Relevant bibliographies by topics / GABA

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'GABA'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 September 2024

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Journal articles on the topic "GABA"

1

Akasu, Takashi, Yoshikazu Munakata, Masashi Tsurusaki, and Hiroshi Hasuo. "Role of GABAA and GABAC Receptors in the Biphasic GABA Responses in Neurons of the Rat Major Pelvic Ganglia." Journal of Neurophysiology 82, no. 3 (September 1, 1999): 1489–96. http://dx.doi.org/10.1152/jn.1999.82.3.1489.

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The role of γ-aminobutyric acid-A (GABAA) and GABAC receptors in the GABA-induced biphasic response in neurons of the rat major pelvic ganglia (MPG) were examined in vitro. Application of GABA (100 μM) to MPG neurons produced a biphasic response, an initial depolarization (GABAd) followed by a hyperpolarization (GABAh). The input resistance of the MPG neurons was decreased during the GABAd, whereas it was increased during the GABAh. The GABAd could be further separated into the early component (early GABAd) with a duration of 27 ± 5 s (mean ± SE; n = 11) and the late component (late GABAd) with a duration of 109 ± 11 s ( n = 11). The duration of the GABAh was 516 ± 64 s ( n = 11). The effects of GABA (5–500 μM) in producing the depolarization and the hyperpolarization were concentration-dependent. GABA (5–30 μM) induced only late depolarizations. The early component of the depolarization appeared when the concentration of GABA was >50 μM. Muscimol produced only early depolarizing responses. Baclofen (100 μM) had no effect on the membrane potential and input resistance of MPG neurons. Bicuculline (60 μM) blocked the early GABAdbut not the late GABAd and the GABAh. Application of picrotoxin (100 μM) with bicuculline (60 μM) blocked both the late GABAd and the GABAh. CGP55845A (3 μM), a selective GABAB receptor antagonist, did not affect the GABA-induced responses. cis-4-Aminocrotonic acid (CACA, 1 mM) and trans-4-aminocrotonic acid (TACA, 1 mM), selective GABAC receptor agonists, produced late biphasic responses in the MPG neurons. The duration of the CACA responses was almost the same as those of the late GABAdand GABAh obtained in the presence of bicuculline. Imidazole-4-acetic acid (I4AA, 100 μM), a GABAC receptor antagonist, depressed the late GABAd and the GABAh but not the early GABAd. I4AA (100 μM) and picrotoxin (100 μM) also suppressed the biphasic response to CACA. The early GABAd and the late GABAd were reversed in polarity at −32 ± 3 mV ( n = 7) and −38 ± 2 mV ( n = 4), respectively, in the Krebs solution. The reversal potential of the GABAh was −34 ± 2 mV ( n = 4) in the Krebs solution. The reversal potentials of the late GABAd and the GABAh shifted to −20 ± 3 mV ( n = 5) and −22 ± 3 mV ( n = 5), respectively, in 85 mM Cl− solution. These results indicate that the late GABAd and the GABAh are mediated predominantly by bicuculline-insensitive, picrotoxin-sensitive GABA receptors, GABAC (or GABAAOr) receptors, in neurons of the rat MPG.
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Qian, H., and J. E. Dowling. "GABAA and GABAC receptors on hybrid bass retinal bipolar cells." Journal of Neurophysiology 74, no. 5 (November 1, 1995): 1920–28. http://dx.doi.org/10.1152/jn.1995.74.5.1920.

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1. gamma-Aminobutyric acid (GABA) responses from solitory hybrid bass retinal bipolar cells were studied with the use of conventional and perforated whole cell patch-clamp recording. 2. GABA elicited a chloride current in bipolar cells that had both transient and sustained components. The transient component was sensitive to bicuculline and resembled GABAA-mediated currents, whereas the more sustained component was resistant to bicuculline and resembled the responses mediated by GABAC receptors. 3. The bicuculline-resistant GABA responses recorded from the bipolar cells could not be modulated by either diazepam or pentobarbital sodium, and they were unaffected by phaclofen and 2-hydroxysaclofen, GABAB receptor antagonists. On the other hand, the bicuculline-resistant GABA responses could be blocked substantially by imidazole-4-acetic acid (I4AA), a competitive antagonist of GABAC receptors. 4. Noise analysis of the GABA-elicited currents suggested a different single channel conductance for GABAA (10.1 pS) and GABAC receptors (3.6 pS). 5. Zinc, a putative modulator of synaptic transmission, strongly inhibited the GABAC responses on bipolar cells, whereas the GABAA responses were not significantly affected by zinc. 6. The proportion of the GABAC to GABAA responses varied widely between bipolar cells. Local application of GABA onto dendrites or axon terminals showed that both types of GABA receptors are present on both regions of the cell. 7. The distinct properties of these two GABA receptor types suggest that they play different roles in retinal function.
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Jackel, C., W. Krenz, and F. Nagy. "BICUCULLINE/BACLOFEN-INSENSITIVE GABA RESPONSE IN CRUSTACEAN NEURONES IN CULTURE." Journal of Experimental Biology 191, no. 1 (June 1, 1994): 167–93. http://dx.doi.org/10.1242/jeb.191.1.167.

