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Search Results: 1 - 10 of 220248 matches for " Sue C Kinnamon "
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Amiloride-sensitive channels in type I fungiform taste cells in mouse
Aurelie Vandenbeuch, Tod R Clapp, Sue C Kinnamon
BMC Neuroscience , 2008, DOI: 10.1186/1471-2202-9-1
Abstract: Taste cell types were identified by their response to depolarizing voltage steps and their presence or absence of GFP fluorescence. TRPM5-GFP taste cells expressed large voltage-gated Na+ and K+ currents, but lacked voltage-gated Ca2+ currents, as expected from previous studies. Approximately half of the unlabeled cells had similar membrane properties, suggesting they comprise a separate population of Type II cells. The other half expressed voltage-gated outward currents only, typical of Type I cells. A single taste cell had voltage-gated Ca2+ current characteristic of Type III cells. Responses to amiloride occurred only in cells that lacked voltage-gated inward currents. Immunocytochemistry showed that fungiform taste buds have significantly fewer Type II cells expressing PLC signalling components, and significantly fewer Type III cells than circumvallate taste buds.The principal finding is that amiloride-sensitive Na+ channels appear to be expressed in cells that lack voltage-gated inward currents, likely the Type I taste cells. These cells were previously assumed to provide only a support function in the taste bud.At the peripheral taste system level, it is still unclear whether each taste quality is transduced by a separate population of taste cells, each connected to distinct nerve fibers (labelled-line model), or whether individual taste cells are sensitive to several taste modalities (across fiber pattern model). Currently, taste cells are categorized into three groups according to morphological, biochemical and physiological properties (for a review, see[1,2]). Type I cells make up about 50% of the total number of cells in a bud and are believed to have a support role, similar to glial cells in the nervous system. Type I cells wrap around other cells in the bud in a glial-like fashion [3]and express enzymes for inactivation and uptake of transmitters [4,5]. Notably, these cells have voltage-dependent outward currents, but they lack a voltage-gated inward cur
Mouse taste cells with G protein-coupled taste receptors lack voltage-gated calcium channels and SNAP-25
Tod R Clapp, Kathryn F Medler, Sami Damak, Robert F Margolskee, Sue C Kinnamon
BMC Biology , 2006, DOI: 10.1186/1741-7007-4-7
Abstract: Depolarization with high K+ resulted in an increase in intracellular Ca2+ in a small subset of non-GFP labeled cells of both transgenic mouse lines. In contrast, no depolarization-evoked Ca2+ responses were observed in GFP-expressing taste cells of either genotype, but GFP-labeled cells responded to the PLC activator m-3M3FBS, suggesting that these cells were viable. Whole cell recording indicated that the GFP-labeled cells of both genotypes had small voltage-dependent Na+ and K+ currents, but no evidence of Ca2+ currents. A subset of non-GFP labeled taste cells exhibited large voltage-dependent Na+ and K+ currents and a high threshold voltage-gated Ca2+ current. Immunocytochemistry indicated that SNAP-25 was expressed in a separate population of taste cells from those expressing T1R3 or TRPM5. These data indicate that G protein-coupled taste receptors and conventional synaptic signaling mechanisms are expressed in separate populations of taste cells.The taste receptor cells responsible for the transduction of bitter, sweet, and umami stimuli are unlikely to communicate with nerve fibers by using conventional chemical synapses.Taste buds, the transducing elements of gustatory sensation, contain a heterogeneous population of 50 to 100 elongate taste receptor cells, which extend from the basal lamina to the surface of the epithelium. Taste stimuli interact with receptors on the apical membrane, while the basolateral membranes of some taste cells associate with gustatory nerve fibers to transmit taste information to the brain.Several types of taste cells have been identified morphologically. Type I cells, also known as "dark" cells, generally comprise about half of the taste bud. These cells are not believed to have a receptive function, but to play a more glial-like role in the taste bud [1,2]. About 35% of the cells are Type II cells, which are also known as "light" cells due to the electron lucent nature of their cytoplasm. Type II cells express T1R and T2R taste re
Evidence for a role of glutamate as an efferent transmitter in taste buds
Aurelie Vandenbeuch, Marco Tizzano, Catherine B Anderson, Leslie M Stone, Daniel Goldberg, Sue C Kinnamon
BMC Neuroscience , 2010, DOI: 10.1186/1471-2202-11-77
