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PubMed1997

Innervation of taste buds in the canine larynx as revealed by immunohistochemistry for the various neurochemical markers.

The distribution and innervation of the canine laryngeal taste buds were observed using immunohistochemistry with antibodies against protein gene product 9.5 (PGP 9.5) and neurofilament protein (NFP). We also observed the immunohistochemical distribution of serotonin, tyrosine hydroxylase (TH) and various neuropeptides including calcitonin gene-related peptide (CGRP), substance P (SP), vasoactive intestinal peptide (VIP), galanin, methionine enkephalin (ENK) and neuropeptide Y (NPY). The taste buds in the canine larynx were densely distributed in the mucosa at the basal portion of the epiglottis and cuneiform process of the arytenoid cartilage. The taste cells were immunoreactive for PGP 9.5 and serotonin. The nerve fibers with immunoreactivity for PGP 9.5 in the taste buds were observed in the perigemmal region and intra- and subgemmal plexuses, and these were classified into two types based on their diameter. The thick nerve fibers corresponded to the fibers immunoreactive for NFP, while the thin nerve fibers corresponded to the fibers immunoreactive for TH and various neuropeptides. Numerous nerve fibers immunoreactive for SP and CGRP were observed in the perigemmal region, and intra- and subgemmal plexuses. A few galanin- and ENK-immunoreactive nerve fibers were also observed in the taste buds, whereas NPY-immunoreactive nerve fibers were noted beneath them. All peptide-containing fibers except for VIP-immunoreactive nerves were situated in the subgemmal regions. In conclusion, the multiple innervation to the laryngeal taste buds were documented. Thick nerve fibers are likely to be irritant receptors, while thin varicose nerve fibers seem to regulate taste buds themselves. The laryngeal taste buds may be among the important structures which are sensitive to exogeneous chemical and/or mechanical stimuli, for the protection of the airway and the regulation of the respiratory function.

Animals↗

PubMed1997

GABAergic neurotransmission in rat taste buds: immunocytochemical study for GABA and GABA transporter subtypes.

Gamma-aminobutyric acid (GABA) is known to be a candidate for the neurotransmitter involved in the sense of taste. We hereby studied GABA and its termination system, GABA transporters, in rat taste buds by immunocytochemical approaches. Immunoblot analysis of three GABA transporter subtypes (GAT1, GAT2 and GAT3) revealed that the immunoreactive bands of GAT2 and GAT3, but not GAT1, were detected in the tongue. GAT3-immunoreactive band was recognized only in the circumvallate papilla containing a large number of taste buds while GAT2-immunoreactive bands were seen in all areas of the tongue. GAT2 immunoreactivity appeared to be specifically in the nerve fibers beneath the lingual epithelium. Both GAT3 and GABA immunoreactivities were detected only in taste buds. A few GAT3-immunoreactive cells were found in a cross-section of each taste bud but most GAT3-immunoreactive cells were localized in the margin of the taste bud. GAT3 was predominantly concentrated in the distal portion of the GAT3-immunoreactive cells. In contrast, GABA-immunoreactive cells were seen more frequently within each taste bud and the immunoreactivity was distributed throughout the perikarya of the cells. These results suggest that the GABA-uptake system is present in the taste buds and the GABAergic neurotransmission involved in the sensation of taste is terminated by the uptake of GABA into certain taste cells via GAT3.

Animals↗

PubMedDate not supplied

Retinoid-induced limb defects 1: inhibition of cell proliferation in distal mesenchyme of limb buds in rats.

The present study was undertaken to investigate the effects of all-trans-retinoic acid (RA) on cell death and limb bud growth in forelimb buds and also to examine whether these events are involved in limb bone defects induced by RA in rats. RA was given at doses of 50 and 100 mg/kg to pregnant rats on Day 12 of pregnancy. Although RA did not show teratogenecity in the 50 mg/kg group, micromelia was observed in the 100 mg/kg group in all live fetuses on Day 21 of gestation. Micromelia was characterized by high incidences of proximodistal reduction of forearm bones without reduction of the humerus. The incidence of cell death in prechondrogenic areas, which differentiate into humerus and forearm bone, significantly increased 24 h after RA treatment in not only the 100 mg/kg, but also the 50 mg/kg, group. There was no difference in the incidence of cell death in the prechondrogenic area between the two groups. These observations indicate that the bone-specific defects were not the result of cell death alone in the prechondrogenic area. We examined the effects of RA on early forelimb bud growth, which is indispensable for the morphogenesis of the forelimb. Proximodistal length and protein content were decreased significantly in the forelimb bud 24 h after RA treatment at a dose of 100 mg/kg, but not 50 mg/kg. The immunohistochemical detection of bromodeoxyuridine (BrdU) incorporated into cells showed that at a dose of 100 mg/kg, cell proliferation was reduced in the distal mesenchyme, but not in the forearm-bone prechondrocytes of the forelimb bud. As the distal margin provides the cells differentiating into the prechondrocytes of future bones in the limb bud, these observations suggested that RA-induced inhibition of cell proliferation in the distal margin resulted in a decrease of forearm-bone prechondrocytes localized at more distal sites. We conclude that RA may inhibit the chondrogenesis of forearm bones by reducing cell proliferation in the distal margin of the forelimb bud, not by increasing cell death, and that this results in reduction defects in forearm bones.