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Neurones were dissociated from thoracic ganglia of embryonic and adult lobsters and kept in primary culture. When gamma-aminobutyric acid (GABA) was applied by pressure ejection, depolarizing or hyperpolarizing responses were produced, depending on the membrane potential. They were accompanied by an increase in membrane conductance. When they were present, action potential firing was inhibited. The pharmacological profile and ionic mechanism of GABA-evoked current were investigated under voltage-clamp with the whole-cell patch-clamp technique. The reversal potential of GABA-evoked current depended on the intracellular and extracellular Cl- concentration but not on extracellular Na+ and K+. Blockade of Ca2+ channels by Mn2+ was also without effect. The GABA-evoked current was mimicked by application of the GABAA agonists muscimol and isoguvacine with an order of potency muscimol>GABA>isoguvacine. cis-4-aminocrotonic acid (CACA), a folded and conformationally restricted GABA analogue, supposed to be diagnostic for the vertebrate GABAC receptor, also induced a bicuculline-resistant chloride current, although with a potency about 10 times lower than that of GABA. The GABA-evoked current was largely blocked by picrotoxin, but was insensitive to the GABAA antagonists bicuculline, bicuculline methiodide and SR 95531 at concentrations of up to 100 µmol l-1. Diazepam and phenobarbital did not exert modulatory effects. The GABAB antagonist phaclophen did not affect the GABA-induced current, while the GABAB agonists baclophen and 3-aminopropylphosphonic acid (3-APA) never evoked any response. Our results suggest that lobster thoracic neurones in culture express a chloride-conducting GABA-receptor channel which conforms to neither the GABAA nor the GABAB types of vertebrates but shows a pharmacology close to that of the novel GABAC receptor described in the vertebrate retina.
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Zhang, J., and M. M. Slaughter. "Preferential suppression of the ON pathway by GABAC receptors in the amphibian retina." Journal of Neurophysiology 74, no. 4 (October 1, 1995): 1583–92. http://dx.doi.org/10.1152/jn.1995.74.4.1583.

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1. Electrophysiological recordings were obtained from neurons in the amphibian intact retina and retinal slice preparations. The effects of gamma-aminobutyric acid (GABA) were evaluated in the presence of bicuculline or SR95531, which block the GABAA receptor, and baclofen, which saturates the GABAB receptor. 2. Under these conditions, GABA preferentially reduced ON light responses in amacrine and ganglion cells, apparently through a presynaptic mechanism that reduced bipolar cell input. GABA also produced a small hyperpolarization in the resting membrane potential of ganglion cells. 3. Picrotoxin blocked these effects of GABA. The action of GABA was duplicated by muscimol and by trans-aminocrotonic acid. Cis-aminocrotonic acid was neither a potent nor selective agonist. This pharmacology is indicative of the GABAC receptor. 4. In voltage-clamp recordings of ganglion cells in the slice preparation, GABA produced a large chloride conductance that was blocked by bicuculline or SR95531, and a smaller chloride conductance that was not blocked by these GABAA receptor antagonists, but was blocked by picrotoxin. This indicates that ganglion cells possess both GABAA and GABAC receptors. 5. The GABAC receptor current was relatively nondesensitized. Consequently, whereas the peak GABAA receptor current was more than fivefold larger than the GABAC receptor current, after desensitization the latter current was larger. Both currents reversed near the chloride equilibrium potential.
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Naffaa, Moawiah M., David E. Hibbs, Mary Chebib, and Jane R. Hanrahan. "Pharmacological Effect of GABA Analogues on GABA-ϱ2 Receptors and Their Subtype Selectivity." Life 12, no. 1 (January 17, 2022): 127. http://dx.doi.org/10.3390/life12010127.

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GABAϱ receptors are distinctive GABAergic receptors from other ionotropic GABAA and metabotropic GABAB receptors in their pharmacological, biochemical, and electrophysiological properties. Although GABA-ϱ1 receptors are the most studied in this subfamily, GABA-ϱ2 receptors are widely distributed in the brain and are considered a potential target for treating neurological disorders such as stroke. The structure of GABA-ϱ2 receptors and their pharmacological features are poorly studied. We generated the first homology model of GABA-ϱ2 channel, which predicts similar major interactions of GABA with the binding-site residues in GABA-ϱ1 and GABA-ϱ2 channels. We also investigated the pharmacological properties of several GABA analogues on the activity of GABA-ϱ2 receptors. In comparison to their pharmacological effect on GABA-ϱ1 receptors, the activation effect of these ligands and their potentiation/inhibition impact on GABA response have interestingly shown inter-selectivity between the two GABA-ϱ receptors. Our results suggest that several GABA analogues can be used as research tools to study the distinctive physiology of GABA-ϱ1 and GABA-ϱ2 receptors. Furthermore, their partial agonist effect may hold promise for the future discovery of selective modulatory agents on GABAA receptors.
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ROTOLO, THOMAS C., and RAMON F. DACHEUX. "Two neuropharmacological types of rabbit ON-alpha ganglion cells express GABAC receptors." Visual Neuroscience 20, no. 4 (July 2003): 373–84. http://dx.doi.org/10.1017/s095252380320403x.

