Binding of [<sup>3</sup>H]‐muscimol to GABA<sub>A</sub> sites in the guinea‐pig urinary bladder: biochemical assay and autoradiography

Erdö, Sándor L.; Mione, Marina; Amenta, Francesco; Wolff, Joachim R.

doi:10.1111/j.1476-5381.1989.tb11819.x

Cited by 15 publications

(7 citation statements)

References 23 publications

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“…The average overexpression of GABA a receptor p subunit in breast tumors vs non-breast normal tissues is 4.0 (Table 2). GABA a receptors were shown to be located on central neurons and astroglia, and were also detected on non-neuronal cells including endocrine cells of the pituitary pars intermediate and smooth muscle cells of the urinary bladder and uterus (Amenta et al, 1988;Erdo et al, 1989). The function of GABA A receptors in non-neuronal cells is not clear, although their function in the uterus appears to be related to the regulation of uterine motility by inhibiting contraction (Majewska and Vaupel, 1991).…”

Section: Identification Of Cdnas Differentially Expressed In Breast Tmentioning

confidence: 99%

Discovery of differentially expressed genes in human breast cancer using subtracted cDNA libraries and cDNA microarrays

et al. 2002

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Identifying novel and known genes that are di erentially expressed in breast cancer has important implications in understanding the biology of breast tumorigenesis and developing new diagnostic and therapeutic agents. In this study we have combined two powerful technologies, PCRbased cDNA subtraction and cDNA microarray, as a high throughput methodology designed to identify cDNA clones that are breast tumor-and tissue-speci®c and are overexpressed in breast tumors. Approximately 2000 cDNA clones generated from the subtracted breast tumor library were arrayed on the microarray chips. The arrayed target cDNAs were then hybridized with 30 pairs of¯uorescent-labeled cDNA probes generated from breast tumors and normal tissues to determine the tissue distribution and tumor speci®city. cDNA clones showing overexpression in breast tumors by microarray were further analysed by DNA sequencing, GenBank and EST database searches, and quantitative real time PCR. We identi®ed several known genes, including mammaglobin, cytokeratin 19, ®bronectin, and hair-speci®c type II keratin, which have previously been shown to be overexpressed in breast tumors and may play an important role in the malignance of breast. We also discovered B726P which appears to be an isoform of NY-BR-1, a breast tissue-speci®c gene. Two additional clones discovered, B709P and GABA A receptor p subunit, were not previously described for their overexpression pro®le in breast tumors. Thus, combining PCRbased cDNA subtraction and cDNA microarray allowed for an e cient way to identify and validate genes with elevated mRNA expression levels in breast cancer that may potentially be involved in breast cancer progression. These di erentially expressed genes may be of potential utility as therapeutic and diagnostic targets for breast cancer.

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Section: Identification Of Cdnas Differentially Expressed In Breast Tmentioning

confidence: 99%

Discovery of differentially expressed genes in human breast cancer using subtracted cDNA libraries and cDNA microarrays

et al. 2002

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“…GABA and GABA A Rs also exist in nonneuronal cells of visceral organs (2,6,10,11,14,24,29). It is known that GABA is a transmitter of enteric interneurons and that GABA regulates the function of the gastrointestinal tract (22).…”

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confidence: 99%

A novel role of intestine epithelial GABAergic signaling in regulating intestinal fluid secretion

Yun

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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γ-Aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the central nervous system, and it is produced via the enzymatic activity of glutamic acid decarboxylase (GAD). GABA generates fast biological signaling through type A receptors (GABA(A)R), an anionic channel. Intriguingly, GABA is found in the jejunum epithelium of rats. The present study intended to determine whether a functional GABA signaling system exists in the intestinal epithelium and if so whether the GABA signaling regulates intestinal epithelial functions. RT-PCR, Western blot, and immunohistochemical assays of small intestinal tissues of various species were performed to determine the expression of GABA-signaling proteins in intestinal epithelial cells. Perforated patch-clamp recording was used to measure GABA-induced transmembrane current in the small intestine epithelial cell line IEC-18. The fluid weight-to-intestine length ratio was measured in mice that were treated with GABA(A)R agonist and antagonist. The effect of GABA(A)R antagonist on allergic diarrhea was examined using a mouse model. GABA, GAD, and GABA(A)R subunits were identified in small intestine epithelial cells of mice, rats, pigs, and humans. GABA(A)R agonist induced an inward current and depolarized IEC-18. Both GABA and the GABA(A)R agonist muscimol increased intestinal fluid secretion of rats. The increased intestinal secretion was largely decreased by the GABA(A)R antagonist picrotoxin or gabazine, but not by tetrodotoxin. The expression levels of GABA-signaling proteins were increased in the intestinal epithelium of mice that were sensitized and challenged with ovalbumin (OVA). The OVA-treated mice exhibited diarrhea, which was alleviated by oral administration of gabazine or picrotoxin. An endogenous autocrine GABAergic signaling exists in the mammalian intestinal epithelium, which upregulates intestinal fluid secretion. The intestinal GABAergic signaling becomes intensified in allergic diarrhea, and inhibition of this GABA-signal system alleviates the allergic diarrhea.

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“…GABA. GABA, glutamate decarboxylase, and the GABA transporter, GAT1, have all been shown to be present in the urinary bladder of guinea pigs and rats (Tanaka, 1985;Erdö et al, 1989;Pehrson and Andersson, 2002), and GABA may influence bladder motility by acting not only in the CNS, but also at the pelvic ganglionic (de Groat, 1970;Maggi et al, 1985a;Kataoka et al, 1994) and postganglionic levels, by reducing neurotransmitter release from neurons innervating the detrusor (Andersson, 1993;Pehrson and Andersson, 2002;Sanger et al, 2002). Pehrson and Andersson (2002) showed in the rat bladder that the GABA reuptake inhibitor tiagabine, by blocking GAT1 and increasing local levels of GABA, attenuated bladder contractions induced by electrical field stimulation, but did not affect contractions induced by carbachol.…”

Section: Peripheral Targetsmentioning

confidence: 99%

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Andersson

Wein²

2004

Pharmacol Rev

454

364

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Binding of [³H]‐muscimol to GABA_A sites in the guinea‐pig urinary bladder: biochemical assay and autoradiography

Cited by 15 publications

References 23 publications

Discovery of differentially expressed genes in human breast cancer using subtracted cDNA libraries and cDNA microarrays

Discovery of differentially expressed genes in human breast cancer using subtracted cDNA libraries and cDNA microarrays

A novel role of intestine epithelial GABAergic signaling in regulating intestinal fluid secretion

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

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Binding of [3H]‐muscimol to GABAA sites in the guinea‐pig urinary bladder: biochemical assay and autoradiography

Cited by 15 publications

References 23 publications

Discovery of differentially expressed genes in human breast cancer using subtracted cDNA libraries and cDNA microarrays

Discovery of differentially expressed genes in human breast cancer using subtracted cDNA libraries and cDNA microarrays

A novel role of intestine epithelial GABAergic signaling in regulating intestinal fluid secretion

Pharmacology of the Lower Urinary Tract: Basis for Current and Future Treatments of Urinary Incontinence

Contact Info

Product

Resources

About

Binding of [³H]‐muscimol to GABA_A sites in the guinea‐pig urinary bladder: biochemical assay and autoradiography