Cooling sensations arise inside the mouth during ingestive and homeostasis behaviors. Oral presence of cooling temperature engages the cold and menthol receptor TRPM8 (transient receptor potential melastatin 8) on trigeminal afferents. Yet, how TRPM8 influences brain and behavioral responses to oral temperature is undefined.
View Article and Find Full Text PDFDevelopmental exposure to ethanol is a leading cause of cognitive, emotional and behavioral problems, with fetal alcohol spectrum disorder (FASD) affecting more than 1:100 children. Recently, comorbid sleep deficits have been highlighted in these disorders, with sleep repair a potential therapeutic target. Animal models of FASD have shown non-REM (NREM) sleep fragmentation and slow-wave oscillation impairments that predict cognitive performance.
View Article and Find Full Text PDFTrigeminal neurons convey somatosensory information from craniofacial tissues. In mouse brain, ascending projections from medullary trigeminal neurons arrive at taste neurons in the parabrachial (PB) nucleus, suggesting that taste neurons participate in somatosensory processing. However, the cell types that support this convergence were undefined.
View Article and Find Full Text PDFCurr Opin Physiol
April 2021
Temperature sensation contributes to human enjoyment of foods and beverages. The mouthfeel of warmed foods or drinking ice-cold water on a hot day are respectively pleasant and refreshing. Although historically under-studied for a role in food preference, new data have shed light on how oral temperature sensing and thermoreceptor mechanisms inside the mouth influence ingestive acceptance behaviors in rodent models used in flavor neurobiology.
View Article and Find Full Text PDFThe flavoring agent menthol elicits complex orosensory and behavioral effects including perceived cooling at low concentrations and irritation and ingestive avoidance at higher intensities. Oral menthol engages the cold-activated transient receptor potential (TRP) ion channel TRP melastatin 8 (TRPM8) on trigeminal fibers, although its aversive feature was discussed to involve activation of TRP ankyrin 1 (TRPA1) associated with nociceptive processing. Here, we studied the roles of TRPM8 and TRPA1 in orosensory responding to menthol by subjecting mice gene deficient for either channel to brief-access exposure tests, which measure immediate licking responses to fluid stimuli to capture sensory/tongue control of behavior.
View Article and Find Full Text PDFTaste and somatosensation both mediate protective behaviors. Bitter taste guides avoidance of ingestion of toxins while pain sensations, such as noxious heat, signal adverse conditions to ward off harm. Although brain pathways for taste and somatosensation are typically studied independently, prior data suggest that they intersect, potentially reflecting their common protective role.
View Article and Find Full Text PDFTaste stimuli have a temperature that can stimulate thermosensitive neural machinery in the mouth during gustatory experience. Although taste and oral temperature are sometimes discussed as different oral sensory modalities, there is a body of literature that demonstrates temperature is an important component and modulator of the intensity of gustatory neural and perceptual responses. Available data indicate that the influence of temperature on taste, herein referred to as "thermogustation," can vary across taste qualities, can also vary among stimuli presumed to share a common taste quality, and is conditioned on taste stimulus concentration, with neuronal and psychophysical data revealing larger modulatory effects of temperature on gustatory responding to weakened taste solutions compared with concentrated.
View Article and Find Full Text PDFOral temperature is a component and modifier of taste perception. Both trigeminal (V) and taste-sensitive cells, including those in the nucleus of the solitary tract (NTS), can respond to oral temperature. However, functional associations in thermal sensitivity between V and gustatory neurons are poorly understood.
View Article and Find Full Text PDFIntroduction: This mini-review discusses some of the parallels between rodent neurophysiological and human psychophysical data concerning temperature effects on sweet taste.
Methods And Purpose: "Sweet" is an innately rewarding taste sensation that is associated in part with foods that contain calories in the form of sugars. Humans and other mammals can show unconditioned preference for select sweet stimuli.
The temperature of taste stimuli can modulate gustatory processing. Perceptual data indicate that the adapted temperature of oral epithelia also influences gustation, although little is known about the neural basis of this effect. Here, we electrophysiologically recorded orosensory responses (spikes) to 25°C (cool) and 35°C (warm) solutions of sucrose (0.
View Article and Find Full Text PDFTemperature can modify neural and behavioral responses to taste stimuli that elicit "sweetness," a perception linked to intake of calorie-laden foods. However, the role of temperature in the neural representation of sweet taste is poorly understood. Here we made electrophysiological recordings from gustatory neurons in the medulla of inbred mice to study how adjustments in taste solution temperature to cool (18°C), ambient (22°C), and warm (30°C and 37°C) values changed the magnitude and latency of gustatory activity to sucrose (0, 0.
