Relevant bibliographies by topics / Receptors, GABA-Benzodiazepine

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Receptors, GABA-Benzodiazepine'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "Receptors, GABA-Benzodiazepine"

1

WAMSLEY, JAMES K. "GABA-Benzodiazepine Receptors." American Journal of Psychiatry 149, no. 4 (April 1992): 582—a—582. http://dx.doi.org/10.1176/ajp.149.4.582-a.

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Lingford-Hughes, Anne R., P. Acton, S. Gacinovic, J. Suckling, G. F. Busatto, S. J. A. Boddington, E. Bullmore, et al. "Reduced levels of GABA-benzodiazepine receptor in alcohol dependency in the absence of grey matter atrophy." British Journal of Psychiatry 173, no. 2 (August 1998): 116–22. http://dx.doi.org/10.1192/bjp.173.2.116.

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BackgroundWe tested the hypothesis that reduced levels of the GABA-benzodiazepine receptor occur in alcohol dependency using single photon emission tomography (SPET) and the specific GABA-benzodiazepine ligand, 123l-iomazenil.MethodNeurologically and cognitively unimpaired abstinent alcohol-dependent (n=12) and non-alcohol-dependent male subjects (n=14) underwent a 123l–iomazenil SPET scan. SPET and magnetic resonance images were co-registered and voxel-based statistical tests performed. Subjects' clinical and alcohol history were obtained with standard questionnaires. The relationships between clinical and alcohol variables and the regional level of GABA-benzodiazepine receptors were investigated using multiple regression analysis.ResultsAbstinent alcohol-dependent subjects had decreased levels of GABA-benzodiazepine receptor compared with non-alcohol-dependent subjects within the frontal, parietal and temporal cortices, including regions in which grey matter atrophy was absent.ConclusionsAlcohol dependency is associated with reduced GABA-benzodiazepine receptor levels in the absence of grey matter atrophy in some cortical regions, such as within the parietal lobe. Regional variability of reduction in GABA-benzodiazepine receptors demonstrates that alcohol does not have a global, toxic effect on the brain.
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Guttman, Mark. "Receptors in the Basal Ganglia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 14, S3 (August 1987): 395–401. http://dx.doi.org/10.1017/s0317167100037793.

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ABSTRACT:The study of neurotransmitter receptors aids in the understanding of the normal anatomy, pharmacology, therapeutics and pathophysiology of disease processes involving the basal ganglia. Receptors may be studied in vitro by homogenate binding experiments, enzyme analysis or quantitative autoradiography and in vivo with positron emission tomography. In the substantia nigra (SN), receptors have been identified for somatostatin, neurotensin, substance P, glycine, benzodiazepine and GABA, opiates, dopamine, angiotensin converting enzyme (ACE) and serotonin. The striatum has receptors for dopamine, GABA and benzodiazepines, acetylcholine, opiates, substance P, glutamate and cholecystokinin. GABA and benzodiazepine receptors are also located in the globus pallidus. In Parkinson's disease, striatal dopamine D-2 receptors are elevated in patients that have not received L-DOPA therapy. This supersensitivity is reversed with agonist therapy. Muscarinic binding to cholinergic receptors seems to correlate with dopamine receptors. Delta opiate receptors are increased in the caudate and mu binding is reduced in the striatum. In the SN of patients with Parkinson's disease, there is reduced binding of somatostatin, neurotensin, mu and kappa opiates, benzodiazepine and GABA and glycine. In Huntington's disease, there is reduced binding of GABA and benzodiazepines, dopamine, acetylcholine, glutamate and CCK. There is increased binding of GABA in both the SN and globus pallidus. Glycine binding is increased in the substantia nigra and ACE is reduced.
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Schnee, M., J. Rauh, S. D. Buckingham, and D. B. Sattelle. "Pharmacology of skeletal muscle GABA-gated chloride channels in the cockroach Periplaneta americana." Journal of Experimental Biology 200, no. 23 (December 1, 1997): 2947–55. http://dx.doi.org/10.1242/jeb.200.23.2947.

