Journal articles: 'Gamma-aminobutyric acid'

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Roberts, Eugene. "Gamma-aminobutyric acid." Scholarpedia 2, no. 10 (2007): 3356. http://dx.doi.org/10.4249/scholarpedia.3356.

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Habibuddin, M., S. Sen, M. Pal, and S. P. Pal. "N-Valproyl gamma aminobutyric acid." Behavioural Pharmacology 6, SUPPLEMENT 1 (May 1995): 95. http://dx.doi.org/10.1097/00008877-199505001-00111.

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Le Vo, Tam Dinh, and Soon-Ho Hong. "Optimization of gamma-Aminobutyric Acid Bioconversion by Recombinant Escherichia coli." KSBB Journal 27, no. 2 (April 30, 2012): 127–30. http://dx.doi.org/10.7841/ksbbj.2012.27.2.127.

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Girard, C. L., J. R. Seoane, and J. J. Matte. "Topographic studies of the effects of microinjections of muscimol on the hypothalamic control of feed intake in sheep." Canadian Journal of Physiology and Pharmacology 64, no. 4 (April 1, 1986): 406–10. http://dx.doi.org/10.1139/y86-065.

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Ten sheep were used to define the anatomical basis for the feeding systems sensitive to gamma-aminobutyric acid, by using intrahypothalamic microinjections of the gamma-aminobutyric acid agonist, muscimol. In satiated sheep, 1 μL of muscimol (0.5 nmol/μL) elicited feeding when injected into paraventricular, ventromedial, and anterior hypothalamic areas. Similar injections into 39 sites tested in 6-h fasted sheep failed to decrease feed intake. The data suggest that neurons sensitive to gamma-aminobutyric acid in medial hypothalamus may be involved in the initiation of feeding.

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Ho, I. K., and Beth Hoskins. "NEUROTOXICANTS AND GAMMA-AMINOBUTYRIC ACID RECEPTORS." Journal of Toxicological Sciences 15, SupplementIV (1990): 3–13. http://dx.doi.org/10.2131/jts.15.supplementiv_3.

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MacNaughton, WK, and A. Krantis. "Gamma-aminobutyric acid-induced chloride secretion." Gastroenterology 112, no. 2 (February 1997): 672–73. http://dx.doi.org/10.1053/gast.1997.v112.agast970672.

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Hardcastle, J., and PT Hardcastle. "gamma-Aminobutyric acid and intestinal secretion." Gastroenterology 111, no. 4 (October 1996): 1163–64. http://dx.doi.org/10.1016/s0016-5085(96)70096-3.

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Minuk, Gerald Y. "Gamma-Aminobutyric Acid and the Liver." Digestive Diseases 11, no. 1 (1993): 45–54. http://dx.doi.org/10.1159/000171400.

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Olsen, R. W. "Absinthe and gamma -aminobutyric acid receptors." Proceedings of the National Academy of Sciences 97, no. 9 (April 25, 2000): 4417–18. http://dx.doi.org/10.1073/pnas.97.9.4417.

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Belokrylov, G. A., and I. V. Molchanova. "Immunostimulating property of gamma-aminobutyric acid." Bulletin of Experimental Biology and Medicine 104, no. 3 (September 1987): 1284–86. http://dx.doi.org/10.1007/bf00842017.

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Liu, Yan, Yue-Hui Li, Feng-Jie Guo, Jia-Jia Wang, Rui-Li Sun, Jin-Yue Hu, and Guan-Cheng Li. "Gamma-aminobutyric acid promotes human hepatocellular carcinoma growth through overexpressed gamma-aminobutyric acid A receptor α3 subunit." World Journal of Gastroenterology 14, no. 47 (2008): 7175. http://dx.doi.org/10.3748/wjg.14.7175.

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Hwang, Eunyeong, and Jae-Yong Park. "Isolation and Characterization of Gamma-Aminobutyric Acid (GABA)-Producing Lactic Acid Bacteria from Kimchi." Current Topic in Lactic Acid Bacteria and Probiotics 6, no. 2 (December 2020): 64–69. http://dx.doi.org/10.35732/ctlabp.2020.6.2.64.

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Moradi-Afrapoli, Fahimeh, Hannes van der Merwe, Maria De Mieri, Anke Wilhelm, Marco Stadler, Pieter Zietsman, Steffen Hering, Kenneth Swart, and Matthias Hamburger. "HPLC-Based Activity Profiling for GABAA Receptor Modulators in Searsia pyroides Using a Larval Zebrafish Locomotor Assay." Planta Medica 83, no. 14/15 (May 16, 2017): 1169–75. http://dx.doi.org/10.1055/s-0043-110768.

