Fetal alcohol exposure reduces responsiveness of taste nerves and trigeminal chemosensory neurons to ethanol and its flavor components.

Fetal alcohol exposure (FAE) leads to increased intake of ethanol in adolescent rats and humans. We asked whether these behavioral changes may be mediated in part by changes in responsiveness of the peripheral taste and oral trigeminal systems. We exposed the experimental rats to ethanol in utero by administering ethanol to dams through a liquid diet; we exposed the control rats to an isocaloric and isonutritive liquid diet. To assess taste responsiveness, we recorded responses of the chorda tympani (CT) and glossopharyngeal (GL) nerves to lingual stimulation with ethanol, quinine, sucrose, and NaCl. To assess trigeminal responsiveness, we measured changes in calcium levels of isolated trigeminal ganglion (TG) neurons during stimulation with ethanol, capsaicin, mustard oil, and KCl. Compared with adolescent control rats, the adolescent experimental rats exhibited diminished CT nerve responses to ethanol, quinine, and sucrose and GL nerve responses to quinine and sucrose. The reductions in taste responsiveness persisted into adulthood for quinine but not for any of the other stimuli. Adolescent experimental rats also exhibited reduced TG neuron responses to ethanol, capsaicin, and mustard oil. The lack of change in responsiveness of the taste nerves to NaCl and the TG neurons to KCl indicates that FAE altered only a subset of the response pathways within each chemosensory system. We propose that FAE reprograms development of the peripheral taste and trigeminal systems in ways that reduce their responsiveness to ethanol and surrogates for its pleasant (i.e., sweet) and unpleasant (i.e., bitterness, oral burning) flavor attributes.NEW & NOTEWORTHY Pregnant mothers are advised to avoid alcohol. This is because even small amounts of alcohol can alter fetal brain development and increase the risk of adolescent alcohol abuse. We asked how fetal alcohol exposure (FAE) produces the latter effect in adolescent rats by measuring responsiveness of taste nerves and trigeminal chemosensory neurons. We found that FAE substantially reduced taste and trigeminal responsiveness to ethanol and its flavor components.

Attenuation of peripheral salt taste responses and local immune function contralateral to gustatory nerve injury: effects of aldosterone.

Dietary sodium restriction coupled with axotomy of the rat chorda tympani nerve (CTX) results in selectively attenuated taste responses to sodium salts in the contralateral, intact chorda tympani nerve. Converging evidence indicates that sodium deficiency also diminishes the activated macrophage response to injury on both the sectioned and contralateral, intact sides of the tongue. Because a sodium-restricted diet causes a robust increase in circulating aldosterone, we tested the hypothesis that changes in neurophysiological and immune responses contralateral to the CTX could be mimicked by aldosterone administration instead of the low-sodium diet. Taste responses in rats with CTX and supplemental aldosterone for 4-6 days were similar to rats with CTX and dietary sodium restriction. Responses to sodium salts were as much as 50% lower compared with sham-operated and vehicle-supplemented rats. The group-related functional differences were eliminated with lingual application of amiloride, suggesting that a major transduction pathway affected was through epithelial sodium channels. Consistent with the functional results, few macrophages were observed on either side of the tongue in rats with CTX and aldosterone. In contrast, macrophages were elevated on both sides of the tongue in rats with CTX and the vehicle. These results show that sodium deficiency or administration of aldosterone suppresses the immune response to neural injury, resulting in attenuation of peripheral gustatory function. They also show a potential key link among downstream consequences of sodium imbalance, taste function, and immune activity.

Stimulus-induced increase of taste responses in the hamster chorda tympani by repeated exposure to 'novel' tastants.

Variations in amplitude of responses of the chorda tympani to repeated application of various novel tastants were measured in familiarized and control groups of adult hamsters. Three groups of 10 hamsters were pre-exposed to 5 mM dulcin, 50 mM potassium L-glutamate (KGlu) or 1 mM 5'guanosine monophosphate (5'GMP). In the fourth group, the tongue was rinsed with 5'GMP for 20 min just prior to recording from the chorda tympani. The tastants were novel to the fifth group (naïve control). A series of 17 stimuli was repeated six times and responses were quantified relative to the initial response of each of the 50 hamsters. The responses of the chorda tympani increased with repetition in the control group. In contrast, no increase in amplitude of response to the pre-exposed tastants or to stimuli with qualitatively related tastes was observed in the group familiarized with either KGlu or 5'GMP. These results indicate that the response of the chorda tympani depends on previous exposure to a tastant. The sensitivity of taste cells appears to be modulated, possibly by stimulus-induced supplementary receptors.

The role of the chorda tympani nerve in the activation of the rat hypothalamic histaminergic system by leptin.