Animals↗

PubMed2000

Localization of the glutamate-aspartate transporter, GLAST, in rat taste buds.

A number of putative neurotransmitter substances have been found in vertebrate taste buds. Amongst these glutamate has been localized in fibres innervating the buds and uptake of glutamate has been shown to occur into receptor cells. It is therefore possible that, in common with other sensory systems, glutamate is a neurotransmitter in taste buds. In the inner ear and retina of mammals, the membranes of supporting cells have been shown to contain the glial glutamate transporter GLAST. In the brain, this protein is involved in glutamate re-uptake into glial cells where the glutamate is converted into glutamine for recycling into glutamatergic terminals. In this study, the presence of GLAST has been investigated in taste buds in the rat vallate papilla and its distribution compared with that of glutamine to determine whether there are cells in this system that play a glia-like role in glutamate handling. Immunofluorescent labelling showed that a subset of cells in the taste bud contains GLAST. Immunogold labelling indicated that it occurs in the plasma membranes of supporting cells, especially on the fine cytoplasmic processes of dark cells towards the basal region of the bud. A protein of molecular mass similar to that of cerebellar GLAST was detected in immunoblots of excised papillae. Double labelling and semiquantitative analysis of glutamine and GLAST immunoreactivity showed that the GLAST-positive cells have a higher level of cytoplasmic glutamine than the adjacent cells. It is proposed that these GLAST-positive cells play a glia-like role in the uptake of glutamate following its release at synapses within the taste bud although the precise location of the latter remains uncertain. The GLAST-positive cells may also be involved in its subsequent conversion to glutamine in a glutamate/glutamine cycle similar to that described in the brain.

ATP-Binding Cassette Transporters↗

PubMed2006

Organ culture studies on the development of mouse embryo limb buds under EMF influence.

PURPOSE: To investigate the effects of an electromagnetic field (EMF) on limb bud development in vitro, an organ culture system was applied. MATERIALS AND METHODS: Three test groups of amputated mouse limb buds included the experimental (E) group which received EMF (50 Hz/13.1 mT, for 2 h), a sham (Sh) group exposed to no EMF treatment and the control (C) group. The limb buds of E and Sh groups (n = 20 per group) were amputated from mouse embryos on day 11.5 of development and cultured in minimum essential medium Eagle (MEM Eagle), supplemented with 15% human embryo cord serum, for 2 days, while those of group C (n = 20) were removed on day 13.5 of development. All samples were fixed in Bouin's fluid, embedded in paraffin, serially sectioned (5 microm thick) and stained with Hematoxylin and Eosin. Limb bud measurements were performed using a scaled graticule. RESULTS: Morphological and histological examinations showed significant changes in the experimental limb bud group as compared with the sham and control groups. The growth rate in both fore and hindlimb buds in proximal-distal (P-D) and anterior-posterior (A-P) axes were significantly increased. Chondrocyte counts and mitotic figures of mesenchymal and red blood cells were significantly increased as compared with those of sham and control groups. There was also a significant reduction of mesenchymal cell counts, while no significant difference was observed in the degenerated cell counts among the three groups. CONCLUSIONS: These findings suggest that EMF, under the conditions applied, has progressive effects on the limb bud development and that both proliferation and differentiation can be stimulated in vitro.

Animals↗

PubMed1994

Keratin 19-like immunoreactivity in receptor cells of mammalian taste buds.