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AbstractA dichloromethane extract from leaves of Searsia pyroides potentiated gamma aminobutyric acid-induced chloride currents by 171.8 ± 54% when tested at 100 µg/mL in Xenopus oocytes transiently expressing gamma aminobutyric acid type A receptors composed of α 1 β 2 γ 2s subunits. In zebrafish larvae, the extract significantly lowered pentylenetetrazol-provoked locomotion when tested at 4 µg/mL. Active compounds of the extract were tracked with the aid of HPLC-based activity profiling utilizing a previously validated zebrafish larval locomotor activity assay. From two active HPLC fractions, compounds 1 – 3 were isolated. Structurally related compounds 4 – 6 were purified from a later eluting inactive HPLC fraction. With the aid of 1H and 13C NMR and high-resolution mass spectrometry, compounds 1 – 6 were identified as analogues of anacardic acid. Compounds 1 – 3 led to a concentration-dependent decrease of pentylenetetrazol-provoked locomotion in the zebrafish larvae model, while 4 – 6 were inactive. Compounds 1 – 3 enhanced gamma aminobutyric acid-induced chloride currents in Xenopus oocytes in a concentration-dependent manner, while 4 – 6 only showed marginal enhancements of gamma aminobutyric acid-induced chloride currents. Compounds 2, 3, and 5 have not been reported previously.

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Shelp, B. "Metabolism and functions of gamma-aminobutyric acid." Trends in Plant Science 4, no. 11 (November 1, 1999): 446–52. http://dx.doi.org/10.1016/s1360-1385(99)01486-7.

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Silverman, R. B., B. J. Invergo, M. A. Levy, and C. R. Andrew. "Substrate stereospecificity and active site topography of gamma-aminobutyric acid aminotransferase for beta-aryl-gamma-aminobutyric acid analogues." Journal of Biological Chemistry 262, no. 7 (March 1987): 3192–95. http://dx.doi.org/10.1016/s0021-9258(18)61489-9.

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Jacob, James N., Victor E. Shashoua, Alexander Campbell, and Ross J. Baldessarini. ".gamma.-Aminobutyric acid esters. 2. Synthesis, brain uptake, and pharmacological properties of lipid esters of .gamma.-aminobutyric acid." Journal of Medicinal Chemistry 28, no. 1 (January 1985): 106–10. http://dx.doi.org/10.1021/jm00379a019.

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Partridge, Brett J., Sandra R. Chaplan, Eiji Sakamoto, and Tony L. Yaksh. "Characterization of the Effects of Gabapentin and 3-Isobutyl-γ-Aminobutyric Acid on Substance P-induced Thermal Hyperalgesia." Anesthesiology 88, no. 1 (January 1, 1998): 196–205. http://dx.doi.org/10.1097/00000542-199801000-00028.

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Background The authors sought to characterize the pharmacologic characteristic and site of action of gabapentin (Neurontin) in a model of thermal hyperalgesia induced by intrathecal substance P administration. Methods Rats were prepared with long-term lumbar intrathecal catheters. Hind paw withdrawal latency was determined using a radiant heat stimulus focused through a glass surface onto the plantar surface of the paw. Results Within 5 min after intrathecal injection of substance P (30 nmol), hind paw withdrawal latency fell from 11 to 8 s. Gabapentin given intrathecally or intraperitoneally produced dose-dependent reversal of the thermal hyperalgesia, with complete reversal (ED100) occurring at 163 microg for intrathecal and 185 mg/kg for intraperitoneal administration. S(+)-3-isobutyl-gamma aminobutyric acid, but not R(-)-3-isobutyl-gamma aminobutyric acid, also produced dose-dependent reversal of the intrathecal substance P-induced thermal hyperalgesia (intrathecal ED100, 65 microg and intraperitonal ED100, 31 mg/kg). The effects of intraperitoneally administered gabapentin and 3-isobutyl-gamma aminobutyric acid were reversed by intrathecal pretreatment with D-serine (100 microg) but not by L-serine. All effects were observed at doses that had little effect on motor function or spontaneous activity. Intrathecal N-methyl-D-aspartate (2 nmol) induced thermal hyperalgesia, which was blocked by gabapentin (100 mg/kg intraperitoneally) and S(+)-3-isobutyl-gamma aminobutyric acid (30 mg/kg intraperitoneally). Conclusions The structure-activity relationship and the stereospecificity noted after intrathecal delivery suggest that gabapentin and S(+)-3-isobutyl-gamma aminobutyric acid act at a common spinal locus to modulate selectively a facilitated state of nociceptive processing.

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Li, Haixing, and Yusheng Cao. "Lactic acid bacterial cell factories for gamma-aminobutyric acid." Amino Acids 39, no. 5 (April 3, 2010): 1107–16. http://dx.doi.org/10.1007/s00726-010-0582-7.

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Menezes, E., F. Santos, A. Velho, T. Dinh, A. Kaya, E. Topper, B. Didion, A. Moura, and E. Memili. "153 Sperm metabolomic landscape associated with bull fertility." Reproduction, Fertility and Development 31, no. 1 (2019): 201. http://dx.doi.org/10.1071/rdv31n1ab153.