A possible pathway through which leptin activates the histaminergic system was studied using in vivo microdialysis in rats. Intraperitoneal injection of leptin (1.3 mg/kg) caused a significant increase in hypothalamic histamine release, however, its intracerebroventricular injection (10 microg/rat) did not cause any significant changes in the release. Furthermore, leptin (1.3 mg/kg) had no effect on histamine release in rats whose chorda tympani nerves, a branch of the facial nerve which mediates taste information, were transected bilaterally. These findings indicate that leptin activates the histaminergic system by the peripheral signal inputs via the chorda tympani resulting in the suppression of food intake.

Neuroanatomical effects of capsaicin on the primary afferent neurons.

Studies by N. JANCSO and his associates in the 1970's established that capsaicin in paprika exerts selective damage on nociceptive primary sensory neurons. The physiological and pharmacological aspects of capsaicin's effect have been repeatedly reviewed, but no report seems available concerning the neuroanatomical changes caused by capsaicin. This paper first reviews the neuroanatomical aspect of the lesion caused by capsaicin. Special attention is paid to quantitative estimations made by our group and others on the loss of dorsal root ganglion (DRG) cells, dorsal root nerve fibers, the saphenous nerve, chorda tympani nerve, and pulp nerves after neonatal treatment with capsaicin. The degenerating process of DRG cells induced by capsaicin is discussed with respect to necrosis and apoptosis. The capsaicin receptors found recently are concisely introduced with reference to their action. A discrepancy between a marked loss of dorsal root C-fibers and an unexpectedly intact response to noxious heat in mice treated with capsaicin at neonate is discussed, and attension is given to nerves sprouting from capsaicin-resistant DRG cells in the superficial dorsal horn. In addition, the architecture of the synapses between the central endings of the capsaicin-sensitive primary afferent neurons and the intrinsic inhibitory interneurons is described and its possible significance considered in terms of the transmission of nociceptive information.

Effects of chorda tympani nerve anesthesia on taste responses in the NST.

Human clinical and psychophysical observations suggest that the taste system is able to compensate for losses in peripheral nerve input, since patients do not commonly report decrements in whole mouth taste following chorda tympani nerve damage or anesthesia. Indeed, neurophysiological data from the rat nucleus of the solitary tract (NST) suggests that a release of inhibition (disinhibition) may occur centrally following chorda tympani nerve anesthesia. Our purpose was to study this possibility further. We recorded from 59 multi- and single-unit taste-responsive sites in the rat NST before, during and after recovery from chorda tympani nerve anesthesia. During anesthesia, average anterior tongue responses were eliminated but no compensatory increases in palatal or posterior tongue responses were observed. However, six individual sites displayed increased taste responsiveness during anesthesia. The average increase was 32.9%. Therefore, disinhibition of taste responses was observed, but infrequently and to a small degree in the NST At a subset of sites, chorda tympani-mediated responses decreased while greater superficial petrosal-mediated responses remained the same during anesthesia. Since this effect was accompanied by a decrease in spontaneous activity, we propose that taste compensation may result in part by a change in signal-to-noise ratio at a subset of sites.

A novel peptide isolated from the leaves of Gymnema sylvestre--I. Characterization and its suppressive effect on the neural responses to sweet taste stimuli in the rat.

1. A new substance that suppressed selectively the neural responses of the rat to sweet taste stimuli was isolated from the leaves of Gymnema sylvestre. 2. The substance was proved to be a peptide consisting of 35 amino acids and having a molecular weight of about 4,000. 3. The inhibitory effect on the sweet responses appeared after treating the tongue surface with the peptide at a concentration of more than 1 x 10(-6) M.

Evaluation of plant extracts for sweetness using the Mongolian gerbil.

Extracts of Thladiantha grosvenorii fruits, Stevia rebaudiana leaves, and Abrus precatorius leaves were investigated using Mongolian gerbil electrophysiological and conditioned taste aversion procedures, which were designed to respond to sucrose. A close correlation was observed between extracts of these sweet plants known to contain sweet principles and those extracts indicated as being sweet by a combination of these gerbil bioassays. The methods employed seem to be suitable for use in aiding the purification of highly sweet compounds of plant origin.

On the effects of gymnemic acid in the hamster and rat.

The gustatory activity of the chorda tympani proper nerve has been recorded before and after the application of gymnemic acid to the tongue of hamster and rat. Concentrations of pure gymnemic acid ranging from 1 mg/ml to 10 mg/ml have been used. In the hamster gymnemic acid suppressed the response to solutions of sucrose especially, but it also caused, at higher concentrations, a general suppression of the tast response. The depression caused in the response to sucrose was directly related to the strength of the gymnemic acid and inversely to that of the sucrose solution. In the rat a suppression of the response to saccharin was obtained but no suppression of the taste response to sucrose by gymnemic acid was observed.