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The major inhibitory neurotransmitters GABA and glycine provide the bulk of input to large-field ganglion cells in the retina. Whole-cell patch-clamp recordings were used to characterize the glycine- and GABA-activated currents for morphologically identified ON-α ganglion cells in the rabbit retina. Cells identified as ON-α cells by light evoked currents were intracellularly stained and examined by light microscopy which revealed dendritic stratification in the vitreal half of the inner plexiform layer and confirmed their physiological identity. All Ca2+-mediated synaptic influences were abolished with Co2+, revealing two types of ON-α cell characterized by their different inhibitory current profiles. One group exhibited larger glycine- than GABA-activated currents, while the other group had larger GABA- than glycine-activated currents. Both cell types demonstrated strychnine-sensitive glycine-activated currents and bicuculline-sensitive GABAA-activated currents. Surprisingly, both cell types expressed functional GABAC receptors demonstrated by their sensitivity to TPMPA. In addition, the cells with larger glycine-activated currents also possessed GABAB receptors, whereas those with larger GABA-activated currents did not. Immunocytochemical experiments confirmed the presence of glycine, GABAA, and GABAC receptor subunits on all physiologically identified ON-α ganglion cells in this study. In addition, the GABAB receptor immunolabeled puncta were present on the cells with larger glycine-activated currents, but not on the cells with the larger GABA-activated currents. In conclusion, the presence of different functional GABA and glycine receptors determined physiologically correlated well with the specific GABA and glycine receptor immunolabeling for two neuropharmacological types of rabbit ON-α ganglion cells.
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Absalom, Nathan, Izumi Yamamoto, David O'Hagan, Luke Hunter, and Mary Chebib. "Probing the Mode of Neurotransmitter Binding to GABA Receptors Using Selectively Fluorinated GABA Analogues." Australian Journal of Chemistry 68, no. 1 (2015): 23. http://dx.doi.org/10.1071/ch14456.

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Stereoselective fluorination is a useful technique for controlling the conformations of organic molecules. This concept has been exploited to create conformationally biased analogues of the neurotransmitter gamma-aminobutyric acid (GABA). Mono- and di-fluorinated GABA analogues are found to adopt different conformations, due to subtle stereoelectronic effects associated with the C–F bond. These conformationally biased GABA analogues exhibit different shape-dependent selectivity patterns towards GABAA, GABAB, and GABAC receptors, providing valuable information on the binding modes of the natural ligand at these medicinally important targets.
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Han, Y., D. Cao, X. Li, R. Zhang, F. Yu, Y. Ren, and L. An. "Attenuation of γ-aminobutyric acid (GABA) transaminase activity contributes to GABA increase in the cerebral cortex of mice exposed to β-cypermethrin." Human & Experimental Toxicology 33, no. 3 (November 12, 2013): 317–24. http://dx.doi.org/10.1177/0960327113497770.

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The current study investigated the γ-aminobutyric acid (GABA) levels and GABA metabolic enzymes (GABA transaminase (GABAT) and glutamate decarboxylase (GAD)) activities at 2 and 4 h after treatment, using a high-performance liquid chromatography with ultraviolet detectors and colorimetric assay, in the cerebral cortex of mice treated with 20, 40 or 80 mg/kg β-cypermethrin by a single oral gavage, with corn oil as vehicle control. In addition, GABA protein (4 h after treatment), GABAT protein (2 h after treatment) and GABA receptors messenger RNA (mRNA) expression were detected by immunohistochemistry, Western blot and real-time quantitative reverse transcriptase polymerase chain reaction, respectively. β-Cypermethrin (80 mg/kg) significantly increased GABA levels in the cerebral cortex of mice, at both 2 and 4 h after treatment, compared with the control. Also, GABA immunohistochemistry results suggested that the number of positive granules was increased in the cerebral cortex of mice 4 h after exposure to 80 mg/kg β-cypermethrin when compared with the control. Furthermore, the results also showed that GABAT activity detected was significantly decreased in the cerebral cortex of mice 2 h after β-cypermethrin administration (40 or 80 mg/kg). No significant changes were found in GAD activity, or the expression of GABAT protein and GABAB receptors mRNA, in the cerebral cortex of mice, except that 80 mg/kg β-cypermethrin caused a significant decrease, compared with the vehicle control, in GABAA receptors mRNA expression 4 h after administration. These results suggested that attenuated GABAT activity induced by β-cypermethrin contributed to increased GABA levels in the mouse brain. The downregulated GABAA receptors mRNA expression is most likely a downstream event.
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Liske, S., and M. E. Morris. "Extrasynaptic effects of GABA (γ-aminobutyric acid) agonists on myelinated axons of peripheral nerve." Canadian Journal of Physiology and Pharmacology 72, no. 4 (April 1, 1994): 368–74. http://dx.doi.org/10.1139/y94-054.