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Sub-fertility fertility in bulls decreases the efficiency and profitability of cattle production because AI allows a single bull to inseminate thousands of cows. In recent decades, there has been a general decline in fertility of bulls, even among those exhibiting normal sperm motility and morphology. Despite advances in technology and knowledge, molecular, cellular and physiological mechanisms underlying the causes of low fertility in bulls are currently unclear. Therefore, the objective of this study was to identify sperm metabolites associated with fertility in Holstein bulls. The metabolome of sperm from 10 mature bulls with high fertility (HF, n=5) and low fertility (LF, n=5) was identified by gas chromatography coupled to mass spectrometry. Bull fertility was based on the sire conception rates deviating from the average. Statistical analysis was performed by using MetaboAnalyst 3.0 (http://www.metaboanalyst.ca/). A total of 22 metabolites were detected and categorized according to their major chemical classes, including amino acids, peptides/analogues, carbohydrates/carbohydrate conjugates, fatty acids, steroids/steroid derivatives, keto acids and derivatives, carboxylic acids, and other organic and inorganic compounds. Organic acids and derivatives as well as fatty acids were the major compounds in bull spermatozoa. Seven organic acids and derivatives were detected, including benzoic acid, carbonate, carbamate dimethyl, carbamate trimethyl, lactic acid, oxalic acid, and urea. Five fatty acids were identified including oleic acid, oleanitrile, nonanoic acid, and palmitic acid. Oleic acid, phosphoric acid, phosphine, carbamate trimethyl, and glycerol were the most abundant metabolites in bull sperm, whereas benzoic acid, acetic acid, l-serine, carbamate, and 2-ketobutyric acid were the least predominant metabolites present in bull sperm. Multivariate analysis (partial least squares-discriminant analysis) of the sperm metabolome showed a clear separation between HF and LF bulls. Variable importance in projection (VIP) score demonstrated that metabolites with VIP >1.5 were gamma-aminobutyric acid (VIP=2.01), carbamate trimethyl (VIP=1.88), benzoic acid (VIP=1.86), and lactic acid (VIP=1.81). Abundance ratios of gamma-aminobutyric acid, carbamate trimethyl, benzoic acid, and lactic acid was greater in HF bulls compared with LF animals. According to univariate analysis, abundance ratios of gamma-aminobutyric acid (P=0.03) and carbamate trimethyl (P=0.047) were greater in HF than in LF bulls. Gamma-aminobutyric acid was positively correlated with carbamate trimethyl (r=0.94; P<0.0001) and benzoic acid (r=0.74; P=0.0139). Benzoic acid was positively correlated with carbamate trimethyl (r=0.75; P=0.0107) and carbamate dimethyl (r=0.68; P=0.0274). The identified metabolites can serve as potential markers to evaluate semen quality and predict bull fertility.

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Khashan, Ismael Sadeq, and Maysaa Jalal Majeed. "The Role of GABA and Insulin Regulated Aminopeptidase on Insulin Resistance and GLUT4 in Prediabetes and Type 2 Diabetes Mellitus." AL-Kindy College Medical Journal 20, no. 1 (April 1, 2024): 65–70. http://dx.doi.org/10.47723/6b3yqa81.

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Background: Different proposed mechanisms for insulin resistance have been put forth to understand the relationship and changes in insulin resistance. Looking at the levels of insulin, the neurotransmitter gamma-aminobutyric acid, glucose transport type 4, and the newly discovered enzyme insulin regulated aminopeptidase may provide an integrated perspective on insulin resistance. Objectives: To study the role of serum gamma-aminobutyric acid and insulin regulated aminopeptidase enzyme levels in pathogenesis of insulin resistance and translocation of glucose transport type 4 in patients with type2 diabetes mellitus and pre-diabetes ones. Subjects and methods: Ninety individuals were divided into three age- and BMI matched groups (diabetics, prediabetics, healthy) were assessed for glycated hemoglobin (turbidometry method), fasting serum glucose (colorimetric method), serum insulin (electrochemiluminescence immunoassay method), homeostatic model assessment for insulin resistance, serum gamma-aminobutyric acid, glucose transporter type 4, and insulin regulated aminopeptidase measured by the sandwich ELISA method. The cut-off value was adopted according to the World Health Organization, individuals with their fasting serum glucose lower than 110 mg/ml, and glycated hemoglobin level not more than 5.7 % are considered healthy individuals. Result: The mean (±SD) values of serum insulin regulated aminopeptidase, gamma-aminobutyric acid and glucose transport type 4 showed significantly lower levels with greater increases in insulin resistance, represented by the significant decrease in diabetics group who have high insulin resistance compared with pre-diabetics and healthy individuals’ groups (p < 0.05). They also significantly decrease in individuals with the pre-diabetic stage compared to healthy individuals without insulin resistance (p < 0.05). Significant negative correlations were found between HOMA-IR values and each of GABA, IRAP, and GLUT4. Conclusion: Decreasing gamma-aminobutyric acid may promote insulin resistance and prediabetes/diabetes onset. Decreased insulin regulated aminopeptidase levels suggest a role alongside glucose transport type 4 in glucose uptake, allowing screening for prediabetes risk.