Three monoclonal antibodies, 4.62, LP2K and 170.2.14, were used to evaluate keratin 19-like immunoreactivity in gustatory epithelia. Keratin 19-like immunoreactivity was restricted to the intragemmal cells for all types of mammalian taste buds examined. These taste buds included fungiform, foliate and vallate taste buds in rat, gerbil and rabbit, and nasopalatine, epiglottal and palatine taste buds in rat. There was no keratin 19-like immunoreactivity in basal cells or in perigemmal cells lateral to the immunoreactive taste receptor cells. Denervation of the rat vallate papilla eliminated all taste buds, as well as all immunoreactive taste cells. That the immunoreactive material in the taste cells was keratin 19 was supported by the comparable staining of rat taste buds with each of three monoclonal antibodies specific for keratin 19. Furthermore, as predicted, these antibodies selectively stained luminal cells of rat bile ducts, bladder, salivary ducts, trachea, ureter and uterus. It was concluded that monoclonal antibodies against keratin 19 can usefully distinguish intragemmal taste receptor cells from keratinocytes, and from the perigemmal and basal cells of gustatory epithelia. Anti-keratin 19 antibodies may serve to identify differentiated taste cells in gustatory epithelia undergoing taste bud development, renewal, degeneration or regeneration.

Animals↗

PubMed1999

The effects of beta-bungarotoxin on the morphogenesis of taste papillae and taste buds in the mouse.

Although it has been long accepted that innervation by a taste nerve is essential for maintenance of taste buds, it is not clear what role, if any, innervation plays in the morphogenesis of taste papillae and taste bud development. The following study was undertaken to determine what effects lack of sensory innervation have on the development of taste papillae and the formation of taste buds in the mouse. Timed-pregnant female mice (n = 3) at gestational day 12 (gd12) were anesthetized and a 1 microl solution (1 microg/microl) of beta-bungarotoxin (beta-BTX), a neurotoxin that disrupts sensory and motor neuron development, was injected into the amniotic cavity of two embryos per dam. Two shams were injected with PBS. Fetuses were harvested at gd18, 1 day before birth, and four beta-BTX-injected embryos, two shams and two controls were fixed in buffered paraformaldehyde. Serial sections were examined for the presence and morphology of taste papillae and taste buds. No nerve profiles were observed in beta-BTX-injected tongues. Although circumvallate papillae were present on beta-BTX tongues, only five fungiform papillae could be identified. Taste buds were present on a large percentage of fungiform papillae profiles (24%) and on circumvallate papillae in sham and control fetuses; in contrast, no taste buds were associated with taste papillae in beta-BTX fetuses. These results implicate a significant role for innervation in taste papillae and taste bud morphogenesis.

Animals↗

PubMed2004

A strong nerve dependence of sonic hedgehog expression in basal cells in mouse taste bud and an autonomous transcriptional control of genes in differentiated taste cells.

The nerve-dependency of gene expression in mouse taste bud was examined through an analysis of changes in gene expression in and around the taste buds in circumvallate papillae after surgery of cranial nerve IXth (glossopharyngeal nerve). The number of cells expressing T1r3, gustducin, Mash1 and Nkx2.2 gradually decreased after denervation. However, the expression intensity of these genes was barely influenced by denervation, and strong expression was observed at 6 days after denervation. In contrast, the basal cell-specific Sonic hedgehog (Shh) expression in the taste buds was decreased markedly at 6 h after denervation. In the regeneration process of taste buds, Shh expression was observed during a very early phase before taste bud formation. These results indicate the autonomous transcriptional control of genes in differentiated taste cells and the strong nerve-dependency of Shh expression in basal cells. Furthermore, in order to reveal the mitotic activity of Shh-expressing cells in taste buds, the BrdU-labeling experiments were performed using a combination of BrdU-immunohistochemistry and in situ hybridization. BrdU-signal was very rarely observed in Shh-expressing cells immediately after BrdU injection, and the signals were noted mainly in Ptc-expressing cells. BrdU signals rapidly increased in Shh-expressing cells in following 12 h and began to decrease after 2 days post-injection. These results suggest that most Shh-expressing cells are not mitotically active, but that Shh-expressing cells may be in the early transient developmental state of taste cells in taste buds.

Animals↗

PubMed1996

Embryonic taste buds develop in the absence of innervation.

