventions and to permit quantification of aggregate Na+ channel behavior using a kinetic model, we obtained chorda tympani nerve responses to NaCl and sodium gluconate (NaGlu) during receptive field voltage clamp in rats aged from 12–14 to 60 days and older (60+ days). Significant, age-dependent increases in chorda tympani responses to these stimuli occurred as expected. Importantly, apical Na+ channel density, estimated from an apical Na+ channel kinetic model, increased monotonically with age. The maximum rate of Na+response increase occurred between postnatal days 12–14 and 29–31. In addition, estimated Na+ channel affinity increased between 12–14 and 19–23 days of age, i.e., on a time course distinct from that of the maximum rate of Na+response increase. Finally, estimates of the fraction of clamp voltage dropped across taste receptor apical membranes decreased between 19–23 and 29–31 days of age for NaCl but remained stable for NaGlu. The stimulus dependence of this change is consistent with a developmental increase in taste bud tight junctional Cl− ion permeability that lags behind the developmental increase in apical Na+ channel density. A significant, indirect anion influence on apical Na+ channel properties was present at all ages tested. This influence was evident in the higher apparent apical Na+ channel affinities obtained for NaCl relative to NaGlu. This stimulus-dependent modulation of apical Na+ channel apparent affinity relies on differences in the transepithelial potentials between NaCl and NaGlu. These originate from differences in paracellular anion permeability but act also on the driving force for Na+ through apical Na+channels. Detection of such an influence on taste depends fundamentally on the preservation of taste bud polarity and on a direct measure of sensory function, such as the response of primary afferents.

scholarly journals Effects of voltage perturbation of the lingual receptive field on chorda tympani responses to Na+ and K+ salts in the rat: implications for gustatory transduction.

1994 ◽  
Vol 104 (5) ◽  
pp. 885-907 ◽  
Author(s):  
Q Ye ◽  
G L Heck ◽  
J A DeSimone
Keyword(s):  
Receptive Field ◽  
Voltage Clamp ◽  
Maximal Response ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Salt Taste ◽  
Negative Voltage ◽  
Voltage Clamp Condition ◽  
Taste Cells ◽  
Clamp Condition

Taste sensory responses from the chorda tympani nerve of the rat were recorded with the lingual receptive field under current or voltage clamp. Consistent with previous results (Ye, Q., G. L. Heck, and J. A. DeSimone. 1993. Journal of Neurophysiology. 70:167-178), responses to NaCl were highly sensitive to lingual voltage clamp condition. This can be attributed to changes in the electrochemical driving force for Na+ ions through apical membrane transducer channels in taste cells. In contrast, responses to KCl over the concentration range 50-500 mM were insensitive to the voltage clamp condition of the receptive field. These results indicate the absence of K+ conductances comparable to those for Na+ in the apical membranes of taste cells. This was supported by the strong anion dependence of K salt responses. At zero current clamp, the potassium gluconate (KGlu) threshold was > 250 mM, and onset kinetics were slow (12 s to reach half-maximal response). Faster onset kinetics and larger responses to KGlu occurred at negative voltage clamp (-50 mV). This indicates that when K+ ion is transported as a current, and thereby uncoupled from gluconate mobility, its rate of delivery to the K+ taste transducer increases. Analysis of conductances shows that the paracellular pathway in the lingual epithelium is 28 times more permeable to KCl than to KGlu. Responses to KGlu under negative voltage clamp were not affected by agents that are K+ channel blockers in other systems. The results indicate that K salt taste transduction is under paracellular diffusion control, which limits chemoreception efficiency. We conclude that rat K salt taste occurs by means of a subtight junctional transducer for K+ ions with access limited by anion mobility. The data suggest that this transducer is not cation selective which also accounts for the voltage and amiloride insensitive part of the response to NaCl.

Existence of two types of postjunctional α-adrenoceptors in the isolated canine internal carotid artery

1988 ◽  
Vol 66 (5) ◽  
pp. 655-659 ◽  
Author(s):  
Yasuaki Kawai ◽  
Shigeaki Kobayashi ◽  
Toshio Ohhashi
Keyword(s):  
Response Curve ◽  
Carotid Arteries ◽  
Internal Carotid ◽  
The Other ◽  
Low Concentrations ◽  
Selective Agonists ◽  
High Concentrations ◽  
The Right ◽  
Internal Carotid Arteries ◽  
Concentration Response Curve