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Nguyen, James An, Gunvant K. Thaker, and Carol A. Tamminga. "Gamma-Aminobutyric Acid (GABA) Pathways in Tardive Dyskinesia." Psychiatric Annals 19, no. 6 (June 1, 1989): 302–9. http://dx.doi.org/10.3928/0048-5713-19890601-08.

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Horie∗, H., and G. A. Rechnitz. "Enzymatic Flow Injection Determination of Gamma-Aminobutyric Acid." Analytical Letters 28, no. 2 (January 1995): 259–66. http://dx.doi.org/10.1080/00032719508000320.

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Bown, A. W., and B. J. Shelp. "The Metabolism and Functions of [gamma]-Aminobutyric Acid." Plant Physiology 115, no. 1 (September 1, 1997): 1–5. http://dx.doi.org/10.1104/pp.115.1.1.

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Kathiresan, A., P. Tung, C. C. Chinnappa, and D. M. Reid. "[gamma]-Aminobutyric Acid Stimulates Ethylene Biosynthesis in Sunflower." Plant Physiology 115, no. 1 (September 1, 1997): 129–35. http://dx.doi.org/10.1104/pp.115.1.129.

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Winder, T. R., G. Y. Minuk, E. J. Sargeant, and T. P. Seland. "Gamma-Aminobutyric Acid (GABA) and Sepsis-Related Encephalopathy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 15, no. 1 (February 1988): 23–25. http://dx.doi.org/10.1017/s0317167100027128.

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ABSTRACT:In order to determine whether disturbances in GABA homeostasis might play a role in the pathogenesis of sepsis-related encephalopathy, serum and brain tissue GABA concentrations from six areas of the brain (cortex, diencephalon, striatum, hippocampus, midbrain, and pons-medulla) were determined in a rat model of bacterial sepsis (cecal ligation and perforation). The results were compared to those obtained from sham operated control animals. All septic animals demonstrated clinical signs of encephalopathy and had elevated serum GABA levels (0.92 ± 0.3 uM versus 0.48 ± 0.15 in controls, p < 0.01). GABA content in the specific subcompartments of the brain, however, were similar in the two groups. These results indicate that although serum GABA levels are elevated during sepsis, GABA is unlikely to play an important role in the pathogenesis of sepsis-related encephalopathy.

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Li, Haixing, Ting Qiu, Yan Chen, and Yusheng Cao. "Separation of gamma-aminobutyric acid from fermented broth." Journal of Industrial Microbiology & Biotechnology 38, no. 12 (May 26, 2011): 1955–59. http://dx.doi.org/10.1007/s10295-011-0984-x.

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Ramos-Martinez, V. H., E. Ramirez-Vargas, F. J. Medellin-Rodriguez, C. A. Ávila-Orta, C. A. Gallardo-Vega, A. B. Jasso-Salcedo, and M. L. Andrade-Guel. "Zeolite 13X modification with gamma-aminobutyric acid (GABA)." Microporous and Mesoporous Materials 295 (March 2020): 109941. http://dx.doi.org/10.1016/j.micromeso.2019.109941.

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Öngür, Dost, Andrew P. Prescot, Julie McCarthy, Bruce M. Cohen, and Perry F. Renshaw. "Elevated Gamma-Aminobutyric Acid Levels in Chronic Schizophrenia." Biological Psychiatry 68, no. 7 (October 2010): 667–70. http://dx.doi.org/10.1016/j.biopsych.2010.05.016.

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Do-Rego, J. L., G. A. Mensah-Nyagan, D. Beaujean, D. Vaudry, W. Sieghart, V. Luu-The, G. Pelletier, and H. Vaudry. "gamma -Aminobutyric acid, acting through gamma -aminobutyric acid type A receptors, inhibits the biosynthesis of neurosteroids in the frog hypothalamus." Proceedings of the National Academy of Sciences 97, no. 25 (November 21, 2000): 13925–30. http://dx.doi.org/10.1073/pnas.240269897.

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Deev, R. V., Yu M. Shatrova, A. I. Sinitskiy, N. S. Molchanova, A. K. Yunusova, O. B. Tseylikman, D. A. Kozochkin, and M. S. Lapshin. "Levels of biogenic amines in the brain of rats at experimental post-traumatic stress disorder development." Kazan medical journal 96, no. 5 (October 15, 2015): 806–10. http://dx.doi.org/10.17750/kmj2015-806.