It has been hypothesized that taste buds are induced by contact with developing cranial nerve fibers late in embryonic development, since descriptive studies indicate that during embryonic development taste cell differentiation occurs concomitantly with or slightly following the advent of innervation. However, experimental evidence delineating the role of innervation in taste bud development is sparse and equivocal. Using two complementary experimental approaches, we demonstrate that taste cells differentiate fully in the complete absence of innervation. When the presumptive oropharyngeal region was taken from a donor axolotl embryo, prior to its innervation and development of taste buds, and grafted ectopically on to the trunk of a host embryo, the graft developed well-differentiated taste buds. Although grafts were invaded by branches of local spinal nerves, these neurites were rarely found near ectopic taste cells. When the oropharyngeal region was raised in culture, numerous taste buds were generated in the complete absence of neural elements. Taste buds in grafts and in explants were identical to those found in situ both in terms of their morphology and their expression of calretinin and serotonin immunoreactivity. Our findings indicate that innervation is not necessary for complete differentiation of taste receptor cells. We propose that taste buds are either induced in response to signals from other tissues, such as the neural crest, or arise independently through intrinsic patterning of the local epithelium.

Ambystoma↗

PubMed2001

Glycoconjugate in rat taste buds.

The taste buds of the fungiform papillae, circumvallate papilla, foliate papillae, soft palate and epiglottis of the rat oral cavity were examined by lectin histochemistry to elucidate the relationships between expression of glycoconjugates and innervation. Seven out of 21 lectins showed moderate to intense staining in at least more than one taste bud. They were succinylated wheat germ agglutinin (s-WGA). Dolichos biflorus agglutinin (DBA), Bandeiraea simplicifolia lectin-I (BSL-I), Ricinus communis agglutinin-I (RCA-I), peanut agglutinin (PNA), Ulex europaeus agglutinin-I (UEA-I) and Phaseolus vulgaris agglutinin-L (PHA-L). UEA-I and BSL-I showed moderate to intense staining in all of the taste buds examined. They strongly stained the taste buds of the epiglottis, which are innervated by the cranial nerve X. UEA-I intensely stained the taste buds of the fungiform papillae and soft palate, both of which are innervated by the cranial nerve VII. The taste buds of circumvallate papilla and foliate papillae were innervated by the cranial nerve IX and strongly stained by BSL-I. Thus, UEA-I and BSL-I binding glycoconjugates, probably alpha-linked fucose and alpha-D-galactose, respectively, might be specific for taste buds. Although the expression of these glycoconjugates would be related to the innervation of the cranial nerve X, the differential expression of alpha-linked fucose and alpha-D-galactose might be related to the innervation of the cranial nerve VII and IX, respectively.

Animals↗

PubMed1995

Innervation in human taste buds and its decrease in Alzheimer's disease patients.

The innervation in human taste buds of the foliate and circumvallate papillae was studied immunohistochemically using several neuronal markers in patients with Alzheimer's disease (AD) and their control (ADC) patients. Antisera to protein gene product 9.5 (PGP 9.5), neuron-specific enolase (NSE), tyrosine hydroxylase (TH), dopamine-beta hydroxylase (DbetaH) and calcitonin gene-related peptide (CGRP) were used in immunofluorescence and streptavidin-biotin-peroxidase complex studies. The antiserum to PGP 9.5 stained a greater number of intragemmal nerve fibers in taste buds than that of other antisera. PGP 9.5 immunoreactivity was strictly localized in the nerve fibers, whereas NSE immunoreactivity was observed not only in the nerve fibers, but also in taste bud cells. Intragemmal TH- and DbetaH-immunoreactive nerve fibers were not identified in taste buds. Only a few intragemmal nerve fibers immunoreactive for anti-CGRP antiserum were observe in a small number of taste buds. Furthermore, quantitive analysis in AD and ADC patients demonstrated that the mean number of PGP 9.5-immunoreactive intragemmal nerve fibers in taste buds of the foliate and circumvallate papillae decreased significantly in AD patients. These results indicated that PGP 9.5 is a most suitable molecular marker for the demonstration of the extrinsic innervation in human taste buds, and that the decreased innervation may account partially for the decrement in chemosensory capacity in AD patients.

Aged↗

PubMed1999

Alterations in size, number, and morphology of gustatory papillae and taste buds in BDNF null mutant mice demonstrate neural dependence of developing taste organs.

