3H-baclofen and 3H-GABA bind to bicuculline-insensitive GABAB sites in rat brain

  title={3H-baclofen and 3H-GABA bind to bicuculline-insensitive GABAB sites in rat brain},
  author={David R. Hill and Norman G. Bowery},
The presence of a novel receptor for the neurotransmitter γ-aminobutyric acid (GABA) on peripheral autononric nerve terminals and in mammalian brain slices has been described recently1–4. This receptor differs from the classical GABA site as it is unaffected by recognized GABA antagonists such as bicuculline and is not sensitive to the majority of accepted GABA-mimetics such as 3-aminopropanesulphonic acid (3-APS) or isoguvacine. We propose to designate the classical site as the GABAA and the… Expand
Studies on [3H]GABA and endogenous GABA release in rat cerebral cortex suggest the presence of autoreceptors of the GABAB type.
It is concluded that the release of GABA from rat cortical nerve endings may be inhibited through the activation of autoreceptors which appear to belong to the GABAB type. Expand
Bicuculline-insensitive GABA receptors: Studies on the binding of (−)-baclofen to rat cerebellar membranes
The effects of some conformationally restricted analogues of gamma-aminobutyric acid (GABA) on [3H](-)-baclofen binding indicated that GABA interacts with (-)-bicuculline-sensitive binding sites ( GABAB) in extended rather than folded conformations, and that folded analogue of GABA may interact with a class of binding site insensitive to (--bacl ofen and bicucULLine. Expand
The Autoradiographic Localization of Baclofen-Sensitive GABAB Sites in Rat Cerebellum
The existence of a receptor for GABA on neurons of the mammalian peripheral and central nervous systems is now firmly established and radiolabelied ligand binding studies have supported the view thatExpand
Bicuculline‐ and Baclofen‐Insensitive γ‐Aminobutyric Acid Binding to Rat Cerebellar Membranes
Abstract: Up to 60% of γ‐[3H]aminobutyric acid ([3H]GABA) bound specifically to rat cerebellar membranes in the absence of Ca2+ was insensitive to the GABAA antagonist bicuculline and to the GABABExpand
3-aminopropanephosphinic acid is a potent agonist at peripheral and central presynaptic GABAB receptors
Data show that 3-APA is a potent agonist at presynaptic GABAB receptors in the periphery and on GABAergic neurons from the central nervous system. Expand
CGP 52432: a novel potent and selective GABAB autoreceptor antagonist in rat cerebral cortex.
The potency and selectivity characteristics of CGP 52432 indicate that the drug is by far the most appropriate tool to investigate the terminal GABAB autoreceptors of the rat cerebral cortex. Expand
Bicuculline-insensitive GABA receptors on peripheral autonomic nerve terminals.
Data suggest the presence of a bicuculline-insensitive GABA receptor on autonomic nerve terminals, and preliminary observations indicate a lack of chloride ion dependence in the action of GABA at this site. Expand
Evidence that SL75102 is an agonist at GABA b as well as GABA a receptors
It is suggested that in addition to any direct action of SL76002 itself the products ofSL76002 metabolism, SL75102 and GABA may exert effects via baclofen-sensitive GABAB as well as GABAA sites in mammalian brain. Expand
Antagonistic effect of δ-aminovaleric acid on bicuculline-insensitive γ-aminobutyric acidB (GABAB) sites in the rat's brain
Abstract The effect of δ-aminovaleric acid (δ-AV) on bicuculline-insensitive γ-aminobutyric acid B (GABA B ) sites in the central nervous system (CNS) was investigated by binding studies andExpand
Are baclofen-sensitive GABAB receptors present on primary afferent terminals of the spinal cord?
It is reported here that GABAB sites, unlike GABAA sites, are present in high concentrations in laminae I, II, III and IV of the dorsal horn and that after the neonatal administration of capsaicin this binding is reduced by 40–50%. Expand


(–)Baclofen decreases neurotransmitter release in the mammalian CNS by an action at a novel GABA receptor
GABA clearly decreased the evoked release of accumulated 3H-noradrenaline from rat atria in vitro and3H-acetylcholine from preganglionic terminals in the rat superior cervical ganglion in vitro without affecting the basal release of tritium. Expand
Inhibition of Na+‐independent [3H]GABA binding to synaptic membranes of rat brain by β‐substituted GABA derivatives
The requirements of the substituents of the PC atom of the GABA molecule to retain affinity for the receptor sites are defined to achieve additional information on the mechanism of action of some GABA derivatives with central inhibitory activity, like P-phenyl-GABA (Phenygam) and fi-(p-chloropheny1)- GABA (Baclofen). Expand
Gamma-aminobutyric acid binding to receptor sites in the rat central nervous system.
Gamma-aminobutyric acid binds to synaptic membrane fractions of rat brain in a selective fashion representing an interaction with postsynaptic GABA receptors, with intermediate values in the thalamus, hippocampus, hypothalamus, cerebral cortex, midbrain, and corpus striatum. Expand
The action of β-phenyl-GABA derivatives on neurones of the cat cerebral cortex
The depressant action of β-p-CPG was not antagonised by bicuculline which suggests that the β-aryl-GABA derivatives do not exert a GABA-like action on cortical neurones. Expand
Central effects of -(p-chlorophenyl)-?-aminobutyric acid
Although less potent than GABA, β-p-CPG depressed the firing of spinal interneurones, pyramidal tract neurones and Purkinje cells of anaesthetised cats and may activate neuronal receptors for an inhibitory transmitter chemically related to phenylethylamine. Expand
Abstract— The treatment of cerebellar membranes of rat brain with a low concentration of Triton X‐100 followed by sufficient washing results in an increase of the Na+‐independent binding of [3H]GABAExpand
Regulation of hippocampal glutamate receptors: evidence for the involvement of a calcium-activated protease.
  • M. Baudry, G. Lynch
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
  • 1980
It is suggested that an endogenous membrane-associated thiol protease regulates the number of [3H]glutamate binding sites in hippocampal membranes and that this is the mechanism by which calcium stimulates glutamate binding. Expand
Regulation of glutamate receptors by cations
It is proposed that the regulation of glutamate binding by cations might account for the extremely long-lasting potentiation of synaptic responses found in the hippocampus following bursts of repetitive electrical stimulation. Expand
Protein measurement with the Folin phenol reagent.
Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein. Expand