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Aim. To study the changes in levels of biogenic amines-neurotransmitters in the brain at experimental post-traumatic stress disorder development in rats. Methods. Post-traumatic stress disorder was modeled by keeping 48 outbred male rats in under constant and inescapable strong unconditioned stimulus. The control group included 16 intact animals, not exposed to stress influences. The levels of 3,4-dihydroxyphenylalanine, dopamine, norepinephrine, epinephrine and gamma-aminobutyric acid were determined by fluorometric methods. Behavioral activity of animals was evaluated on the day 3, 7, 10 and 14 by «open field» and «elevated plus maze» actinographs. Results. When comparing the concentrations of studied neurotransmitters in the brain of control animals with experimental groups, reflecting the development of post-traumatic stress disorder at the time, adrenaline and 3,4-dihydroxyphenylalanine levels were increased on the third day, level of norepinephrine was reduced on the seventh day, 3,4-dihydroxyphenylalanine, dopamine, norepinephrine levels were elevaled, gamma-aminobutyric acid level was reduced on the tenth day, gamma-aminobutyric acid level was increased on the fourteenth day after the stress. Conclusion. According to the results of the correlation analysis, the largest contribution to the development of behavioral disorders are made by altered brain level of gamma-aminobutyric acid at the time of post-traumatic stress disorder formation (tenth and fourteenth day). At the earlier stages (third and seventh day), the relationship of rats behavioral activity and altered 3,4-dihydroxyphenylalanine and norepinephrine brain levels was shown.

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E.I, Bon. "The Place of Mood Stabilizers in The Treatment of Anxiety Disorders." Neuroscience and Neurological Surgery 14, no. 03 (May 3, 2024): 01–04. http://dx.doi.org/10.31579/2578-8868/312.

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Mood stabilizers are used to treat bipolar disorder, but some drugs, in particular valproate, have anti-anxiety activity. This property is determined by the effect of valproate on the GABAergic system. Gamma-aminobutyric acid is involved in neurotransmission through interneuronal synapses in areas of the brain that control mood, such as the striatum, globus pallidus, and cerebral cortex. One of the most widespread mediators that plays a central role in the pathophysiology of anxiety disorders is the gamma-aminobutyric acid (GABA) system. This fact allows us to consider valproic acid as the drug of choice in the treatment of anxiety disorders.

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Wang, Xin, Zheng-Gui Huang, Olga Dergacheva, Evguenia Bouairi, Christopher Gorini, Christopher Stephens, Michael C. Andresen, and David Mendelowitz. "Ketamine Inhibits Inspiratory-evoked γ-Aminobutyric Acid and Glycine Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus." Anesthesiology 103, no. 2 (August 1, 2005): 353–59. http://dx.doi.org/10.1097/00000542-200508000-00019.

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Background Ketamine can be used for perioperative pain management as well as a dissociative anesthetic agent in emergency situations. However, ketamine can induce both cardiovascular and respiratory depression, especially in pediatric patients. Although ketamine has usually been regarded as sympathoexcitatory, recent work has demonstrated that ketamine has important actions on parasympathetic cardiac vagal efferent activity. The current study tests the hypothesis that ketamine, at clinical relevant concentrations, alters central cardiorespiratory interactions in the brainstem and, in particular, the inspiration-evoked increase in gamma-aminobutyric acid-mediated and glycinergic neurotransmission to parasympathetic cardiac efferent neurons. Methods Cardiac vagal neurons were identified by the presence of a retrograde fluorescent tracer. Respiratory evoked gamma-aminobutyric acid-mediated and glycinergic synaptic currents were recorded in cardiac vagal neurons using whole cell patch clamp techniques while spontaneous rhythmic respiratory activity was recorded simultaneously. Results : Ketamine, at concentrations from 0.1 to 10 microM, evoked a concentration-dependent inhibition of inspiratory burst frequency. Inspiration-evoked gamma-aminobutyric acid-mediated neurotransmission to cardiac vagal neurons was inhibited at ketamine concentrations of 0.5 and 1 microM. The increase in glycinergic activity to cardiac vagal neurons during inspiration was also inhibited at ketamine concentrations of 0.5 and 1 microM. Conclusions At clinically relevant concentrations (0.5 and 1 microM), ketamine alters central respiratory activity and diminishes both inspiration-evoked gamma-aminobutyric acid-mediated and glycinergic neurotransmission to parasympathetic cardiac efferent neurons. This reduction in inhibitory neurotransmission to cardiac vagal neurons is likely responsible for the compromised respiratory sinus arrhythmia that occurs with ketamine anesthesia.

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Aanesen, A. "Carrier-mediated gamma-aminobutyric acid uptake in human spermatozoa indicating the presence of a high-affinity gamma-aminobutyric acid transport protein." Biology of Reproduction 54, no. 4 (April 1, 1996): 841–46. http://dx.doi.org/10.1095/biolreprod54.4.841.

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Kazemi, H., and B. Hoop. "Glutamic acid and gamma-aminobutyric acid neurotransmitters in central control of breathing." Journal of Applied Physiology 70, no. 1 (January 1, 1991): 1–7. http://dx.doi.org/10.1152/jappl.1991.70.1.1.