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The pharmacology of -aminobutyric acid (GABA)-gated chloride channels of the coxal levator (182c,d) muscle of the cockroach Periplaneta americana has been investigated and the data compared with similar findings for the cell body of the cockroach fast coxal depressor motor neurone (Df). Muscle GABA receptors resembled those of the motor neurone cell body in their sensitivity to picrotoxinin and insensitivity to bicuculline. However, muscle GABA receptors were insensitive to the neuronal GABA receptor agonists isoguvacine (10(-4) mol l-1) and 3-aminopropane sulphonic acid (10(-3 )mol l-1). The benzodiazepine flunitrazepam, which at 10(-6 )mol l-1 greatly enhances the amplitude of the motor neurone GABA-induced responses, failed to affect muscle responses to GABA when tested at the same and at a higher (10(-4 )mol l-1) concentration. The convulsant t-butylbicyclophosphorothionate was a weak antagonist of cockroach muscle GABA receptors, whereas several cyclodienes were much more effective antagonists. Thus, studies using a benzodiazepine and several convulsant antagonists reveal differences in the pharmacology of muscle and neuronal GABA receptors of the cockroach Periplaneta americana.
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Meldrum, B. "Classification of GABA and benzodiazepine receptors." Journal of Psychopharmacology 1, no. 1 (January 1987): 1–5. http://dx.doi.org/10.1177/026988118700100102.

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Weizman, Abraham, and Moshe Gavish. "Gonadal hormones, GABA and benzodiazepine receptors." European Neuropsychopharmacology 6 (June 1996): 97. http://dx.doi.org/10.1016/0924-977x(96)87749-2.

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Li, Ping, Megan M. Eaton, Joe Henry Steinbach, and Gustav Akk. "The Benzodiazepine Diazepam Potentiates Responses of α1β2γ2L γ-Aminobutyric Acid Type A Receptors Activated by either γ-Aminobutyric Acid or Allosteric Agonists." Anesthesiology 118, no. 6 (June 1, 2013): 1417–25. http://dx.doi.org/10.1097/aln.0b013e318289bcd3.

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Abstract Background: The γ-aminobutyric acid (GABA) type A receptor is a target for several anesthetics, anticonvulsants, anxiolytics, and sedatives. Neurosteroids, barbiturates, and etomidate both potentiate responses to GABA and allosterically activate the receptor. We examined the ability of a benzodiazepine, diazepam, to potentiate responses to allosteric agonists. Methods: The GABA type A receptors were expressed in human embryonic kidney 293 cells and studied using whole-cell and single-channel patch clamp. The receptors were activated by the orthosteric agonist GABA and allosteric agonists pentobarbital, etomidate, and alfaxalone. Results: Diazepam is equally potent at enhancing responses to orthosteric and allosteric agonists. Diazepam EC50s were 25 ± 4, 26 ± 6, 33 ± 6, and 26 ± 3 nm for receptors activated by GABA, pentobarbital, etomidate, and alfaxalone, respectively (mean ± SD, 5–6 cells at each condition). Mutations to the benzodiazepine-binding site (α1(H101C), γ2(R144C), γ2(R197C)) reduced or removed potentiation for all agonists, and an inverse agonist at the benzodiazepine site reduced responses to all agonists. Single-channel data elicited by GABA demonstrate that in the presence of 1 μm diazepam the prevalence of the longest open-time component is increased from 13 ± 7 (mean ± SD, n = 5 patches) to 27 ± 8% (n = 3 patches) and the rate of channel closing is decreased from 129 ± 28 s−1 to 47 ± 6 s−1 (mean±SD) Conclusions: We conclude that benzodiazepines do not act by enhancing affinity of the orthosteric site for GABA but rather by increasing channel gating efficacy. The results also demonstrate the presence of interactions between allosteric activators and potentiators, raising a possibility of effects on dosage requirements or changes in side effects.
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Teuber, L., F. Watjen, and L. H. Jensen. "Ligands for the Benzodiazepine Binding Site - a Survey." Current Pharmaceutical Design 5, no. 5 (May 1999): 317–43. http://dx.doi.org/10.2174/138161280505230110100242.