Sensory ganglia that innervate taste buds and gustatory papillae (geniculate and petrosal) are reduced in volume by about 40% in mice with a targeted deletion of the gene for brain-derived neurotrophic factor (BDNF). In contrast, the trigeminal ganglion, which innervates papillae but not taste buds on the anterior tongue, is reduced by only about 18%. These specific alterations in ganglia that innervate taste organs make possible a test for roles of lingual innervation in the development of appropriate number, morphology, and spatial pattern of fungiform and circumvallate papillae and associated taste buds. We studied tongues of BDNF null mutant and wild-type littermates and made quantitative analyses of all fungiform papillae on the anterior tongue, the single circumvallate papilla on the posterior tongue, and all taste buds in both papilla types. Fungiform papillae and taste buds were reduced in number by about 60% and were substantially smaller in diameter in mutant mice 15-25 days postnatal. Remaining fungiform papillae were selectively concentrated in the tongue tip region. The circumvallate papilla was reduced in diameter and length by about 40%, and papilla morphology was disrupted. Taste bud number in the circumvallate was reduced by about 70% in mutant tongues, and the remaining taste buds were smaller than those on wild-type tongues. Our results demonstrate a selective dependence of taste organs on a full complement of appropriate innervation for normal growth and morphogenesis. Effects on papillae are not random but are more pronounced in specific lingual regions. Although the geniculate and petrosal ganglia sustain at least half of their normal complement of cell number in BDNF -/- mice, remaining ganglion cells do not substitute for lost neurons to rescue taste organs at control numbers. Whereas gustatory ganglia and the taste papillae initially form independently, our results suggest interdependence in later development because ganglia derive BDNF support from target organs and papillae require sensory innervation for morphogenesis.

Animals↗

PubMed1999

Involvement of Frzb-1 in mesenchymal condensation and cartilage differentiation in the chick limb bud.

In developing limb bud, mesenchymal cells form cellular aggregates called "mesenchymal condensations". These condensations show the prepattern of skeletal elements of the limb prior to cartilage differentiation. Roles of various signaling molecules in chondrogenesis in the limb bud have been reported. One group of signaling factors includes the Wnt proteins, which have been shown to have an inhibitory effect on chondrogenesis in the limb bud. Therefore, regulation of Wnt activity may be important in regulating cartilage differentiation. Here we show that Frzb-1, which encodes a secreted frizzled-related protein that can bind to Wnt proteins and can antagonize the activity of some Wnts, is expressed in the developing limb bud. At early stages of limb development, Frzb-1 is expressed in the ventral core mesenchyme of the limb bud, and later Frzb-1 expression becomes restricted to the central core region where mesenchymal condensations occur. At these stages, a chondrogenic marker gene, aggrecan, is not yet expressed. As limb development proceeds, expression of Frzb-1 is detected in cartilage primordial cells, although ultimately Frzb-1 expression is down-regulated. Similar results were obtained in the recombinant limb bud, which was constructed from dissociated and re-aggregated mesenchymal cells and an ectodermal jacket with the apical ectodermal ridge. In addition, Frzb-1 expression preceded aggrecan expression in micromass cultures. These results suggest that Frzb-1 has a role in condensation formation and cartilage differentiation by regulating Wnt activity in the limb bud.

Aggrecans↗

PubMed2004

[Changes of taste bud and fungiform papillae after 60Co radiation in rat].

OBJECTIVE: To observe the morphological changes and the regenerating ability of the fungiform papillae and taste buds after 60Co radiation with clinical doses in rats. METHODS: The heads, faces and necks of 30 SD rats were radiated with a large dose and one time of 60Co in the clinical radiation. The general living condition and the number and shape of the fungiform papillae and taste buds of the tongues were observed after the radiation in rats. RESULTS: In the group of 60Co radiation, the animals had wilting, decreasing appetite, losing weight. The heads, faces and necks of animals appeared redness, peeling of hair, increasing of secretions in 5 days after the 60Co radiation. The changes reached the summit in 10 days and the general living condition of the animals recovered in 60 days. The fungiform papillae and taste buds of the animals appeared degeneration, atrophy and collapsing in 5 days after the 60Co radiation. The injuries reached the summit in 10-20 days and the fungiform papillae and taste buds regenerated partially, and the some atrophied fungiform papillae and taste buds were not regenerated in 60 days. CONCLUSION: The damage to fungiform papillae and taste buds of tongue following the 60Co radiation with the clinical doses was very serious. The damaged fungiform papillae and taste buds can regenerate partially, but not completely.

Animals↗

PubMed1989

Morphological changes in taste buds of the fungiform papillae after a single dose of x-ray irradiation in rats.