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We review recent cross-disciplinary experimental and theoretical investigations on metabolism of the amino acid neurotransmitters glutamic acid and gamma-aminobutyric acid (GABA) in the brain during hypoxia and hypercapnia and their possible role in central control of breathing. The roles of classical modifiers of central chemical drive to breathing (H+ and cholinergic mechanisms) are summarized. A brief perspective on the current widespread interest in GABA and glutamate in central control is given. The basic biochemistry of these amino acids and their roles in ammonia and bicarbonate metabolism are discussed. This review further addresses recent work on central respiratory effects of inhibitory GABA and excitatory glutamate. Current understanding of the sites and mechanisms of action of these amino acids on or near the ventral surface of the medulla is reviewed. We focus particularly on tracer kinetic investigations of glutamatergic and GABAergic mechanisms in hypoxia and hypercapnia and their possible role in the ventilatory response to hypoxia. We conclude with some speculative remarks on the critical importance of these investigations and suggest specific directions of research in central mechanisms of respiratory control.

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Koch, Stephanie C., Maria Fitzgerald, and Gareth J. Hathway. "Midazolam Potentiates Nociceptive Behavior, Sensitizes Cutaneous Reflexes, and Is Devoid of Sedative Action in Neonatal Rats." Anesthesiology 108, no. 1 (January 1, 2008): 122–29. http://dx.doi.org/10.1097/01.anes.0000296079.45446.15.

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Background The significant postnatal maturation of gamma-aminobutyric acid signaling in the developing brain is likely to have important implications for infant pain processing. Gamma-aminobutyric acid receptor activation evokes analgesia and sedation in the adult, but the impact of immature gamma-aminobutyric acid signaling on modulators of the gamma-aminobutyric acid type A receptor, such as the benzodiazepines, is not known in infants. Methods Nociceptive processing was measured using behavioral and electrophysiological recordings of hind limb flexor withdrawal threshold and magnitude to mechanical and thermal stimulation of the hind paw. The effects of midazolam (0.1-10 mg/kg subcutaneously, 0.1 mg/kg intrathecally) or saline treatment were compared in rats aged 3, 10, 21, and 40 days (adult). The sedative action of midazolam was assessed at each age using righting reflex latencies. Results Midazolam dose-dependently decreased mechanical reflex thresholds and increased mechanical and thermal reflex magnitudes in neonates. In older rat pups and adults, midazolam had the reverse effect, increasing thresholds and decreasing reflex magnitude. These differences were mediated supraspinally; intrathecal administration of midazolam did not affect flexion reflexes at any age. Midazolam had no sedative action in the youngest rats; sedation increased gradually through postnatal development. Conclusions The results show a striking reversal in the effects of midazolam on nociception and sedation in rats between postnatal days 3 and 10. Midazolam fails to sedate young rats and sensitizes their flexor reflex activity. The sedative and desensitizing effects of midazolam are not observed until later in life after maturation in supraspinal centers. The results indicate a need to better understand the pharmacology of drugs used routinely in neonatal intensive care.

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Drexler, Berthold, Rachel Jurd, Uwe Rudolph, and Bernd Antkowiak. "Dual Actions of Enflurane on Postsynaptic Currents Abolished by the γ-Aminobutyric Acid Type A Receptor β3(N265M) Point Mutation." Anesthesiology 105, no. 2 (August 1, 2006): 297–304. http://dx.doi.org/10.1097/00000542-200608000-00012.

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Background At concentrations close to 1 minimum alveolar concentration (MAC)-immobility, volatile anesthetics display blocking and prolonging effects on gamma-aminobutyric acid type A receptor-mediated postsynaptic currents. It has been proposed that distinct molecular mechanisms underlie these dual actions. The authors investigated whether the blocking or the prolonging effect of enflurane is altered by a point mutation (N265M) in the beta3 subunit of the gamma-aminobutyric acid type A receptor. Furthermore, the role of the beta3 subunit in producing the depressant actions of enflurane on neocortical neurons was elucidated. Methods Spontaneous inhibitory postsynaptic currents were sampled from neocortical neurons in cultured slices derived from wild-type and beta3(N265M) mutant mice. The effects of 0.3 and 0.6 mm enflurane on decay kinetics, peak amplitude, and charge transfer were quantified. Furthermore, the impact of enflurane-induced changes in spontaneous action potential firing was evaluated by extracellular recordings in slices from wild-type and mutant mice. Results In slices derived from wild-type mice, enflurane prolonged inhibitory postsynaptic current decays and decreased peak amplitudes. Both effects were almost absent in slices from beta3(N265M) mutant mice. At clinically relevant concentrations between MAC-awake and MAC-immobility, the anesthetic was less effective in depressing spontaneous action potential firing in slices from beta3(N265M) mutant mice compared with wild-type mice. Conclusion At concentrations between MAC-awake and MAC-immobility, beta3-containing gamma-aminobutyric acid type A receptors contribute to the depressant actions of enflurane in the neocortex. The beta3(N265M) mutation affects both the prolonging and blocking effects of enflurane on gamma-aminobutyric acid type A receptor-mediated inhibitory postsynaptic currents in neocortical neurons.