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Abstract: y-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian Central Nervous System (CNS). GABA participates in the 1·egulation of neuronal excitability through interaction with specific membrane proteins (the GABAA receptors). The binding of GABA to these postsynaptic receptors, results in an opening of a chloride channel integrated in the receptor which allows the entry of c1- and consequently leads to hyperpolarization of the recipient cell. The action of GABA is allosterically modulated by a wide variety of chemical entities which interact with distinct binding sites at the GABAA receptor complex. One of the most thoroughly investigated rnodulatory site is the benzodiazepin binding site. The benzodiazepines constitute a well-known class of therapeutics displaying hypnotic, anxiolytic and anticonvulsant effects. Their usefulness, however, is limited by a broad range of side effects comprising sedation, ataxia, amnesia, alcohol and barbiturate potentiation, tolerance development and abuse potential. Consequently, there has been an intensive search for modulatory agents with an improved profile, and a diversity of chemical entities distinct from the benzodiazepines. but with GABA modulatory effects have been identified. The existence of endogenous ligands for the GABAA receptor complex beside GABA has often been described, but their role in the regulation of GABA action is still a matter of controversy. The progress of molecular biology during the last decade has contributed enormously to the understanding of benzodiazepine receptor pharmacology. A total of 14 GABAA receptor subunits have been cloned from mammalian brain and have been expressed/co-expressed in stable cell lines. These transfected cells constitute an important tool in the characterization of subtype selective ligands. In spite of the rapidly expanding knowledge of the molecular and pharmacological mechanisms involved in GABA/benzodiazepine related CNS disorders. the identification of clinically selective acting drugs is still to come.
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Shilov, Georgii N., Oleg N. Bubel, and Petr D. Shabanov. "A new approach to understanding structure, functions and classificasion of GABA-benzodiazepine receptor complex, a molecular target for creation of new anticonvulsants on the base of inhibitory amino acids." Reviews on Clinical Pharmacology and Drug Therapy 14, no. 3 (September 15, 2016): 34–45. http://dx.doi.org/10.17816/rcf14334-45.

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The GABA molecule was shown to the methods of quantum mechanic characteristics and molecular geometry has three conformational states: linear (GABA-1 conformer), cyclic (GABA-2 comformer) and bucket-like (GABA-3 conformer). The play different functions in the brain neurons: cyclic and bucket-like conformers play role of endogenous transmitters, and linear conformer participates in neuronal metabolism. The theoretical conformational analysis shows there are two types of GABA receptors in the CNS neurons: GABA-2 receptors, agonists of which are cyclic conformer of GABA, glycine and β-alanine and antagonists are bemegride, pentilentetrazol and strychnine; and GABA-3 receptors, agonists of which is bucket-like conformer of GABA and antagonists are picrotoxin and bicuculline. Anticonvulsive and other behavioral effects of derivatives of barbituric acid, benzazepine, benzodiazepine, gidantoine, succinimide and oxasolidindione are realized probably via GABA-2 receptors to switch on them the following functional centers of their structure are nessesary: α, γ and [δ-ε] for barbitirates; β, [δ-ε] and γ for carbamazepine; β and [δ-ε] for benzodiazepine derivatives, gabapentine and vigabatrine; α, β, γ and [δ-ε] for gidantoine and oxasolidindione derivatives; α, β, γ for succinimide derivatives. The power of any behavioral effect of anticonvulsants and inhibitory amino acids depends on power, location and numbers of hydrogen bounds developed between active centers of pharmacophore of anticonvulsant or inhibitory amino acids and active centers of functional skeleton of GABA-2 receptor complex, these properties determine absense of nootropic activity in anticonvulsive drugs and presense of them in inhibitory amino acids. It is concluded there are perspectives of synthesis of conpounds, pharmacophore of which should be like as cyclic conformer of GABA, glycine and β-alanine on their quantum mechanic characteristics and molecular geometry
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Dietl, M. M., R. Cortés, and J. M. Palacios. "Neurotransmitter receptors in the avian brain. III. GABA-benzodiazepine receptors." Brain Research 439, no. 1-2 (January 1988): 366–71. http://dx.doi.org/10.1016/0006-8993(88)91496-5.