Abstract: Using molecular and immunohistochemical techniques, we show that the vesicular transporters for glutamate, VGLUT 1 and 2, but not VGLUT3, are expressed in the nerve fibers surrounding taste buds but likely not in taste cells themselves. Further, we show that P2X2, a specific marker for gustatory but not trigeminal fibers, co-localizes with VGLUT2, suggesting the VGLUT-expressing nerve fibers are of gustatory origin. Calcium imaging indicates that GAD67-GFP Type III taste cells, but not T1R3-GFP Type II cells, respond to glutamate at concentrations expected for a glutamate transmitter, and further, that these responses are partially blocked by NBQX, a specific AMPA/Kainate receptor antagonist. RT-PCR and immunohistochemistry confirm the presence of the Kainate receptor GluR7 in Type III taste cells, suggesting it may be a target of glutamate released from gustatory nerve fibers.Taken together, the results suggest that glutamate may be released from gustatory nerve fibers using a vesicular mechanism to modulate Type III taste cells via GluR7.L-glutamate (hereafter referred to as glutamate) has been proposed to play a role in neurotransmission in the peripheral taste system [1,2]. Evidence supporting a role for glutamate as a transmitter includes the expression of glutamate receptors in taste cells [3-8] as well as the presence of the glutamate transporter GLAST [9]. However, the origin of glutamate and its sites of action in the taste bud are not well understood. For example, glutamate could be released from taste cells to activate glutamate receptors on adjacent taste cells or afferent nerve fibers. Alternatively, glutamate could be released from either gustatory or somatosensory nerve fibers to modulate the activity of taste cells. Studies examining the function of glutamate as a transmitter in the taste system are complicated by the fact that glutamate is also a taste stimulus that elicits the umami taste (for review, [10-12]. However, gustatory nerve responses to
Immunocytochemical evidence for co-expression of Type III IP3 receptor with signaling components of bitter taste transduction
Tod R Clapp, Leslie M Stone, Robert F Margolskee, Sue C Kinnamon
BMC Neuroscience , 2001, DOI: 10.1186/1471-2202-2-6
Abstract: Antibodies against Type I, II, and III IP3 receptors were tested on sections of rat and mouse circumvallate papillae. Robust cytoplasmic labeling for the Type III IP3 receptor (IP3R3) was found in a large subset of taste cells in both species. In contrast, little or no immunoreactivity was seen with antibodies against the Type I or Type II IP3 receptors. To investigate the potential role of IP3R3 in bitter taste transduction, we used double-label immunocytochemistry to determine whether IP3R3 is expressed in the same subset of cells expressing other bitter signaling components. IP3R3 immunoreactive taste cells were also immunoreactive for PLCβ2 and γ13. Alpha-gustducin immunoreactivity was present in a subset of IP3R3, PLCβ2, and γ13 positive cells.IP3R3 is the dominant form of the IP3 receptor expressed in taste cells and our data suggest it plays an important role in bitter taste transduction.Taste receptor cells are specialized epithelial cells, which are organized into discrete endorgans called taste buds. Typical taste buds contain 50-100 polarized taste cells, which extend from the basal lamina to the taste pore, where apical microvilli protrude into the oral cavity. The basolateral membrane forms chemical synapses with primary gustatory neurons (Fig. 1A). In mammals, lingual taste buds are housed in connective tissue structures called papillae. Fungiform papillae are located on the anterior two-thirds of the tongue and typically contain 1-2 taste buds each. Vallate and foliate papillae are found on the posterior tongue and house several hundred taste buds each. Taste transduction begins when sapid stimuli interact with the apical membrane of taste cells, usually resulting in taste cell depolarization, calcium influx, and transmitter release onto gustatory afferent neurons. Simple stimuli, such as salts and acids depolarize taste cells by direct interaction with apical ion channels. In contrast, complex stimuli, such as sugars, amino acids, and most bitter com
A2BR Adenosine Receptor Modulates Sweet Taste in Circumvallate Taste Buds
Shinji Kataoka, Arian Baquero, Dan Yang, Nicole Shultz, Aurelie Vandenbeuch, Katya Ravid, Sue C. Kinnamon, Thomas E. Finger
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030032
Abstract: In response to taste stimulation, taste buds release ATP, which activates ionotropic ATP receptors (P2X2/P2X3) on taste nerves as well as metabotropic (P2Y) purinergic receptors on taste bud cells. The action of the extracellular ATP is terminated by ectonucleotidases, ultimately generating adenosine, which itself can activate one or more G-protein coupled adenosine receptors: A1, A2A, A2B, and A3. Here we investigated the expression of adenosine receptors in mouse taste buds at both the nucleotide and protein expression levels. Of the adenosine receptors, only A2B receptor (A2BR) is expressed specifically in taste epithelia. Further, A2BR is expressed abundantly only in a subset of taste bud cells of posterior (circumvallate, foliate), but not anterior (fungiform, palate) taste fields in mice. Analysis of double-labeled tissue indicates that A2BR occurs on Type II taste bud cells that also express Gα14, which is present only in sweet-sensitive taste cells of the foliate and circumvallate papillae. Glossopharyngeal nerve recordings from A2BR knockout mice show significantly reduced responses to both sucrose and synthetic sweeteners, but normal responses to tastants representing other qualities. Thus, our study identified a novel regulator of sweet taste, the A2BR, which functions to potentiate sweet responses in posterior lingual taste fields.