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Butovas, Sergejus, Uwe Rudolph, Rachel Jurd, Cornelius Schwarz, and Bernd Antkowiak. "Activity Patterns in the Prefrontal Cortex and Hippocampus during and after Awakening from Etomidate Anesthesia." Anesthesiology 113, no. 1 (July 1, 2010): 48–57. http://dx.doi.org/10.1097/aln.0b013e3181dc1db7.

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Background The anesthetic properties of etomidate are largely mediated by gamma-aminobutyric acid type A receptors. There is evidence for the existence of gamma-aminobutyric acid type A receptor subtypes in the brain, which respond to small concentrations of etomidate. After awakening from anesthesia, these subtypes are expected to cause cognitive dysfunction for a yet unknown period of time. The corresponding patterns of brain electrical activity and the molecular identity of gamma-aminobutyric acid type A receptors contributing to these actions remain to be elucidated. Methods Anesthesia was induced in wild-type and beta3(N265M) knock-in mice by intravenous injection of 10 mg/kg etomidate. Local field potentials were recorded simultaneously in the prefrontal cortex and hippocampus using chronically implanted electrode arrays. Local field potentials were sampled before, during, and after anesthesia. Results In the prefrontal cortex and hippocampus of wild-type mice, intravenous bolus injection of etomidate evoked isoelectric baselines and subsequent burst suppression. These effects were largely attenuated by the beta3(N265M) mutation. During emergence from anesthesia, power density in the theta band (5-15 Hz) transiently increased in the hippocampus of wild types, but not in the mutants, indicating that this action was caused by the receptors harboring beta3 subunits. In both genotypes, etomidate produced a long-lasting (> 1 h after recovery of righting reflexes) decrease in theta-peak frequency. Significant slowing of theta activity was apparent in the hippocampus and prefrontal cortex. Conclusions Etomidate-induced patterns of brain activity during deep anesthesia mostly involve actions at beta3 containing gamma-aminobutyric acid type A receptors. During the postanesthesia period, altered theta-band activity indicates ongoing anesthetic action.

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Jezewska, E., A. Scinska, W. Kukwa, A. Sobolewska, D. Turzynska, J. Samochowiec, and P. Bienkowski. "Gamma-aminobutyric acid concentrations in benign parotid tumours and unstimulated parotid saliva." Journal of Laryngology & Otology 125, no. 5 (December 17, 2010): 492–96. http://dx.doi.org/10.1017/s0022215110002574.

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AbstractObjective:Apart from its role as an inhibitory neurotransmitter, γ-aminobutyric acid is also thought to regulate various stages of cell proliferation and differentiation in the brain and periphery. The present study aimed to assess the levels of γ-aminobutyric acid and its biochemical precursor glutamic acid (glutamate) in benign parotid tumours and in unstimulated parotid saliva.Method:Unstimulated parotid saliva was collected bilaterally, using the swab method, in 20 patients with unilateral pleomorphic adenoma or Warthin's tumour. Samples of tumour and adjacent salivary tissue were collected during tumour resection.Results:Concentrations of γ-aminobutyric acid and glutamate, but not aspartate, were significantly higher in the tumour tissue than in the non-tumour tissue. There was no significant difference in salivary concentrations of γ-aminobutyric acid, glutamate or aspartate, comparing the involved and non-involved side.Conclusion:The present results provide preliminary evidence that γ-aminobutyric acid may be involved in the growth of benign parotid tumours.

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Ohisa, Naganori, Tosihisa Ohno, and Katsumi Mori. "Free Amino Acid and .GAMMA.-Aminobutyric acid Contents of Germinated Rice." NIPPON SHOKUHIN KAGAKU KOGAKU KAISHI 50, no. 7 (2003): 316–18. http://dx.doi.org/10.3136/nskkk.50.316.

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Prommer, Eric. "Midazolam: an essential palliative care drug." Palliative Care and Social Practice 14 (January 2020): 263235241989552. http://dx.doi.org/10.1177/2632352419895527.

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Midazolam is a commonly used benzodiazepine in palliative care and is considered one of the four essential drugs needed for the promotion of quality care in dying patients. Acting on the benzodiazepine receptor, it promotes the action of gamma-aminobutyric acid. Gamma-aminobutyric acid action promotes sedative, anxiolytic, and anticonvulsant properties. Midazolam has a faster onset and shorter duration of action than other benzodiazepines such as diazepam and lorazepam lending itself to greater flexibility in dosing than other benzodiazepines. The kidneys excrete midazolam and its active metabolite. Metabolism occurs in the liver by the P450 system. This article examines the pharmacology, pharmacodynamics, and clinical uses of midazolam in palliative care.