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Dissertations / Theses on the topic "Receptors, GABA-Benzodiazepine"

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Chen, Jianping. "The Effects of Chronic Ethanol Intake on the Allosteric Interaction Between GABA and Benzodiazepine at the GABAA Receptor." Thesis, University of North Texas, 1992. https://digital.library.unt.edu/ark:/67531/metadc501231/.

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This study examined the effects of chronic ethanol intake on the density, affinity, and allosteric modulation of rat brain GABAA receptor subtypes. In the presence of GABA, the apparent affinity for the benzodiazepine agonist flunitrazepam was increased and for the inverse agonist R015-4513 was decreased. No alteration in the capacity of GABA to modulate flunitrazepam and R015-4513 binding was observed in membranes prepared from cortex, hippocampus or cerebellum following chronic ethanol intake or withdrawal. The results also demonstrate two different binding sites for [3H]RO 15-4513 in rat cerebellum that differ in their affinities for diazepam. Chronic ethanol treatment and withdrawal did not significantly change the apparent affinity or density of these two receptor subtypes.
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Xiang, Kun. "The role of L-type voltage-gated calcium channels in hippocampal CA1 neuron glutamate and GABA-A receptor-mediated synaptic plasticity following chronic benzodiazepine administration." Connect to Online Resource-OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1181737040.

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Dissertation (Ph.D.)--University of Toledo, 2007.
"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 70-78, p. 93, p. 132-140, p. 164-168, p. 194-221.
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Bilbe, Graeme. "Molecular studies on the gaba-benzodiazepine receptor." Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37639.

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Ai, Jinglu. "Medicinal plants as a source of novel brain GABA A/benzodiazepine receptor ligands /." Roskilde : Roskilde University, Department of Life sciences & Chemistry ; Sct. Hans Hospital, Department of Biochemistry, Research Institute of Biological Psychiatry, 1999.

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Alenfall, Jan. "Peripheral benzodiazepine receptors in prostate and prostatic tumors characterization, hormonal regulation and possible role in tumorigenesis /." Lund : Dept. of Pharmacology, University of Lund, 1995. http://books.google.com/books?id=_xlrAAAAMAAJ.

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Taylor, S. C. "Interactions of drugs acting at the benzodiazepine/gaba receptor-ionophone complex : Acute and chronic studies." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382669.

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BLANOT, FRANCOIS. "Vers le clonage du recepteur gaba/benzodiazepine : apport de l'electrophysiologie et de la biologie moleculaire." Paris 6, 1987. http://www.theses.fr/1987PA066701.

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Le recepteur central de l'acide g-aminobutyrique et des benzodiazepines a ete etudie par deux approches complementaires: l'une electrophysiologique, l'autre faisant appel aux techniques de la biologie moleculaire. L'etude electrophysiologique a ete realisee sur des ovocytes de xenopus injecte d'arn messager extrait de cerveau de poulet. Divers parametres caracterisant le recepteur de l'acide g-amino-butyrique ainsi que l'interaction d'une -carboline avec celui-ci ont ete etudies
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GUERINEAU, DE LAMERIE GUILLAUME. "Interet de la mesure des recepteurs gaba-benzodiazepines en tomographie par emission de positons dans les pathologies psychiatriques." Lyon 1, 1993. http://www.theses.fr/1993LYO1M268.

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Wu, Chieh-Hsi. "The effects of acute and chronic ethanol administration on the expression of GABA(A)/benzodiazepine receptor subunit mRNA in the mouse cerebellum /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487849696965995.