Qualitative and quantitative differences between taste buds of the rat and mouse
Huazhi Ma, Ruibiao Yang, Stacey M Thomas, John C Kinnamon
BMC Neuroscience , 2007, DOI: 10.1186/1471-2202-8-5
Abstract: There are significant differences (p < 0.05) between mouse and rat taste buds in the percentages of taste cells displaying immunoreactivity for all five markers. Rat taste buds display significantly more immunoreactivity than mice for PLCβ2 (31.8% vs 19.6%), α-gustducin (18% vs 14.6%), and synaptobrevin-2 (31.2% vs 26.3%). Mice, however, have more cells that display immunoreactivity to 5-HT (15.9% vs 13.7%) and PGP 9.5 (14.3% vs 9.4%). Mouse taste buds contain an average of 85.8 taste cells vs 68.4 taste cells in rat taste buds. The average volume of a mouse taste bud (42,000 μm3) is smaller than a rat taste bud (64,200 μm3). The numerical density of taste cells in mouse circumvallate taste buds (2.1 cells/1000 μm3) is significantly higher than that in the rat (1.2 cells/1000 μm3).These results suggest that rats and mice differ significantly in the percentages of taste cells expressing signaling molecules. We speculate that these observed dissimilarities may reflect differences in their gustatory processing.Mammalian taste buds are onion-shaped structures specialized for the detection of aqueous stimuli. Based on morphological criteria, rodent taste cells have been classified into types I, II, III, peripheral and basal cells [1-12]. Type I cells in rodents are slender and possess an electron-dense cytoplasm and several long, apical microvilli extending into the oral cavity. A distinguishing feature of a type I cell is the presence of many 100–400 nm dense granules in the apical cytoplasm. Type II cells are characterized by the presence of an electron-lucent cytoplasm and large circular or ovoid nuclei. Type II cells possess several short microvilli of uniform length extending into the taste pore. Type III cells are slender and exhibit morphology and cytoplasmic electron density intermediate between type I and type II cells. The nuclei of type III cells are slender and possess prominent invaginations. Two distinguishing features of type III cells are the single blunt
Immunocytochemical analysis of P2X2 in rat circumvallate taste buds
Ruibiao Yang, Alana Montoya, Amanda Bond, Jenna Walton, John C Kinnamon
BMC Neuroscience , 2012, DOI: 10.1186/1471-2202-13-51
Abstract: P2X2-like immunoreactivity is present in intragemmal nerve processes in rat circumvallate taste buds. Intense immunoreactivity can also be seen in the subgemmal nerve plexuses located below the basal lamina. The P2X2 immunoreactive nerve processes also display syntaxin-1-LIR. The immunoreactive nerves are in close contact with the IP3R3-LIR Type II cells and syntaxin-1-LIR and/or 5-HT-LIR Type III cells. Taste cell synapses are observed only from Type III taste cells onto P2X2-LIR nerve processes. Unusually large, “atypical” mitochondria in the Type II taste cells are found only at close appositions with P2X2-LIR nerve processes. P2X2 immunogold particles are concentrated at the membranes of nerve processes at close appositions with taste cells.Based on our immunofluorescence and immunoelectron microscopical studies we believe that both perigemmal and most all intragemmal nerve processes display P2X2-LIR. Moreover, colloidal gold immunoelectron microscopy indicates that P2X2-LIR in nerve processes is concentrated at sites of close apposition with Type II cells. This supports the hypothesis that ATP may be a key neurotransmitter in taste transduction and that Type II cells release ATP, activating P2X2 receptors in nerve processes.