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Effects of the inhibitory neurotransmitter, GABA (γ-aminobutyric acid) on the excitability of myelinated fibers of isolated amphibian sciatic nerves and their dorsal and ventral spinal roots have been compared with those of a GABAA agonist, THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol), and the GABAB agonist baclofen. Graded, prolonged increases in the amplitude of A-fiber half-maximal compound action potentials of Rana ballenderi sciatic nerves were evoked by GABA (Rmax = 49%, EC50 = 0.1 mM); responses to THIP were smaller (Rmax = 34%, EC50 = 1.1 mM) and with a different, distinctly biphasic recovery phase. In studies of Rana catesbeiana nerves and their attached spinal roots, excitability increases produced in fibers of the ventral roots by GABA were smaller than those of the dorsal roots. Peak changes evoked by THIP in both roots were similar to the effects of GABA on the ventral root; however, THIP's ventral root response showed much less sensitivity and was followed by a rapid recovery phase, undershoot, and secondary, prolonged enhancement. Bicuculline methiodide antagonized agonist-induced increases, and revealed the presence of significant decreases in excitability of the ventral root fibers at concentrations of GABA or THIP < 3 mM. Baclofen evoked inconsistent changes in the excitability of whole nerve and root fibers; small increases occurred with lower doses and secondary, delayed decreases with higher doses. The high concentration (≥ 0.1 mM) of the active isomer needed to cause a small response suggests a limited contribution and (or) presence of GABAB receptors. GABA and its agonists evoke complex, multiphasic excitability changes in the myelinated axons of the spinal roots and peripheral nerve. Contributions of different phases of increase and directions of change signify the participation of multiple receptors and (or) mechanisms. Responses of the dorsal root appear to reflect mainly GABAA-mediated increases in excitability; those of the ventral root include an additional or greater decrease, which may reflect a hyperpolarizing component mediated by a GABAC-like or bicuculline methiodide insensitive GABAA receptor. The large, prolonged responses of the sensory axons to GABA may be linked to their greater K+ channel conductance and related to the inhibitory transmitter's depolarizing action at the more proximal site of their central presynaptic terminals.Key words: dorsal and ventral roots, amphibian, excitability, GABAA, GABAB, GABAC.
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Fischer, Y., and I. Parnas. "Activation of GABAB receptors at individual release boutons of the crayfish opener neuromuscular junction produces presynaptic inhibition." Journal of Neurophysiology 75, no. 4 (April 1, 1996): 1377–85. http://dx.doi.org/10.1152/jn.1996.75.4.1377.

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1. Presynaptic inhibition in crustaceans involves the activation of gamma-aminobutyric acid-A (GABAA) receptors that produce an increase in chloride conductance at excitatory axon terminals. Such inhibition produced by single inhibitory pulses is blocked by picrotoxin, a GABAA antagonist. 2. Presynaptic inhibition produced by bath application of GABA was not blocked by picrotoxin. Measurements of the membrane resistance of the excitatory axon terminals revealed that substantial presynaptic inhibition still persisted after 50 microM picrotoxin had completely blocked the increase in conductance produced by 10 microM GABA. 3. Baclofen, a GABAB agonist, reduced release from the excitatory nerve terminals, and 20H-Saclofen, a GABAB antagonist, blocked the effect of baclofen and the presynaptic inhibition produced by 10 microM GABA. 4. 20H-Saclofen alone did not block presynaptic inhibition produced by 100 microM GABA, and the combined action of both 20H-Saclofen and picrotoxin was required to block such effects. 5. The excitatory nerve terminals seem to contain GABAA and GABAB receptors. The GABAB receptors are preferentially activated at lower GABA concentrations (in the microM range), whereas both the GABAA and GABAB receptors are activated at high GABA concentrations.
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Dissertations / Theses on the topic "GABA"

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Kragler, Andrea. "GABA-Transporter." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-9774.

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Picard, Raymonde. "Charakterisierung funktioneller Domänen für GABA und Furosemid auf GABAA-Rezeptoren." [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=971995141.

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Ong, Jennifer. "GABA and GABA-receptors in the enteric nervous system /." Title page, contents and summary only, 1985. http://web4.library.adelaide.edu.au/theses/09PH/09pho582.pdf.

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Davies, Martin. "The GABA transporter and the regulation of the GABA¦A receptor." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1993. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23915.pdf.

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Aanesen, Arthur. "Gaba and human spermatozoa : characterization and regulation of gaba transport proteins /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980925aane.

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Mendu, Suresh Kumar. "Role of GABA and GABAA Channels in T lymphocytes and Stem cells." Doctoral thesis, Uppsala universitet, Institutionen för neurovetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-172541.

