Expression of Mash1 in basal cells of rat circumvallate taste buds is dependent upon gustatory innervation.
Mash1, a mammalian homologue of the Drosophila achaete-scute proneural gene complex, plays an essential role in differentiation of subsets of peripheral neurons. In this study, using RT-PCR and in situ RT-PCR, we investigated if Mash1 gene expression occurs in rat taste buds. Further, we examined dynamics of Mash1 expression in the process of degeneration and regeneration in denervated rat taste buds. In rat tongue epithelium, Mash1 gene expression is confined to circumvallate, foliate, and fungiform papilla epithelia that include taste buds. In taste buds, Mash1-expressing cells are round cells in the basal compartment. In contrast, the mature taste bud cells do not express the Mash1 gene. Denervation and regeneration experiments show that the expression of Mash1 requires gustatory innervation. We conclude that Mash1 is expressed in cells of the taste bud lineage, and that the expression of Mash1 in rat taste buds is dependent upon gustatory innervation. (+info)
Glossopharyngeal nerve transection eliminates quinine-stimulated fos-like immunoreactivity in the nucleus of the solitary tract: implications for a functional topography of gustatory nerve input in rats.
The relationship between specific gustatory nerve activity and central patterns of taste-evoked neuronal activation is poorly understood. To address this issue within the first central synaptic relay in the gustatory system, we examined the distribution of neurons in the nucleus of the solitary tract (NST) activated by the intraoral infusion of quinine using Fos immunohistochemistry in rats with bilateral transection of the chorda tympani (CTX), bilateral transection of the glossopharyngeal nerve (GLX), or combined neurotomy (DBLX). Compared with nonstimulated and water-stimulated controls, quinine evoked significantly more Fos-like-immunoreactive (FLI) neurons across the rostrocaudal extent of the gustatory NST (gNST), especially within its dorsomedial portion (subfield 5). Although the somatosensory aspects of fluid stimulation contributed to the observed increase in FLI neurons, the elevated number and spatial distribution of FLI neurons in response to quinine were remarkably distinguishable from those in response to water. GLX and DBLX produced a dramatic attenuation of quinine-evoked FLI neurons and a shift in their spatial distribution such that their number and pattern were indiscernable from those observed in water-stimulated controls. Although CTX had no effect on the number of quinine-evoked FLI neurons within subfield 5 at intermediate levels of the gNST, it produced intermediate effects elsewhere; yet, the spatial distribution of the quinine-evoked FLI neurons was not altered by CTX. These findings suggest that the GL provides input to all FLI neurons responsive to quinine, however, some degree of convergence with CT input apparently occurs in this subpopulation of neurons. Although the role of these FLI neurons in taste-guided behavioral responses to quinine remains speculative, their possible function in oromotor reflex control is considered. (+info)
Taste qualities of solutions preferred by hamsters.
Molecules of diverse chemical structure are sweet to humans and several lines of evidence (genetic, physiological, behavioral) suggest that there may be distinct sweet perceptual qualities. To address how many perceptual categories these molecules elicit in hamsters (Mesocricetus auratus), we studied patterns of generalization of conditioned taste aversions for seven sweeteners: 100 mM sucrose, 320 mM maltose, 32 mM D-phenylalanine, 3.2 mM sodium saccharin, 16 mM calcium cyclamate, 10 mM dulcin and 32 mM sodium m-nitrobenzene sulfonate. Each stimulus was preferred versus water in two-bottle intake tests and stimulated the chorda tympani nerve. For each of seven experimental groups the conditional stimulus (CS) was a sweetener and for the control group the CS was water. Apomorphine.HCl was injected i.p. after a CS was sampled and, after recovery, test stimuli (TS) were presented for 1 h daily. The intake (ml) of each TS consumed by experimental animals was compared with mean TS intake by the control group. Learned aversions for 18/21 stimulus pairs cross-generalized, resulting in a single cluster of generalization patterns for the seven stimuli. Cross-generalization failures (maltose-cyclamate, maltose-sucrose, cyclamate-NaNBS) may be the consequence of particular stimulus features (e.g. salience, cation taste), rather than the absence of a 'sucrose-like' quality. The results are consistent with a single hamster perceptual quality for a diverse set of chemical structures that are sweet to humans. (+info)
Citrate ions enhance taste responses to amino acids in the largemouth bass.
The glossopharyngeal (IX) taste system of the largemouth bass, Micropterus salmoides, is highly selective to amino acids and is poorly responsive to trisodium citrate; however, IX taste responses to specific concentrations of L- and D-arginine and L-lysine but not L-proline were enhanced by citrate but not sodium ions. Binary mixtures of L-arginine (3 x 10(-4)M and 10(-3)M) or D-arginine (10(-3)M) + trisodium citrate (10(-3)M; pH 7-9) resulted in enhanced taste activity, whereas binary mixtures of higher concentrations (10(-2)M and 10(-1)M) of L- or D-arginine + 10(-3)M trisodium citrate were not significantly different from the response to the amino acid alone. Under continuous adaptation to 10(-3)M citrate, taste responses to L-arginine were also enhanced at the identical concentrations previously indicated, but responses to 10(-2)M and 10(-1)M L-arginine were significantly suppressed. Under continuous adaptation to 10(-2)M L-arginine, taste responses to 10(-2)M, 10(-1)M, and 10(0) M citrate were significantly enhanced. Cellular concentrations of both citrate and amino acids in prey of the carnivorous largemouth bass are sufficient for this taste-enhancing effect to occur naturally during consummatory feeding behavior. Citrate acting as a calcium chelator is presented as a possible mechanism of action for the enhancement effect. (+info)
Responses of single taste fibers and whole chorda tympani and glossopharyngeal nerve in the domestic pig, Sus scrofa.