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Takigawa, Shigenobu, Takashi Ohsasa, Tatsuro Suzuki, Chie Matsuura-Endo, Naoto Hashimoto, Katsuichi Saito, Hiroaki Yamauchi, and Takahiro Noda. "Effective Production of .GAMMA.-Aminobutyric Acid Using Wheat Germ." Nippon Shokuhin Kagaku Kogaku Kaishi 56, no. 2 (2009): 114–17. http://dx.doi.org/10.3136/nskkk.56.114.

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Watanabe, Yasuo, Eriko Torii, Seiya Watanabe, and Kousaku Maeda. "Production of Gamma-aminobutyric Acid in Mules Barley Bran." Nippon Shokuhin Kagaku Kogaku Kaishi 59, no. 6 (2012): 291–94. http://dx.doi.org/10.3136/nskkk.59.291.

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SHIMAHARA, T., Y. PICHON, G. LEES, C. A. BEADLE, and D. J. BEADLE. "Gamma-Aminobutyric Acid Receptors on Cultured Cockroach Brain Neurones." Journal of Experimental Biology 131, no. 1 (September 1, 1987): 231–44. http://dx.doi.org/10.1242/jeb.131.1.231.

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Gamma-aminobutyric acid (GABA) at 10−1 moll−1 inhibited spontaneous activity and produced conductance changes in 60% of cultured cockroach neurones tested. The reversal potential for the GABA-evoked response was between −65 mV and −75 mV. Under whole-cell voltage-clamp conditions, with 114mmoll−1 potassium chloride in the electrode, the reversal potential had a similar value to that predicted for a chloride current. The response was blocked by 10−5 moll−1 picrotoxin but was not affected by 10−5 moll−1 bicuculline. In the whole-cell voltage-clamp conditions, 50 μmoll−1 GABA evoked an inward current that was accompanied by an increase in current noise. Fluctuation analysis of the noise gave a mean channel opening time of 11.8 ms for GABA and 6.5 ms for muscimol. The single-channel conductance was 18.6 pS for GABA and 15.2 pS for muscimol. When 50 μmoll−1 GABA was applied in the presence of the benzodiazepine, flunitrazepam, there was an increase in both the evoked current and the accompanying current noise. Analysis of this noise gave values of 14.3 ms for the mean channel opening time and 18.3 pS for the singlechannel conductance. The variance of the noise was increased by approximately 60% in the presence of flunitrazepam, suggesting that this drug potentiates the GABA responses of cockroach neurones by increasing the frequency of channel events. Note: Present address: Pesticide Research Department, Wellcome Research Laboratories, Berkhamsted, Herts, UK. Present address: Department of Biology, Oxford Polytechnic, Gipsy Lane, Headington, Oxford.

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Soltani, Nepton, Hossein Rezazadeh, and MohammadReza Sharifi. "Insulin resistance and the role of gamma-aminobutyric acid." Journal of Research in Medical Sciences 26, no. 1 (2021): 39. http://dx.doi.org/10.4103/jrms.jrms_374_20.

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Zhao, Yunyan, Zhong Li, Danni Chen, Qingfeng Lei, Lu He, and Rui Wei. "Systematic regulatory network of gamma-aminobutyric acid receptor genes." Journal of Shenzhen University Science and Engineering 32, no. 2 (2015): 128. http://dx.doi.org/10.3724/sp.j.1249.2015.02128.

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Kaspar, Heinrich F., Douglas O. Mountfort, and Vivien Pybus. "Degradation of gamma-aminobutyric acid (GABA) by marine microorganisms." FEMS Microbiology Ecology 8, no. 4 (July 1991): 313–18. http://dx.doi.org/10.1111/j.1574-6941.1991.tb01776.x.

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Kaspar, Heinrich F., Douglas O. Mountfort, and Vivien Pybus. "Degradation of gamma-aminobutyric acid (GABA) by marine microorganisms." FEMS Microbiology Letters 85, no. 4 (July 1991): 313–18. http://dx.doi.org/10.1111/j.1574-6968.1991.tb04757.x.

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Kinnersley, Alan M., and Frank J. Turano. "Gamma Aminobutyric Acid (GABA) and Plant Responses to Stress." Critical Reviews in Plant Sciences 19, no. 6 (November 2000): 479–509. http://dx.doi.org/10.1080/07352680091139277.

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Sokolov, A. Y., O. A. Lyubashina, A. V. Amelin, and S. S. Panteleev. "The role of gamma-aminobutyric acid in migraine pathogenesis." Neurochemical Journal 8, no. 2 (April 2014): 89–102. http://dx.doi.org/10.1134/s1819712414020093.

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Brady, Roscoe O., Julie M. McCarthy, Andrew P. Prescot, J. Eric Jensen, Alissa J. Cooper, Bruce M. Cohen, Perry F. Renshaw, and Dost Öngür. "Brain gamma-aminobutyric acid (GABA) abnormalities in bipolar disorder." Bipolar Disorders 15, no. 4 (May 2, 2013): 434–39. http://dx.doi.org/10.1111/bdi.12074.

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Journal articles on the topic 'Gamma-aminobutyric acid'

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