The pharmacological characteristics of postjunctional α-adrenoceptors in isolated canine internal carotid arteries were investigated by the use of selective agonists and antagonists for α1 and α2-adrenoceptors. Norepinephrine, phenylephrine, and xylazine caused concentration-dependent contractions in the helical strips. The contraction induced by 10−4 M xylazine was significantly smaller than that produced by 10−4 M norepinephrine or 10−4 M phenylephrine. The contraction induced by 10−4 M phenylephrine was almost the same value as that induced by 10−4 M norepinephrine. Phentolamine (10−8 and 10−7 M) caused a parallel shift to the right of the concentration–response curve to norepinephrine. The contractile responses to low concentrations of norepinephrine were significantly suppressed by pretreatment with an α2-antagonist such as yohimbine (10−9 and 10−8 M) or DG 5128(10−7 and 10−6 M). On the other hand, the responses to higher concentrations of norepinephrine were mainly reduced by low concentrations of an α1-antagonist, prazosin (3 × 10−10 and 3 × 10−9 M). These results suggest that both α1- and α2-adrenoceptors are located on the plasma membrane of smooth muscle cells in canine internal carotid arteries and that the norepinephrine-induced contractions at low and high concentrations are mainly mediated by activation of α2- and α1-adrenoceptors, respectively.

scholarly journals Immunoglobulin E decapeptide-induced 5-hydroxytryptamine release from rat peritoneal mast cells. Comparison with corticotropin-(1–24)-peptide, polyarginine, polylysine and antigen

1981 ◽  
Vol 198 (3) ◽  
pp. 615-619 ◽  
Author(s):  
J W Coleman ◽  
S T Holgate ◽  
M K Church ◽  
R C Godfrey
Keyword(s):  
Mast Cells ◽  
Benzalkonium Chloride ◽  
Immunoglobulin E ◽  
Response Curves ◽  
Low Concentrations ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
High Concentrations ◽  
Concentration Response Curve ◽  
Net Release

A synthetic basic decapeptide from the C4 domain of human immunoglobulin E, corticotropin-(1-24)-peptide, polyarginine and polylysine stimulated up to 90% net release of 5-hydroxytryptamine from mast cells in rat peritoneal-cell suspensions. Concentration-response curves to all four polypeptides were parallel. Polyarginine and polylysine (EC50 congruent to 0.05 microM) were approximately 100-fold more potent than immunoglobulin E decapeptide and corticotropin-(1-24)-peptide (EC50 congruent to 5 microM). Polypeptide-induced release was complete within 5-10s. Immunoglobulin-E-decapeptide-induced 5-hydroxytryptamine release was additive to that induced by low concentrations of polyarginine, but non-additive to that induced by high concentrations of polyarginine. In contrast, release induced by antigen was additive along the whole length of the concentration-response curve to polyarginine. Benzalkonium chloride inhibited immunoglobulin-E-decapeptide- and polyarginine-induced 5-hydroxytryptamine release but enhanced release induced by immunological stimulation.

scholarly journals Strain differences in the neural, behavioral, and molecular correlates of sweet and salty taste in naive, ethanol- and sucrose-exposed P and NP rats

2011 ◽  
Vol 106 (5) ◽  
pp. 2606-2621 ◽  
Author(s):  
Jamison Coleman ◽  
Ashley Williams ◽  
Tam-Hao T. Phan ◽  
Shobha Mummalaneni ◽  
Pamela Melone ◽  
...  
Keyword(s):  
Behavioral Responses ◽  
Strain Differences ◽  
Ethanol Exposure ◽  
Chorda Tympani ◽  
Maximum Enhancement ◽  
Low Concentrations ◽  
Salty Taste ◽  
Chronic Ingestion ◽  
Response Profiles ◽  
High Concentrations

Strain differences between naive, sucrose- and ethanol-exposed alcohol-preferring (P) and alcohol-nonpreferring (NP) rats were investigated in their consumption of ethanol, sucrose, and NaCl; chorda tympani (CT) nerve responses to sweet and salty stimuli; and gene expression in the anterior tongue of T1R3 and TRPV1/TRPV1t. Preference for 5% ethanol and 10% sucrose, CT responses to sweet stimuli, and T1R3 expression were greater in naive P rats than NP rats. The enhancement of the CT response to 0.5 M sucrose in the presence of varying ethanol concentrations (0.5–40%) in naive P rats was higher and shifted to lower ethanol concentrations than NP rats. Chronic ingestion of 5% sucrose or 5% ethanol decreased T1R3 mRNA in NP and P rats. Naive P rats also demonstrated bigger CT responses to NaCl+benzamil and greater TRPV1/TRPV1t expression. TRPV1t agonists produced biphasic effects on NaCl+benzamil CT responses, enhancing the response at low concentrations and inhibiting it at high concentrations. The concentration of a TRPV1/TRPV1t agonist (Maillard reacted peptides conjugated with galacturonic acid) that produced a maximum enhancement in the NaCl+benzamil CT response induced a decrease in NaCl intake and preference in P rats. In naive P rats and NP rats exposed to 5% ethanol in a no-choice paradigm, the biphasic TRPV1t agonist vs. NaCl+benzamil CT response profiles were higher and shifted to lower agonist concentrations than in naive NP rats. TRPV1/TRPV1t mRNA expression increased in NP rats but not in P rats exposed to 5% ethanol in a no-choice paradigm. We conclude that P and NP rats differ in T1R3 and TRPV1/TRPV1t expression and neural and behavioral responses to sweet and salty stimuli and to chronic sucrose and ethanol exposure.

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