Whole nerve, as well as single fiber, responses in the chorda tympani proper (CT) and glossopharyngeal (NG) nerves of 1- to 7-week-old pigs were recorded during taste stimulation. In the CT acids and in the NG bitter compounds gave the largest responses. Both nerves exhibited large responses to monosodium glutamate (MSG), MSG with guanosine 5'-monophosphate (GMP) and MSG with inositine 5'-monophosphate (IMP) as well as to glycine, xylitol, sucrose, fructose and glucose. Alitame, aspartame, betaine, neohesperedin dihydrochalcone (NHDHC), super-aspartame, saccharin and thaumatin elicited no or little response. Hierarchical cluster analysis of 49 CT fibers separated four major clusters. The M cluster, comprising 28.5% of all fibers, is characterized by strong responses to MSG, KCl, LiCl and NaCl. The responses to NaCl and LiCl were unaffected by amiloride. The H cluster (24.5%) includes units responding principally to acids. The Q cluster (18.5%) responds to quinine hydrochloride (QHCl), sucrose octaacetate (SOA) and salts with amiloride. The S cluster (28.5%) exhibits strong responses to xylitol, glycine and the carbohydrates as well as to MSG alone and to MSG with GMP or IMP. In 31 NG fibers, hierarchical cluster analysis revealed four clusters: the M cluster (10%), responding to MSG and MSG with GMP or IMP; the H cluster (13%), responding to acids; the Q cluster (29%), responding strongly to QHCl, SOA and tilmicosinR; and the S cluster (48%), responding best to xylitol, carbohydrates and glycine but also to the umami compounds. Multidimensional scaling analysis across fiber responses to all stimuli showed the best separation between compounds with different taste qualities when information from both nerves was utilized. (+info)
Developmental changes in membrane properties of chemoreceptor afferent neurons of the rat petrosal ganglia.
Carotid body chemoreceptors increase their responsiveness to hypoxia in the postnatal period, but the mechanism for this increase is unresolved. The purpose of the present study was to examine developmental changes in cellular characteristics of chemoreceptor afferent neurons in the petrosal ganglia with the underlying hypothesis that developmental changes occur and may account for the developmental increase in chemoreceptor responsiveness. Chemoreceptor complexes (carotid body, sinus nerve, glossopharyngeal nerve, and petrosal ganglia) were harvested from rats, aged 3-40 days, and intracellular recordings were obtained from petrosal ganglion neurons using sharp electrode impalement. All chemoreceptor neurons across ages were C fibers with conduction velocities <1 m/s and generated repetitive action potentials with depolarization. Resting membrane potential was -61.3 +/- 0.9 (SE) mV (n = 78) and input resistance was 108 +/- 6 MOmega and did not significantly change with age. Cell capacitance was 32.4 +/- 1.7 pF and did not change with age. Rheobase averaged 0.21 +/- 0.02 nA and slightly increased with age. Action potentials were followed by an afterhyperpolarization of 12.4 +/- 0.6 mV and time constant 6.9 +/- 0.5 ms; only the time constant decreased with age. These results, obtained in rat, demonstrate electrophysiologic characteristics which differ substantially from that previously described in cat chemoreceptor neurons. In general developmental changes in cell characteristics are small and are unlikely to account for the developmental increase in chemoreceptor responsiveness with age. (+info)
Directing gene expression to gustducin-positive taste receptor cells.
We have demonstrated that an 8.4 kb segment (GUS(8.4)) from the upstream region of the mouse alpha-gustducin gene acts as a fully functional promoter to target lacZ transgene expression to the gustducin-positive subset of taste receptor cells (TRCs). The GUS(8. 4) promoter drove TRC expression of the beta-galactosidase marker at high levels and in a developmentally appropriate pattern. The gustducin minimal 1.4 kb promoter (GUS(1.4)) by itself was insufficient to specify TRC expression. We also identified an upstream enhancer from the distal portion of the murine gustducin gene that, in combination with the minimal promoter, specified TRC expression of transgenes. Expression of the lacZ transgene from the GUS(8.4) promoter and of endogenous gustducin was coordinately lost after nerve section and simultaneously recovered after reinnervation, confirming the functionality of this promoter. Transgenic expression of rat alpha-gustducin restored responsiveness of gustducin null mice to both bitter and sweet compounds, demonstrating the utility of the gustducin promoter. (+info)
Blocking taste receptor activation of gustducin inhibits gustatory responses to bitter compounds.
Gustducin, a transducin-like guanine nucleotide-binding regulatory protein (G protein), and transducin are expressed in taste receptor cells where they are thought to mediate taste transduction. Gustducin and transducin are activated in the presence of bovine taste membranes by several compounds that humans perceive to be bitter. We have monitored this activation with an in vitro assay to identify compounds that inhibited taste receptor activation of transducin by bitter tastants: AMP and chemically related compounds inhibited in vitro responses to several bitter compounds (e.g., denatonium, quinine, strychnine, and atropine). AMP also inhibited behavioral and electrophysiological responses of mice to bitter tastants, but not to NaCl, HCl, or sucrose. GMP, although chemically similar to AMP, inhibited neither the bitter-responsive taste receptor activation of transducin nor the gustatory responses of mice to bitter compounds. AMP and certain related compounds may bind to bitter-responsive taste receptors or interfere with receptor-G protein coupling to serve as naturally occurring taste modifiers. (+info)