Search results for " jun"
showing 10 items of 611 documents
Expression of connexin36 in the adult and developing rat brain.
2000
The distribution of connexin36 (Cx36) in the adult rat brain and retina has been analysed at the protein (immunofluorescence) and mRNA (in situ hybridization) level. Cx36 immunoreactivity, consisting primarily of round or elongated puncta, is highly enriched in specific brain regions (inferior olive and the olfactory bulb), in the retina, in the anterior pituitary and in the pineal gland, in agreement with the high levels of Cx36 mRNA in the same regions. A lower density of immunoreactive puncta can be observed in several brain regions, where only scattered subpopulations of cells express Cx36 mRNA. By combining in situ hybridization for Cx36 mRNA with immunohistochemistry for a general neu…
Facial alveolar bone thickness and modifying factors of anterior maxillary teeth: a systematic review and meta-analysis of cone-beam computed tomogra…
2021
Abstract Background Understanding the anatomy of the facial alveolar bone (FAB), provides a prognostic tool for estimating the degree of dimensional ridge alterations after tooth extraction. This systematic review and meta-analysis aims to determine the FAB thickness and modifying factors of anterior maxillary teeth measured by CBCT scans. A secondary objective was to assess the facial distance from the cementoenamel junction (CEJ) to the bone crest. Methods An electronic search was made of Medline, Embase, Web of Science, Cochrane Library and Google Scholar up to December 2019. Studies that analyze and quantitatively compare FAB thickness at maxillary teeth by CBCT scans were included. The…
Effects of K(ATP) channel modulators on acetylcholine release from guinea-pig isolated atria and small intestine.
2002
The effects of K(ATP) channel blockers (glibenclamide, HMR 1883, HMR 1372) and openers (cromakalim, pinacidil, diazoxide) on the electrically-evoked (5 Hz) release of [(3)H]acetylcholine were studied in isolated guinea-pig atria and myenteric plexus-longitudinal muscle preparations which had been preincubated with [(3)H]choline. Atria: Cromakalim (0.3 microM and 1 microM), pinacidil (10 microM) and diazoxide (30 microM) significantly reduced the stimulation-evoked release of [(3)H]acetylcholine. The inhibition produced by cromakalim and pinacidil was prevented by 1 microM of either HMR 1883, HMR 1372 or glibenclamide. The blockers alone significantly increased the release at concentrations …
Deficient membrane integration of the novel p.N14D-GJB2mutant associated with non-syndromic hearing impairment
2006
Mutations in GJB2, the gene encoding for the Gap Junction protein Connexin 26 (Cx26), have been established as the major cause of hereditary, non-syndromic hearing impairment (HI). We report here the identification of a novel point mutation in GJB2, c.40A>G [p.N14D], detected in compound heterozygosity with the c.35delG mutation in two brothers with moderate non-syndromic sensorineural HI. The mother who carried one wildtype and a p.N14D allele displayed normal hearing. The mutation leads to substitution of the neutral amino acid asparagine (N) by the negatively charged aspartic acid (D) at amino acid number 14, a position that is conserved among Cx26 of different organisms and among many o…
Release of [3H]acetylcholine from a modified rat phrenic nerve-hemidiaphragm preparation
1986
Two different preparations of the rat phrenic nerve-hemidiaphragm (whole nerve-muscle preparation, end-plate preparation) were used for studying synthesis and release of radioactive acetylcholine in the absence and presence of cholinesterase inhibitors. When the whole nerve-muscle preparation (110-180 mg) was incubated with [3H]choline, only small amounts of radioactive acetylcholine were synthesized within the tissue. Electrical nerve stimulation of the whole nerve-muscle preparation produced no increase in tritium outflow. Incubation of the end-plate preparation (16-29 mg) which was obtained after removal of most of the muscle mass led to the formation of large amounts of [3H]acetylcholin…
Altered electrical activity in colonic smooth muscle cells from dystrophic (mdx) mice
2001
Because the colon from dystrophic (mdx) mice shows an altered motor pattern, probably due to neural disorders, our aim was to examine the electrophysiological properties of muscle cells and the functionality of nitrergic transmission in circular muscle from normal and mdx colon. Normal colonic cells (resting membrane potential [RMP] about -50 mV) showed spontaneous hyperpolarizations (inhibitory junction potentials; IJPs) and cyclic slow depolarizations were sometimes recorded. Mdx colon had a depolarized RMP (about -36 mV) and spontaneous IJPs, but the cyclic activity was never observed. In the normal colon, Nomega-nitro-L-arginine methyl ester (L-NAME) induced depolarization and abolished…
Prejunctional M1 and postjunctional M3 muscarinic receptors in the circular muscle of the guinea-pig ileum.
1995
The effects of subtype-selective muscarinic receptor antagonists on electrically evoked release of acetylcholine and muscle contraction were compared in circular muscle preparations of the guinea-pig ileum. Incubation of the preparation with [3H]choline resulted in the formation of [3H]acetylcholine. Electrical stimulation caused the release of [3H]acetylcholine which was abolished by tetrodotoxin and omission of calcium from the medium. 5-Hydroxytryptamine (10 microM) and the nicotinic agonist 1,1-dimethyl-4-phenyl-piperazinium (300 microM) did not change acetylcholine release. The muscarinic antagonists pirenzepine (M1 selective), AF-DX 116 (M2 selective) and hexahydrosiladifenidol (M3 se…
Loss of desmoglein 2 suggests essential functions for early embryonic development and proliferation of embryonal stem cells.
2002
Summary Desmoglein 2 (Dsg2) is a Ca 2+ -dependent adhesion molecule of desmosomes and is synthesized in all desmosome-bearing tissues from their earliest appearance onward. To examine the function of Dsg2, its gene was inactivated by homologous recombination in embryonal stem (ES) cells for the generation of knockout mice. DSG2 −/− mice and a considerable number of DSG2 +/− mice died at or shortly after implantation. On the other hand, DSG2 −/− blastocysts developed an apparently normal trophectoderm layer, the first tissue known to produce desmosomes, and hatched properly. Immunofluorescence analyses of these blastocysts showed, however, that the distribution of the desmosomal plaque prote…
Expression of the rat connexin 39 (rCx39) gene in myoblasts and myotubes in developing and regenerating skeletal muscles: an in situ hybridization st…
2005
We report a detailed analysis of the expression pattern of the recently identified rat connexin gene, named rat connexin 39 (rCx39), both during embryonic development and in adult life. Qualitative and quantitative reverse transcription/polymerase chain reaction analysis showed intense expression of rCx39 restricted to differentiating skeletal muscles, with a peak of expression detected at 18 days of embryonic life, followed by a rapid decline to undetectable levels within the first week of postnatal life. A combination of the in situ hybridization technique for the detection of rCx39 mRNA and immunohistochemistry for myogenin, a myoblast-specific marker, allowed us to establish that the mR…
Hypothalamic Astroglial Connexins are Required for Brain Glucose Sensing-Induced Insulin Secretion
2014
Supplementary Information accompanies the paper on the Journal of Cerebral Blood Flow & Metabolism website; Hypothalamic glucose detection participates in maintaining glycemic balance, food intake, and thermogenesis. Although hypothalamic neurons are the executive cells involved in these responses, there is increasing evidence that astrocytes participate in glucose sensing (GS); however, it is unknown whether astroglial networking is required for glucose sensitivity. Astroglial connexins 30 and 43 (Cx30 and Cx43) form hexameric channels, which are apposed in gap junctions, allowing for the intercellular transfer of small molecules such as glucose throughout the astroglial networks. Here, we…