Electrophysiological Studies on Human Taste Nerves

Diamant, H; Funakoshi, Mitsuaki; Ström, Lennart; Zotterman, Yngve

doi:10.1016/b978-1-4831-9834-7.50020-2

Cited by 44 publications

(19 citation statements)

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“…Rodents also perceive similarities in the oral properties of ethanol and sweet-tasting stimuli, as conditioned aversions to the orosensory features of ethanol generalize to sucrose mixtures in rats (Di Lorenzo et al 1986;Kiefer et al 1990; Kiefer and Lawrence 1988;Kiefer and Mahadevan 1993) and taste aversions to sucrose alone generalize to ethanol in C57BL/6J (B6) mice (Blizard and McClearn 2000). Furthermore, neurophysiological studies across multiple species have demonstrated positive associations between responses to oral alcohol and sweet stimuli in peripheral gustatory fibers (Danilova and Hellekant 2000;Diamant et al 1963;Hellekant et al 1997;Sako and Yamamoto 1999) and central taste-sensitive neurons (Brasser et al 2010;Di Lorenzo et al 1986;Lemon et al 2004;Lemon and Smith 2005). Selective antagonism of sweet taste receptors also directly suppresses oral responses to alcohol by gustatory-sensitive sensory neurons (Lemon et al 2004;Sako and Yamamoto 1999), implicating sweet receptors in the transduction of alcohol taste.…”

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confidence: 99%

Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats

Lemon

Wilson

Brasser

2011

Journal of Neurophysiology

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Lemon CH, Wilson DM, Brasser SM. Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats. J Neurophysiol 106: 3145-3156, 2011. First published September 14, 2011 doi:10.1152/jn.00580.2011In randomly bred rats, orally applied ethanol stimulates neural substrates for appetitive sweet taste. To study associations between ethanol's oral sensory characteristics and genetically mediated ethanol preference, we made electrophysiological recordings of oral responses (spike density) by taste-sensitive nucleus tractus solitarii neurons in anesthetized selectively bred ethanol-preferring (P) rats and their genetically heterogeneous Wistar (W) control strain. Stimuli (25 total) included ethanol [3%, 5%, 10%, 15%, 25%, and 40% (vol/vol)], a sucrose series (0.01, 0.03, 0.1, 0.3, 0.5, and 1 M), and other sweet, salt, acidic, and bitter stimuli; 50 P and 39 W neurons were sampled. k-means clustering applied to the sucrose response series identified cells showing high (S 1 ) or relatively low (S 0 ) sensitivity to sucrose. A three-way factorial analysis revealed that activity to ethanol was influenced by a neuron's sensitivity to sucrose, ethanol concentration, and rat line (P ϭ 0.01). Ethanol produced concentration-dependent responses in S 1 neurons that were larger than those in S 0 cells. Although responses to ethanol by S 1 cells did not differ between lines, neuronal firing rates to ethanol in S 0 cells increased across concentration only in P rats. Correlation and multivariate analyses revealed that ethanol evoked responses in W neurons that were strongly and selectively associated with activity to sweet stimuli, whereas responses to ethanol by P neurons were not easily associated with activity to representative sweet, sodium salt, acidic, or bitter stimuli. These findings show differential central neural representation of oral ethanol between genetically heterogeneous rats and P rats genetically selected to prefer alcohol.

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confidence: 99%

Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats

Lemon

Wilson

Brasser

2011

Journal of Neurophysiology

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“…Primary trigeminal afferents in primates have also been reported to respond to orally applied ethanol at concentrations as low as 0.7 M (~4%; Danilova and Hellekant 2002). Ethanol’s trigeminal stimulant effects, however, have been shown to increase as a function of concentration in both peripheral trigeminal nerve fibers (Danilova and Hellekant 2002) and central neurons in the brain stem trigeminal subnucleus caudalis (>15%; Carstens et al 1998), consistent with psychophysical ratings in humans of greater burning and irritant sensations with increasing alcohol concentration (Diamant et al 1963; Green 1987, 1988; Wilson et al 1973). The present findings of a uniform reduction in ethanol avoidance in TRPV1 deficient mice independent of concentration would suggest that mechanisms other than TRPV1 may be responsible for concentration-dependent increases in trigeminal activity with rising ethanol concentration.…”