The qualitative and quantitative changes occurring in the taste buds of the fungiform papillae of male Sprague-Dawley rats (aged 51-125 days old) after x-ray irradiation were studied. A single dose of 2000 Roentgen (R) was delivered and observations were made at 0, 3, 7, 14, 21 and 30 days after x-ray irradiation. The changes in taste bud morphology were interpreted first as degenerative and then as regenerative at various stages of the study. The degenerative process appeared at about the third day and reached a peak at 7 days. Regeneration then began after a further week and the taste buds appeared mature at about 30 days. While the number of fungiform papillae remained constant throughout the study, there was a marked loss of taste buds on these papillae at 7 days. At 14 days, the number of taste buds increased from this low level, and by 30 days the number approached the control values. Initial taste bud loss could be attributed to a direct irradiation damage leading to taste bud cell desquamation combined with a concomitant mitotic inhibition of the stratum germinativum.

Animals↗

PubMed1988

Proliferation of taste buds in the foliate and vallate papillae of postnatal hamsters.

The growth of the taste system in the hamster is considered in comparison to the postnatal development of other organ systems and the entire animal. No taste buds are present in vallate or foliate papillae of the hamster at birth, but they attain both the appearance and numbers of adult taste buds within 5 weeks of age. The most rapid increase in the number of taste buds occurs within the first 10 days of life, and this proliferation anticipates the weaning of hamsters which occurs by about three weeks of age. Foliate taste buds reach a maximal number within two months, but vallate taste buds continue to increase in number through 4 months of age. Taste bud proliferation and development occur earlier and more rapidly than in other organ systems. This early development of taste buds may protect the weanling hamster against accidental poisoning by noxious plants, and it may also reinforce the food intake which is required for normal growth.

Animals↗

PubMed1983

Chronic impairment of axonal transport eliminates taste responses and taste buds.

A Silastic nerve cuff containing colchicine (1% w/v) was placed around the combined lingualchorda tympani nerve of the Mongolian gerbil (Meriones unguiculatus) to evaluate the role of axonal transport in the maintenance of taste buds. After 3 days the summated gustatory impulse discharges recorded from the chorda tympani nerve were reduced by 60%, while compound action potentials had not changed appreciably. The lingual-chorda tympani nerve underwent ultrastructural changes including a loss of microtubules, an increased prominence and disorientation of neurofilaments, and a significant shrinkage in the cross-sectional area of axoplasm. The shrinkage of axoplasm and the accumulation of mitochondria and cholinesterase at the nerve cuff provided evidence that the colchicine treatment acted to impair axonal transport. More substantial pathological changes were evident in nerve ultrastructure by 15 days when both the ipsilateral chorda tympani taste responses and fungiform taste buds were nearly absent. Control cuffs lacking colchicine had little effect on chorda tympani taste responses, taste buds, or nerve ultrastructure. Eight or 15 days of nerve exposure to lumicolchicine, an isomer of colchicine with low affinity for tubulin, had no significant effect on taste responses. [3H]Colchicine was used in the nerve cuff to demonstrate that colchicine must have acted directly upon the nerve trunk, rather than the taste buds, to cause the loss of taste responses and taste buds. [3H]Colchicine levels were equal in the two sides of the tongue, whereas both the functional and structural deterioration of the taste buds were restricted to the ipsilateral side. We conclude that the loss of taste responses and taste buds was caused by chronically impaired axonal transport in gustatory axons.

Animals↗

PubMed1982

Taste bud adenosine -3'5'-monophosphate phosphodiesterase: activity, subcellular distribution and kinetic parameters.

Higher activity of cyclic adenosine 3',5'-monophosphate (cAMP) phosphodiesterase (PDE) was found in homogenates from bovine circumvellate papillae bearing taste buds compared to activity in homogenates from areas surrounding these papillae in which no taste buds were present. With progressive purification of these homogenates cAMP PDE activity increased in the taste bud enriched fractions relative to that measured in the non-taste bud bearing epithelial tissue. The highest levels of cAMP PDE activity were measured in those taste bud fractions in which purification was greatest. Kinetic studies in both taste bud derived and control tissues showed two apparent Km values, one relatively high, the other, lower. cAMP PDE activity of taste bud membranes was enhanced by Mg++, Mn++ and imidazole and inhibited by ethylene-bis (beta-aminoethylether) N,N-tetra-acetic acid (EGTA), isobutyl methyl xanthine (IBMX), theophylline, and cyclic guanosine 3',5'-monophosphate (cGMP). The possible role for cAMP PDE in taste function is discussed.

3',5'-Cyclic-AMP Phosphodiesterases↗