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GABA (gamma-aminobutyric acid) is best known for its physiological function in the central nervous system.  In the brain GABA is the main inhibitory neurotransmitter where it decreases excitability of neurons and neuronal networks.  The balance between excitation evoked by glutamate and inhibition evoked by GABA is the base from where the brain works. It is fair to say that glutamate is like the gas-pedal and GABA the brake that keeps the brain running at a normal speed.  But, it is not only in the brain that GABA is taking a part in a physiological process vital to life. GABA is present in blood and is even released in the pancreatic islets. What function GABA has in these tissues is still being examined and is the focus of this thesis. The GABA concentration in the peripheral tissues is in the submicromolar concentration range.  The studies in this thesis support the idea that GABA reduces the proliferation and cytokine secretion from immune cells by activating high-affinity GABAA channels in the cells. In contrast, in retinal progenitor stem cells GABA promotes cell proliferation.  These studies demonstrate that the effect of GABA on proliferation is cell-type specific. The GABAA channel subunit isoforms expressed in human, mice and rats T cells differ between the species.  This interspecies variability will result in different pharmacological profile of the subtypes of GABAA channels expressed whereas the physiological process most likely is the same.  Clearly, GABA is not only a neurotransmitter molecule but is also an immunomodulator and an important signal molecule in peripheral tissues.
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Gardner-Fortier, Catherine. "Développement d'un fromage fonctionnel renfermant un composé bioactif, l'acide gama-aminobutyrique (GABA)." Thesis, Université Laval, 2011. http://www.theses.ulaval.ca/2011/28143/28143.pdf.

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CHAMBON, JEAN-PIERRE. "Caracterisation de derives pyridazinyl-gaba comme ligands antagonistes du recepteur gaba-a." Université Louis Pasteur (Strasbourg) (1971-2008), 1987. http://www.theses.fr/1987STR13002.

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Chambon, Jean-Pierre. "Caractérisation de dérivés pyridazinyl-gaba comme ligands antagonistiques du récepteur gaba-A." Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37603758b.

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Namwindwa, Ernest Sinvula. "GABA and glutamate mimetics." Thesis, University of Bath, 1987. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376436.

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Books on the topic "GABA"

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J, Enna S., ed. GABA. San Diego: Academic Press/Elsevier, 2006.

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Enna, S. J., and Hanns Möhler, eds. The GABA Receptors. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-465-0.

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Monti, Jaime M., Seithikurippu Ratnas Pandi-Perumal, and Hanns Möhler, eds. GABA and Sleep. Basel: Springer Basel, 2010. http://dx.doi.org/10.1007/978-3-0346-0226-6.

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Enna, S. J., and Norman G. Bowery, eds. The GABA Receptors. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4757-2597-1.

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J, Enna S., and Bowery N. G, eds. The GABA receptors. 2nd ed. Totowa, N.J: Humana Press, 1997.

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J, Enna S., and Möhler Hanns, eds. The GABA receptors. 3rd ed. Totowa, N.J: Humana Press, 2007.

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Ibrahim, Houmedgaba Maki. Gaba-caxxa =: Bâton. [Djibouti]: ILD, Gabbutíh Afitteh Maqhadá, 2008.

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Subai, Nadu. Al gaba al naimaa'. Alep: Centre essor et civilisation, 1993.

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Erdö, Sándor L., ed. GABA Outside the CNS. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-76915-3.

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International, Symposium on Peripheral GABAergic Mechanisms (1990 Rome Italy). GABA outside the CNS. Berlin: Springer-Verlag, 1992.

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Book chapters on the topic "GABA"

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Manji, Husseini K., Jorge Quiroz, R. Andrew Chambers, Anthony Absalom, David Menon, Patrizia Porcu, A. Leslie Morrow, et al. "GABA." In Encyclopedia of Psychopharmacology, 549. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_444.

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Rey, Jose A. "GABA." In Encyclopedia of Clinical Neuropsychology, 1123–24. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1765.

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Rey, Jose A. "GABA." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1765-2.

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Rey, Jose A. "GABA." In Encyclopedia of Clinical Neuropsychology, 1533–34. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1765.

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King, Maedbh. "GABA." In Encyclopedia of Personality and Individual Differences, 1713–15. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_752.

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King, Maedbh. "GABA." In Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_752-1.

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Robinson, Timothy N., and Richard W. Olsen. "GABA." In Comparative Invertebrate Neurochemistry, 90–123. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9804-6_3.

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Murala, Sireesha, Anudeep Yelam, Mahmoud M. Ismail, and Pradeep C. Bollu. "GABA." In Neurochemistry in Clinical Practice, 73–89. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-07897-2_4.

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Petroianu, Georg, and Peter Michael Osswald. "GABA-Rezeptor." In Anästhesie in Frage und Antwort, 71–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-05715-5_25.

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Petroianu, Georg, and Peter Michael Osswald. "GABA-Rezeptor." In Anästhesie in Frage und Antwort, 83–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-05717-9_36.

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Conference papers on the topic "GABA"

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Asriany, Sherly, Adnan Sofyan, and Ridwan Ridwan. "Analisis Pencahayaan pada Material Lokal Gaba-gaba." In Temu Ilmiah IPLBI 2018. Ikatan Peneliti Lingkungan Binaan Indonesia, 2018. http://dx.doi.org/10.32315/ti.7.g048.