Geographic analysis of low birthweight and infant mortality in Michigan using automated zoning methodology
Sue C Grady, Helen Enander
International Journal of Health Geographics , 2009, DOI: 10.1186/1476-072x-8-10
Abstract: For a majority of Zip Codes the relative standard errors (RSEs) of rates calculated prior to AZM were greater than 20%. Spurious results were the result of too few case and birth counts. Applying AZM with a target population of 25 cases and minimum threshold of 20 cases resulted in the reconstruction of zones with at least 50 births and RSEs of rates 20–22% and below respectively, demonstrating the stability reliability of these new estimates. Other AZM parameters included homogeneity constraints on maternal race and maximum shape compactness of zones to minimize potential confounding. AZM identified areas with elevated low birthweight and infant mortality rates and standardized incidence and mortality ratios. Most but not all of these areas were also detected by SaTScan.Understanding the spatial patterns of low birthweight and infant deaths in Michigan was an important first step in conducting a geographic evaluation of the State's reported high infant mortality rates. AZM proved to be a useful tool for visualizing and exploring the spatial patterns of low birthweight and infant deaths for public health surveillance. Future research should also consider AZM as a tool for health services research.Infant mortality refers to infants born alive who die within their first year of life. In 2006, Michigan's infant mortality rate was 7.6 infant deaths per 1,000 live births with African American infants at substantially higher risk (17.7) than white infants (5.2) of death [1]. The primary adverse reproductive outcomes that increase newborn's risk of death are premature birth (i.e., infants born less than 37 weeks gestation), low birthweight (i.e., infants born less than 2,500 grams), which includes very low birthweight (i.e., infants born less than 1,500 grams) and congenital defects [1]. Infants born prematurely, low birthweight and/or with congenital defects are at increased risk of death because of undeveloped or poorly developed organs and/or organ systems and the inabi
Improving the patient's experience
C Patricia Fathers,Sue Stevens
Community Eye Health Journal , 2008,
Abstract: When arriving at the eye care unit, patients often feel unsure of what is going to happen, anxious, and vulnerable. Many have never found themselves in a hospital setting before or have never travelled or slept away from home.It is an integral part of eye care to make sure a patient's experience is a positive one. This article offers suggestions for good, evidence-based, practice to improve this experience.Our suggestions should necessarily be adapted to local context: resource-poor settings are particularly challenging work environments and staff may need to display more ingenuity in working towards good practice, when striving to achieve the goals of VISION 2020.
Dramatic Increases in Obesity and Overweight Prevalence among Asian Subgroups in the United States, 1992–2011
Gopal K. Singh,Sue C. Lin
ISRN Preventive Medicine , 2013, DOI: 10.5402/2013/898691
Abstract: We examined trends in adult obesity and overweight prevalence among major Asian/Pacific Islander (API) subgroups and the non-Hispanic whites from 1992 to 2011. Using 1992–2011 National Health Interview Surveys, obesity, overweight, and BMI differentials were analyzed by logistic, linear, and log-linear regression. Between 1992 and 2011, obesity prevalence doubled for the Chinese, the Asian Indians, the Japanese, and the Hawaiians/Pacific Islanders; and tripled for the Filipinos. Obesity prevalence among API adults tripled from 3.7% in 1992 to 13.3% in 2010, and overweight prevalence doubled from 23.2% to 43.1%. Immigrants in each API subgroup had lower prevalence than their US-born counterparts, with immigrants’ obesity and overweight risks increasing with increasing duration of residence. During 2006–2011, obesity prevalence ranged from 3.3% for Chinese immigrants to 22.3% for the US-born Filipinos and 41.1% for the Native Hawaiians/Pacific Islanders. The Asian Indians, the Filipinos, and the Hawaiians/Pacific Islanders had, respectively, 3.1, 3.8, and 10.9 times higher odds of obesity than those of the Chinese adults. Compared with Chinese immigrants, the adjusted odds of obesity were 3.5–4.6 times higher for the US-born Chinese and the foreign-born Filipinos, 9 times higher for the US-born Filipinos and whites, 3.8–5.5 times higher for the US-born and foreign-born Asian Indians, and 21.9 times higher for the Native Hawaiians. Substantial ethnic heterogeneity and rising prevalence underscore the need for increased monitoring of obesity and obesity-related risk factors among API subgroups. 1. Introduction Adult obesity rates have increased dramatically in the United States, with the prevalence having risen more than twofold during the past 35 years [1]. Marked increases in obesity prevalence have occurred among both males and females and across all racial/ethnic and socioeconomic groups [1–3]. Due to high prevalence, a rapidly increasing trend, large racial/ethnic and socioeconomic disparities, and an unfavorable international ranking, current obesity levels in both children and adults are seen as a major public health problem in the USA [1–5]. While trend and current data on obesity for US adults are routinely available for such major racial/ethnic groups as the whites, the blacks, and the Hispanics [1, 6], prevalence estimates for specific Asian/Pacific Islander (API) subgroups are less well analyzed, particularly temporal obesity patterns among them [2]. Only a few studies have examined obesity differentials among APIs at the national level [2,
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