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Hazime, Mahmoud. "Etude de l’effet de l’octadécaneuropeptide sur l’activité du cortex cérébral : intérêt pour la récupération fonctionnelle post-ischémique The gliopeptide ODN, a ligand for the benzodiazepine site of GABAA receptors, boosts functional recovery after stroke Prolonged deficit of gamma oscillations in the peri-infarct cortex of mice after stroke Bi-directional effect of the endozepine ODN on neuronal activity in vivo." Thesis, Normandie, 2019. http://www.theses.fr/2019NORMR127.

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L’ischémie cérébrale demeure un problème de santé publique majeur pour lequel on manque de solution thérapeutique permettant de favoriser la récupération des fonctions perdues. L’équipe de recherche dans laquelle cette thèse fut menée a mis en évidence que l’octadécaneuropeptide (ODN), un ligand endogène du récepteur GABAA, permet d’améliorer la récupération sensori-motrice après une ischémie cérébrale chez la souris. L’objectif de cette thèse était de caractériser les effets de l’ODN sur l’activité neuronale in vivo afin de mieux comprendre par quel mécanisme ce peptide agit sur la réparation des circuits neuronaux. Dans une première partie, nous avons montré que l’ODN, in vivo, se comporte comme un pro-excitateur à une concentration micromolaire (la concentration à laquelle il permet la récupération fonctionnelle) en revanche, à faible concentration (10-12 M) l’ODN inhibe l’activité des neurones du cortex. Dans ce travail, nous proposons, sur la base d’expériences in vitro, que cette inhibition est induite par une libération astrocytaire de GABA. Dans une deuxième partie, nous avons démontré que le régime oscillatoire du cortex perilésionnel (fluctuations rythmiques de l’excitabilité neuronale) est appauvri en oscillations gamma 7 et 21 jours après une ischémie cérébrale, mais que l’ODN n’a aucun effet sur leur puissance. Ces travaux confirment l’intérêt de renforcer l’excitabilité du cortex après un AVC et montrent qu’à cette fin, l’ODN peut-être un outil pharmacologique efficace
Cerebral ischemia remains a major public health problem for which there is a lack of a therapeutic solution to promote the recovery of lost functions. The research team in which this thesis was conducted found that octadecaneuropeptide (ODN), an endogenous ligand of the GABAᴀ receptor, improves sensory-motor recovery after cerebral ischemia in mice. The aim of this thesis was to characterize the effects of ODN in neural activity in vivo in order to better understand by what mechanism this peptide can act on the repair of neural circuits. In a first part, we showed that ODN, in vivo, behaves as an excitability enhancer at micromolar concentration (the concentration at which it improves functional recovery). On the other hand, at low concentrations (10¯¹² M) ODN inhibits the activity of neurons in the cortex. Based on complementary in vitro experiences, we propose that this inhibition is induced by an astrocytic release of GABA. In a second part of the thesis, we demonstrated that the oscillatory regimen of the peri-lesional cortex (rythmic fluctuations of neural excitability) is depressed in gamma oscillation 7 and 21 days after cerebral ischemia. However, ODN has no effect on the oscillatory spectral power. This work confirms the value of enhancing the excitability of the cortex after a stroke and shows that for this purpose ODN can be an effective pharmacological tool
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Books on the topic "Receptors, GABA-Benzodiazepine"

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1944-, Hindmarch I., ed. Benzodiazepines: Current concepts : biological, clinical, and social perspectives. Chichester [England]: Wiley, 1990.

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Giovanni, Biggio, Costa Erminio, and Capo Boi Conference on Neuroscience (6th : 1989 : Villasimius, Italy), eds. GABA and benzodiazepine receptor subtypes: Molecular biology, pharmacology, and clinical aspects. New York: Raven Press, 1990.

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W, Olsen Richard, and Venter J. Craig, eds. Benzodiazepine/GABA receptors and chloride channels: Structural and functional properties. New York: A.R. Liss, 1986.

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Martin, Sarter, Nutt David J. 1951-, and Lister Richard G, eds. Benzodiazepine receptor inverse agonists. New York: Wiley-Liss, 1995.