Section: Discussionmentioning

confidence: 59%

“…Oral application of ethanol to the tongue activates peripheral lingual afferent fibers of the trigeminal nerve in the cat (Hellekant 1965), rat (Simon and Sostman 1991) and non-human primate (Danilova and Hellekant 2002), and produces a concentration-dependent increase in activity of central neurons in the rodent brain stem trigeminal subnucleus caudalis (Carstens et al 1998). Stimulation of such substrates presumably underlies the burning and irritant sensations to oral alcohol reported in human psychophysical studies, particularly at higher concentrations (Diamant et al 1963; Green 1987, 1988, 1990; Wilson et al 1973). …”

Section: Introductionmentioning

confidence: 99%

Reduced Oral Ethanol Avoidance in Mice Lacking Transient Receptor Potential Channel Vanilloid Receptor 1

2008

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Ethanol is a known oral trigeminal stimulant and recent data indicate that these effects are mediated in part by transient receptor potential channel vanilloid receptor 1 (TRPV1). The importance of this receptor in orally mediated ethanol avoidance is presently unknown. Here, we compared orosensory responding to ethanol in TRPV1-deficient and wild type mice in a brief-access paradigm that assesses orosensory influences by measuring immediate licking responses to small stimulus volumes. TRPV1−/− and control mice were tested with six concentrations of ethanol (3, 5, 10, 15, 25, 40%), capsaicin (0.003, 0.01, 0.03, 0.1, 0.3, 1 mM), sucrose (0.003, 0.01, 0.03, 0.1, 0.3, 1 M), and quinine (0.01, 0.03, 0.1, 0.3, 1, 3 mM) and psychophysical concentration-response functions were generated for each genotype and stimulus. TRPV1 knockouts displayed reduced oral avoidance responses to ethanol regardless of concentration, insensitivity to capsaicin, and little to no difference in sweet or bitter taste responding relative to wild type mice. These data indicate that the TRPV1 channel plays a role in orosensory-mediated ethanol avoidance, but that other receptor mechanisms likely also contribute to aversive oral responses to alcohol.

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“…Ethanol also directly activates sensory nociceptors including transient receptor potential channel vanilloid receptor 1 [TRPV1; 53], the receptor for capsaicin [54–55], which shows heavy localization on sensory fibers that innervate the oral epithelium [56–57]. These trigeminal circuits process noxious chemical and thermal input from the oral cavity, and ethanol’s ability to stimulate these pathways presumably underlies the burning and irritant sensations to oral alcohol reported in human psychophysical studies, especially at high concentrations [58–62]. Human psychophysical data have further shown that noxious oral sensations processed by the trigeminal system can be confused with bitter taste [63], and thus potentially such cross-modal generalization could account for the perception of a “bitter” taste component to ethanol by humans, as well as the conditioned taste aversion generalization between ethanol and sweet-bitter mixtures in rodents [40,42].…”

Section: Oral Sensory Processing Of Ethanolmentioning

confidence: 99%

Alcohol sensory processing and its relevance for ingestion

Brasser

Castro

Feretic

2015

Physiology & Behavior

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Alcohol possesses complex sensory attributes that are first detected by the body via sensory receptors and afferent fibers that promptly transmit signals to brain areas involved in mediating ingestive motivation, reinforcement, and addictive behavior. Given that the chemosensory cues accompanying alcohol consumption are among the most intimate, consistent, and immediate predictors of alcohol’s postabsorptive effects, with experience these stimuli also gain powerful associative incentive value to elicit craving and related physiologic changes, maintenance of ongoing alcohol use, and reinstatement of drug seeking after periods of abstinence. Despite the above, preclinical research has traditionally dichotomized alcohol’s taste and postingestive influences as independent regulators of motivation to drink. The present review summarizes current evidence regarding alcohol’s ability to directly activate peripheral and central oral chemosensory circuits, relevance for intake of the drug, and provides a framework for moving beyond a dissociation between the sensory and postabsorptive effects of alcohol to understand their neurobiological integration and significance for alcohol addiction.

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Electrophysiological Studies on Human Taste Nerves

Cited by 44 publications

References 4 publications

Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats

Differential neural representation of oral ethanol by central taste-sensitive neurons in ethanol-preferring and genetically heterogeneous rats

Reduced Oral Ethanol Avoidance in Mice Lacking Transient Receptor Potential Channel Vanilloid Receptor 1

Alcohol sensory processing and its relevance for ingestion

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