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Asriany, Sherly, and Adnan Sofyan. "Analisis Termal pada Material Alami Gaba-gaba (Pelepah Sagu) sebagai Bahan Alternatif Hemat Energi." In Temu Ilmiah Ikatan Peneliti Lingkungan Binaan Indonesia 6. Ikatan Peneliti Lingkungan Binaan Indonesia, 2017. http://dx.doi.org/10.32315/ti.6.h001.

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Dampf, Sara J., and Timothy M. Korter. "Low-frequency Vibrational Spectroscopy of $\gamma$-Aminobutyric Acid Derivatives: GABA Hydrochloride and $\beta$-Phenyl-GABA Hydrochloride." In 2020 45th International Conference on Infrared, Millimeter and Terahertz Waves (IRMMW-THz). IEEE, 2020. http://dx.doi.org/10.1109/irmmw-thz46771.2020.9370844.

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REBER, ANNIE, MARIE-HELENE LEROY, and BERNARD POITEVIN. "VISUO-VESTIBULAR REFLEXES ADJUSTMENT BY GABA ANTAGONISTS." In Proceedings of the International School of Biophysics. WORLD SCIENTIFIC, 1998. http://dx.doi.org/10.1142/9789812816887_0028.

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Tan, Chuanxin, Xiaohui Yan, Xiaoguang Wu, Chang Zhu, Mengxing Gou, and Xuejun Liu. "Research Progress of Gamma-Aminobutyric Acid(GABA)." In 2017 6th International Conference on Energy, Environment and Sustainable Development (ICEESD 2017). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/iceesd-17.2017.114.

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Costa, Susana, Maria Fernandes, and M. Sameiro Gonçalves. "Photocleavage Studies of γ-aminobutyric acid (GABA) Conjugates." In The 11th International Electronic Conference on Synthetic Organic Chemistry. Basel, Switzerland: MDPI, 2007. http://dx.doi.org/10.3390/ecsoc-11-01338.

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Azevedo, Ruan Ruan Gambardella Rosalina de, Adriel Rêgo Barbosa, Felipe Felipe Candeas Amorim, Gabriel Pinheiro Martins de Almeida e. Souza, João Victor Cabral Correia Férrer, Márcio Pinheiro Lima, Pedro Henrique Almeida Fraiman, et al. "Atypical manifestation of Anti-Gaba-Br autoimmune encephalitis." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.583.

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Introduction: Anti-GABA-Br is an autoantibody associated with autoimmune encephalitis and small cell lung carcinoma. Clinical seizures, including status epilepticus, represent the most common feature of anti-GABA-Br related disorders. This case reports a previously healthy 40-year-old man with rapidly progressive dementia and Anti-GABA-Br positive cerebrospinal fluid (CSF). This is a case report based on retrospective analysis of a single patient’s medical record. Case report: From May 2019 to October 2020, the patient presented with dulling, decreased speech frequency and gait disturbance. He became unable to perform all basic and instrumental activities of daily living. Physical examination was marked by: pancerebellar dysfunction and impaired working memory. Brain magnetic resonance imaging (MRI) showed global brain volumetric reduction with bilateral T2/FLAIR (T2-weighted-Fluid-Attenuated Inversion Recovery) hypersignal in cortical regions of insula and mesial temporal lobes, without contrast enhancement. Analysis of CSF: 8.3 cells/ mm³ (96% lymphocytes) and protein 64 mg/ml. There was no evidence of: clinical/electroencephalographic seizures or pathological patterns on electroencephalograms. He received methylprednisolone for five days followed by cyclophosphamide infusions (one per month for seven months). Azathioprine started after tapering prednisone. On March 2022, the patient underwent a new MRI with hypersignal improvement although atrophy had persisted. CSF after treatment had no inflammatory changes and was antiGABA-Br positive. The patient presented a partial recovery and was still dependent on instrumental activities. Conclusion: Anti-GABA-Br encephalitis has a predilection for males, affects variable ages and is best characterized by generalized seizures with evolution to refractory status epilepticus although behavioral changes may occur. There are few reports of seizure free cases.
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Ebrahimi, Mansour, and Esmaeil Ebrahimie. "Application of bioinformatics algorithms to define the most important protein features contribute to GABA receptors diversity GABA receptors' diversity, bioinformatic applications." In 2010 2nd International Conference on Chemical, Biological and Environmental Engineering (ICBEE). IEEE, 2010. http://dx.doi.org/10.1109/icbee.2010.5649594.

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Syafiie, S., and I. H. Mustafa. "Single compartment modeling glutamine-glutamate-GABA system in neuron." In 2016 IEEE EMBS Conference on Biomedical Engineering and Sciences (IECBES). IEEE, 2016. http://dx.doi.org/10.1109/iecbes.2016.7843506.

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Nakao, Toshifumi. "Mechanisms of resistance to insecticides targeting RDL GABA receptors." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.91234.

