Results 271 to 280 of about 163,092 (297)
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Journal of Neural Transmission, 1985
Treatment of mice with DSP4 (a neurotoxin that abolishes the presynaptic noradrenergic neuron; Dooley et al., 1983) resulted in: (A) a decrease in the Bmax for the low affinity GABA-B receptor site in the cerebral cortex and hippocampus, whereas the Bmax for the high affinity GABA-B receptor site was unaffected; (B) a greater potentiation of ...
P. D. Suzdak, G. Gianutsos
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Treatment of mice with DSP4 (a neurotoxin that abolishes the presynaptic noradrenergic neuron; Dooley et al., 1983) resulted in: (A) a decrease in the Bmax for the low affinity GABA-B receptor site in the cerebral cortex and hippocampus, whereas the Bmax for the high affinity GABA-B receptor site was unaffected; (B) a greater potentiation of ...
P. D. Suzdak, G. Gianutsos
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Effects of γ-acetylenic GABA and γ-vinyl GABA on synaptosomal release and uptake of GABA
Biochemical Pharmacology, 1981Abstract The effects of the irreversible inhibitors of GABA-transaminase (E.C.2.6.1.19), γ-acetylenic GABA (4-amino-hex-5-ynoic acid, RMI 71645) and γ-vinyl GABA (4-amino-hex-5-enoic acid, RMI 71754) on the release and uptake of endogenous and exogenous GABA by rat cerebral cortical synaptosomes were studied.
Abdul-Salam Abdul-Ghani +3 more
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GABA and GABA receptors in invertebrates
Seminars in Neuroscience, 1991Abstract GABA is the major inhibitory transmitter at invertebrate synapses in both the central and peripheral nervous systems. The receptors for GABA are well characterised electrophysiologically in a wide variety of invertebrate organisms but their biochemical and pharmacological profiles are less well defined. In general invertebrate GABA receptors
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GABA, a forgotten gliotransmitter
Progress in Neurobiology, 2008The amino acid gamma-aminobutiric acid (GABA) is a major inhibitory transmitter in the vertebrate central nervous system (CNS) where it can be released by neurons and by glial cells. Neuronal GABAergic signaling is well characterized: the mechanisms of GABA release, the receptors it targets and the functional consequences of their activation have been ...
Etienne Audinat +10 more
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Clinical Neuropharmacology, 1982
GABA-ergic systems are involved in all the main functions of the brain. In most brain regions impairment of this system produces epileptic activity. GABA-mediated inhibitory function can be enhanced by drugs of at least seven different types. They act on the metabolism or synaptic release of GABA, or its reuptake into neurones of glia, or on various ...
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GABA-ergic systems are involved in all the main functions of the brain. In most brain regions impairment of this system produces epileptic activity. GABA-mediated inhibitory function can be enhanced by drugs of at least seven different types. They act on the metabolism or synaptic release of GABA, or its reuptake into neurones of glia, or on various ...
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Locating GABA in GABA receptor binding sites
Biochemical Society Transactions, 2009The Cys-loop family of ligand-gated ion channels contains both vertebrate and invertebrate members that are activated by GABA (γ-aminobutyric acid). Many of the residues that are critical for ligand binding have been identified in vertebrate GABAA and GABAC receptors, and specific interactions between GABA and some of these residues have been ...
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General Pharmacology: The Vascular System, 1983
The role of both novel GABAB and classical GABAA receptors in GAG-induced anti-nociception was investigated using the tail flick and hot plate tests. To this end, manipulations known to increase baclofen-induced antinociception (GABAB) and the receptor antagonist bicuculline (GABAA) were used.
C. Dickson, J. Sawynok
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The role of both novel GABAB and classical GABAA receptors in GAG-induced anti-nociception was investigated using the tail flick and hot plate tests. To this end, manipulations known to increase baclofen-induced antinociception (GABAB) and the receptor antagonist bicuculline (GABAA) were used.
C. Dickson, J. Sawynok
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Endogenous GABA determines the characteristics of [3H]GABA-binding
European Journal of Pharmacology, 1981Since the identification of sodium-independent GABA-binding sites in membrane preparations from the mammalian central nervous system numerous publications have dealt with the effects of putative endogenous inhibitors of GABA-binding. However, controversy has arisen over the existence and identity of such inhibitors and the possible artifactural role of
Jeffrey Grove +2 more
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GABA and GABA-receptors in the enteric nervous system
Neuropharmacology, 1984Abstract GABA and its metabolic enzymes are present in the intestinal myenteric plexus. High affinity GABA uptake in the plexus has been shown by release studies and autoradiography of labelled GABAergic neurones. Both GABA A - and GABA B -receptor sites on plexus neurones have been established pharmacologically, and GABA-barbiturate-benzo-diazepine ...
Jennifer Ong, David I.B. Kerr
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Molecular and Cellular Biochemistry, 1981
This review describes the development of GABA receptor agonists with no detectable affinity for other recognition sites in GABA-mediated synapses. The key compounds are THIP, isoguvacine, and piperidine-4-sulphonic acid (P4S), developed via extensive structural modifications of the potent but not strictly specific GABA agonist muscimol.
Erik Falch, Povl Krogsgaard-Larsen
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This review describes the development of GABA receptor agonists with no detectable affinity for other recognition sites in GABA-mediated synapses. The key compounds are THIP, isoguvacine, and piperidine-4-sulphonic acid (P4S), developed via extensive structural modifications of the potent but not strictly specific GABA agonist muscimol.
Erik Falch, Povl Krogsgaard-Larsen
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