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1951-, Marescaux C., Vergnes M. 1935-, and Bernasconi R. 1929-, eds. Generalized non convulsive epilepsy: Focus on GABA-B receptors. Wien: Springer-Verlag, 1992.

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1944-, Martin Ian L., ed. The GABAA/benzodiazepine receptor as a target for psychoactive drugs. Austin: R.G. Landes, 1995.

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J, Rodger R., and Cooper S. J, eds. 5-HT1A agonists, 5-HT3 antagonists and benzodiazepines: Their comparative behavioural pharmacology. Chichester, West Sussex, Englad: Wiley, 1991.

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L, Erdő Sándor, and Bowery N. G, eds. GABAergic mechanisms in the mammalian periphery. New York: Raven Press, 1986.

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NATO Advanced Research Workshop on Molecular Biology of Neuroreceptors and Ion Channels (1988 Thera Island, Greece). Molecular biology of neuroreceptors and ion channels. Berlin: Springer-Verlag, 1989.

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Malison, Robert Thomas. Structural homology of the GABAa/benzodiazepine receptor as demonstrated by monoclonal antibodies and limited proteolysis. [New Haven: s.n.], 1987.

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Book chapters on the topic "Receptors, GABA-Benzodiazepine"

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Schliebs, Reinhard, and Thomas Rothe. "GABA and Benzodiazepine Receptors in the Developing Visual System." In Receptors in the Developing Nervous System, 127–40. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1544-5_7.

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Bristow, David R., and Ian L. Martin. "Incorporation of GABA/Benzodiazepine Receptors into Natural Brain Lipid Liposomes: Biochemical Characterization." In Membrane Receptors, Dynamics, and Energetics, 161–71. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5335-5_13.

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Eldefrawi, Amira T., Ibrahim M. Abalis, and Mohyee E. Eldefrawi. "The GABA/Benzodiazepine Receptor · Chloride Channel: Biochemical Identification in Insects and Stereospecific Binding of Insecticides." In Membrane Receptors and Enzymes as Targets of Insecticidal Action, 107–24. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5113-9_5.

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Pauli, S., H. Hall, C. Halldin, and G. Sedvall. "Spatial Benzodiazepine Receptor Imaging in the Human Brain." In GABA: Receptors, Transporters and Metabolism, 267–74. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8990-2_29.

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Kawasaki, Kazuo, Tsuyoshi Kihara, Shunji Murata, Katsumi Koike, Masato Ikeda, Masami Eigyo, and Susumu Takada. "A Novel Benzodiazepine Partial Inverse Agonist, S-8510, as a Cognitive Enhancer." In GABA: Receptors, Transporters and Metabolism, 259–66. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8990-2_28.

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Möhler, H., P. Schoch, and J. G. Richards. "The GABA/Benzodiazepine Receptor Complex: Function, Structure and Location." In Proceedings in Life Sciences, 91–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70690-5_18.

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Deutsch, Stephen I., Abraham Weizman, Ronit Weizman, Frank J. Vocci, and Karin A. Kook. "Role of the GABA—Benzodiazepine Receptor Complex in Stress." In Application of Basic Neuroscience to Child Psychiatry, 61–76. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0525-5_4.

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Jones, E. Anthony, Anthony S. Basile, and Phil Skolnick. "Hepatic Encephalopathy, GABA-ergic Neurotransmission and Benzodiazepine Receptor Ligands." In Advances in Experimental Medicine and Biology, 121–34. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5826-8_7.

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Möhler, H., P. Schoch, and J. G. Richards. "The GABA Receptor/Benzodiazepine Complex in the Central Nervous System." In Neurobiochemistry, 120–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70940-1_14.

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Gee, Kelvin W. "Steroid Modulation of the GABA/Benzodiazepine Receptor-Linked Chloride lonophore." In Molecular Neurobiology · 1988 ·, 291–317. Totowa, NJ: Humana Press, 1989. http://dx.doi.org/10.1007/978-1-4612-4520-9_11.

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