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Reports on the topic "GABA"

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Koh, Wee Yin, Babak Rasti, Xiao Xian Lim, and Wan June Tan. GABA DACHO: Dark chocolate enriched with gamma-aminobutyric acid (GABA) and inulin as prebiotic. Peeref, June 2023. http://dx.doi.org/10.54985/peeref.2306p1335975.

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Locy, Robert D., Hillel Fromm, Joe H. Cherry, and Narendra K. Singh. Regulation of Arabidopsis Glutamate Decarboxylase in Response to Heat Stress: Modulation of Enzyme Activity and Gene Expression. United States Department of Agriculture, January 2001. http://dx.doi.org/10.32747/2001.7575288.bard.

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Most plants accumulate the nonprotein amino acid, g-aminobutyric acid (GABA), in response to heat stress. GABA is made from glutamate in a reaction catalyzed by glutamate decarboxylase (GAD), an enzyme that has been shown by the Israeli PI to be a calmodulin (CaM) binding protein whose activity is regulated in vitro by calcium and CaM. In Arabidopsis there are at least 5 GAD genes, two isoforms of GAD, GAD1 and GAD2, are known to be expressed, both of which appear to be calmodulin-binding proteins. The role of GABA accumulation in stress tolerance remains unclear, and thus the objectives of the proposed work are intended to clarify the possible roles of GABA in stress tolerance by studying the factors which regulate the activity of GAD in vivo. Our intent was to demonstrate the factors that mediate the expression of GAD activity by analyzing the promoters of the GAD1 and GAD2 genes, to determine the role of stress induced calcium signaling in the regulation of GAD activity, to investigate the role of phosphorylation of the CaM-binding domain in the regulation of GAD activity, and to investigate whether ABA signaling could be involved in GAD regulation via the following set of original Project Objectives: 1. Construction of chimeric GAD1 and GAD2 promoter/reporter gene fusions and their utilization for determining cell-specific expression of GAD genes in Arabidopsis. 2. Utilizing transgenic plants harboring chimeric GAD1 promoter-luciferase constructs for isolating mutants in genes controlling GAD1 gene activation in response to heat shock. 3. Assess the role of Ca2+/CaM in the regulation of GAD activity in vivo in Arabidopsis. 4. Study the possible phosphorylation of GAD as a means of regulation of GAD activity. 5. Utilize ABA mutants of Arabidopsis to assess the involvement of this phytohormone in GAD activation by stress stimuli. The major conclusions of Objective 1 was that GAD1 was strongly expressed in the elongating region of the root, while GAD2 was mainly expressed along the phloem in both roots and shoots. In addition, GAD activity was found not to be transcriptionally regulated in response to heat stress. Subsequently, The Israeli side obtained a GAD1 knockout mutation, and in light of the objective 1 results it was determined that characterization of this knockout mutation would contribute more to the project than the proposed Objective 2. The major conclusion of Objective 3 is that heat-stress-induced changes in GAD activity can be explained by heat-stress-induced changes in cytosolic calcium levels. No evidence that GAD activity was transcriptionally or translationally regulated or that protein phosphorylation was involved in GAD regulation (objective 4) was obtained. Previously published data by others showing that in wheat roots ABA regulated GABA accumulation proved not to be the case in Arabidopsis (Objective 5). Consequently, we put the remaining effort in the project into the selection of mutants related to temperature adaptation and GABA utilization and attempting to characterize events resulting from GABA accumulation. A set of 3 heat sensitive mutants that appear to have GABA related mutations have been isolated and partially characterized, and a study linking GABA accumulation to growth stimulation and altered nitrate assimilation were conducted. By providing a better understanding of how GAD activity was and was not regulated in vivo, we have ruled out the use of certain genes for genetically engineering thermotolerance, and suggested other areas of endeavor related to the thrust of the project that may be more likely approaches to genetically engineering thermotolerance.
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Gee, Kelvin W. Dual Modulators of GABA-A and Alpha7 Nicotinic Receptors for Treating Autism. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada610984.

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Fromm, Hillel, and Joe Poovaiah. Calcium- and Calmodulin-Mediated Regulation of Plant Responses to Stress. United States Department of Agriculture, September 1993. http://dx.doi.org/10.32747/1993.7568096.bard.