View Article and Find Full Text PDFChanges in oral temperature can influence taste perception, indicating overlap among mechanisms for taste and oral somesthesis. Medullary gustatory neurons can show cosensitivity to temperature, albeit how these cells process combined taste and thermal input is poorly understood. Here, we electrophysiologically recorded orosensory responses (spikes) from 39 taste-sensitive neurons in the nucleus tractus solitarii of anesthetized mice during oral delivery of tastants adjusted to innocuous cool (16 and 18°C), room (22°C, baseline), and warm (30 and 37°C) oral temperatures.
View Article and Find Full Text PDFA growing literature suggests taste stimuli commonly classified as "bitter" induce heterogeneous neural and perceptual responses. Here, the central processing of bitter stimuli was studied in mice with genetically controlled bitter taste profiles. Using these mice removed genetic heterogeneity as a factor influencing gustatory neural codes for bitter stimuli.
View Article and Find Full Text PDFAlcohol activates orosensory circuits that project to motivationally relevant limbic forebrain areas that control appetite, feeding and drinking. To date, limited data exists regarding the contribution of chemosensory-derived ethanol reinforcement to ethanol preference and consumption. Measures of taste reactivity to intra-orally infused ethanol have not found differences in initial orofacial responses to alcohol between alcohol-preferring (P) and alcohol-non-preferring (NP) genetically selected rat lines.
View Article and Find Full Text PDFIn 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.
View Article and Find Full Text PDFThis paper reviews the physiology of taste processing and ingestive decisions.
View Article and Find Full Text PDFElevated alcohol consumption is associated with enhanced preference for sweet substances across species and may be mediated by oral alcohol-induced activation of neurobiological substrates for sweet taste. Here, we directly examined the contribution of the T1r3 receptor protein, important for sweet taste detection in mammals, to ethanol intake and preference and the neural processing of ethanol taste by measuring behavioral and central neurophysiological responses to oral alcohol in T1r3 receptor-deficient mice and their C57BL/6J background strain. T1r3 knockout and wild-type mice were tested in behavioral preference assays for long-term voluntary intake of a broad concentration range of ethanol, sucrose, and quinine.
View Article and Find Full Text PDFT1r3 is a critical subunit of T1r sweet taste receptors. Here we studied how the absence of T1r3 impacts responses to sweet stimuli by taste neurons in the nucleus tractus solitarius (NTS) of the mouse. The consequences bear on the multiplicity of sweet taste receptors and how T1r3 influences the distribution of central gustatory neurons.
View Article and Find Full Text PDFAlthough there have been many recent advances in the field of gustatory neurobiology, our knowledge of how the nervous system is organized to process information about taste is still far from complete. Many studies on this topic have focused on understanding how gustatory neural circuits are spatially organized to represent information about taste quality (e.g.
View Article and Find Full Text PDFWe explored how variability in responding to taste stimuli could impact the signaling of taste quality information by neuron types and individual cells in the nucleus of the solitary tract. One hundred sixty-two neurons recorded from anesthetized rats were grouped using multivariate analysis of taste responses to the following (in m): 0.5 sucrose, 0.
View Article and Find Full Text PDFJ Neurophysiol
December 2005
Based on the molecular findings that many bitter taste receptors (T2Rs) are expressed within the same receptor cells, it has been proposed that bitter taste is encoded by the activation of discrete neural elements. Here we examined how a variety of bitter stimuli are represented by neural activity in central gustatory neurons. Taste responses (spikes/s) evoked by bathing the tongue and palate with intensity-matched concentrations (in M) of 2 sugars (0.
View Article and Find Full Text PDFA strong positive association exists between the ingestion of alcohol and sweet-tasting solutions. The neural mechanisms underlying this relationship are unknown, although recent data suggest that gustatory substrates are involved. Here, we examined the role of sweet taste receptors and central neural circuits for sugar taste in the gustatory processing of ethanol.
View Article and Find Full Text PDFRecent studies have suggested that the response profiles of taste-responsive cells in the brainstem may be modulated by inhibitory interactions, potentially originating from activity in peripheral taste nerves. This idea was explored by testing the hypothesis that brief (100 msec) pulses of taste stimuli would alter the responses to subsequently presented tastants in the nucleus of the solitary tract (NTS) of urethane-anesthetized rats. Pulses of taste stimuli, called prepulses, were followed by a 3 sec presentation of the same or different taste stimulus.
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