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We have taken a molecular approach to clone cellular targets of calcium/calmodulin (Ca2+/CaM). A 35S-labeled recombinant CaM was used as a probe to screen various cDNA expression libraries. One of the isolated clones from petunia codes for the enzyme glutamate decarboxylase (GAD) which catalyzes the conversion of glutamate to g-aminobutyric acid (GABA). The activity of plant GAD has been shown to be dramatically enhanced in response to cold and heat shock, anoxia, drought, mechanical manipulations and by exogenous application of the stress phytohormone ABA in wheat roots. We have purified the recombinant GAD by CaM-affinity chromatography and studied its regulation by Ca2+/CaM. At a physiological pH range (7.0-7.5), the purified enzyme was inactive in the absence of Ca2+ and CaM but could be stimulated to high levels of activity by the addition of exogenous CaM (K0.5 = 15 nM) in the presence of Ca2+ (K 0.5 = 0.8 mM). Neither Ca2+ nor CaM alone had any effect on GAD activity. Transgenic tobacco plants expressing a mutant petunia GAD lacking the CaM-binding domain, or transgenic plants expressing the intact GAD were prepared and studied in detail. We have shown that the CaM-binding domain is necessary for the regulation of glutamate and GABA metabolism and for normal plant development. Moreover, we found that CaM is tightly associated with a 500 kDa GAD complex. The tight association of CaM with its target may be important for the rapid modulation of GAD activity by Ca2+ signaling in response to stresses.
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Ron, Eliora, and Eugene Eugene Nester. Global functional genomics of plant cell transformation by agrobacterium. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7695860.bard.

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The aim of this study was to carry out a global functional genomics analysis of plant cell transformation by Agrobacterium in order to define and characterize the physiology of Agrobacterium in the acidic environment of a wounded plant. We planed to study the proteome and transcriptome of Agrobacterium in response to a change in pH, from 7.2 to 5.5 and identify genes and circuits directly involved in this change. Bacteria-plant interactions involve a large number of global regulatory systems, which are essential for protection against new stressful conditions. The interaction of bacteria with their hosts has been previously studied by genetic-physiological methods. We wanted to make use of the new capabilities to study these interactions on a global scale, using transcription analysis (transcriptomics, microarrays) and proteomics (2D gel electrophoresis and mass spectrometry). The results provided extensive data on the functional genomics under conditions that partially mimic plant infection and – in addition - revealed some surprising and significant data. Thus, we identified the genes whose expression is modulated when Agrobacterium is grown under the acidic conditions found in the rhizosphere (pH 5.5), an essential environmental factor in Agrobacterium – plant interactions essential for induction of the virulence program by plant signal molecules. Among the 45 genes whose expression was significantly elevated, of special interest is the two-component chromosomally encoded system, ChvG/I which is involved in regulating acid inducible genes. A second exciting system under acid and ChvG/Icontrol is a secretion system for proteins, T6SS, encoded by 14 genes which appears to be important for Rhizobium leguminosarum nodule formation and nitrogen fixation and for virulence of Agrobacterium. The proteome analysis revealed that gamma aminobutyric acid (GABA), a metabolite secreted by wounded plants, induces the synthesis of an Agrobacterium lactonase which degrades the quorum sensing signal, N-acyl homoserine lactone (AHL), resulting in attenuation of virulence. In addition, through a transcriptomic analysis of Agrobacterium growing at the pH of the rhizosphere (pH=5.5), we demonstrated that salicylic acid (SA) a well-studied plant signal molecule important in plant defense, attenuates Agrobacterium virulence in two distinct ways - by down regulating the synthesis of the virulence (vir) genes required for the processing and transfer of the T-DNA and by inducing the same lactonase, which in turn degrades the AHL. Thus, GABA and SA with different molecular structures, induce the expression of these same genes. The identification of genes whose expression is modulated by conditions that mimic plant infection, as well as the identification of regulatory molecules that help control the early stages of infection, advance our understanding of this complex bacterial-plant interaction and has immediate potential applications to modify it. We expect that the data generated by our research will be used to develop novel strategies for the control of crown gall disease. Moreover, these results will also provide the basis for future biotechnological approaches that will use genetic manipulations to improve bacterial-plant interactions, leading to more efficient DNA transfer to recalcitrant plants and robust symbiosis. These advances will, in turn, contribute to plant protection by introducing genes for resistance against other bacteria, pests and environmental stress.
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Chaudhury, Saswata, and Sanchit S. Agarwal. Will Gaza jeopardise India's energy resilience? Edited by Bharat Bhushan and Chris Bartlett. Monash University, October 2023. http://dx.doi.org/10.54377/3624-919a.

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Pimpo, Mark R. After Gaza: The Next Moves Toward Peace. Fort Belvoir, VA: Defense Technical Information Center, March 2006. http://dx.doi.org/10.21236/ada449721.

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Miller, Erin A., Leon E. Smith, Richard S. Wittman, Luke W. Campbell, Nikhil S. Deshmukh, Mital A. Zalavadia, Margo A. Batie, and Vladimir V. Mozin. Hybrid Gama Emission Tomography (HGET): FY16 Annual Report. Office of Scientific and Technical Information (OSTI), February 2017. http://dx.doi.org/10.2172/1390447.

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Visser, A., G. Eppich, R. Bibby, M. Singleton, D. Hillegonds, J. Moran, and B. Esser. California GAMA Special Study:Archival Data Conversion & Upload. Office of Scientific and Technical Information (OSTI), February 2014. http://dx.doi.org/10.2172/1248319.

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Bhushan, Bharat. How the war in Gaza is reshaping geopolitics. Monash University, November 2023. http://dx.doi.org/10.54377/de3f-139e.

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