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R W Olsen

Publications and source records attributed to R W Olsen.

At least 73 records · Page 4Linked to original sources

Phosphorylation of the GABAA receptor by cAMP-dependent protein kinase and by protein kinase C: analysis of the substrate domain.

Previous work has shown that the GABAA-receptor (GABAA-R) could be phosphorylated by cAMP-dependent protein kinase (PKA), protein kinase C (PKC), and a receptor associated kinase. However, no clear picture has yet emerged concerning the particular subunit/subtypes of the GABAA-R that were phosphorylated by PKA and PKC. In the present report we show that an antibody raised against a 23 amino acid polypeptide corresponding to a sequence in the putative intracellular loop of the beta 1 subunit of the receptor blocks the in vitro phosphorylation of the purified receptor by PKA and PKC. Moreover, N-terminal sequence analysis of the principal phosphopeptide fragment obtained after proteolysis of the receptor yielded a sequence that corresponds to the beta 3 subunit of the receptor. Such data provide additional support for our hypothesis (Browning et al., 1990, Proc. Natl. Acad. Sci. USA 87:1315-1317) that both PKA and PKC phosphorylate the beta-subunit of the GABAA-R.

Amino Acid Sequence↗

Antibodies specific for alpha-subunit subtypes of GABAA receptors reveal brain regional heterogeneity.

Antisera were produced in rabbits against synthetic peptides based on subtype-specific regions of the cDNA sequences of the alpha 1, alpha 2, alpha 3, and alpha 4 (also termed alpha 5) subunits of mammalian GABAA receptors. The antigen peptides were chosen from the putative cytoplasmic loop between the proposed third and fourth membrane spanning helices; they were not only subtype-specific sequences, but also their hydrophilicity and predicted secondary structures suggested high potential antigenicity. In all cases, antipeptide antisera recognized on western blots the corresponding alpha-subunit polypeptide of the GABAA receptors purified from bovine brain by benzodiazepine-affinity chromatography, and were able to immunoprecipitate binding activity from detergent-solubilized purified receptors. The four antisera each recognized a unique polypeptide, and only one, in the purified receptor, with alpha 1, alpha 2, alpha 3, and alpha 4 identified at 51, 52, 56, and 57 kDa, respectively. This represents the first identification of the alpha 4 gene product on a gel. Both the relative amount of staining in immunoblots and the fraction of receptor binding that could be immunoprecipitated by saturating concentrations of each of the four subtype-specific antibodies varied in a consistent manner between receptors purified from different brain regions. Thus, cerebral cortex receptor contained all four alpha polypeptides on western blots, and significant activity could be precipitated by all four. Hippocampal receptor lacked alpha 3 immunoreactivity on blotting and by immunoprecipitation; alpha 1 was less, whereas both alpha 2 and alpha 4 were more abundant in hippocampus than in cortex by both techniques. Cerebellum receptor contained only alpha 1 of the four alpha subunits tested, and the anti-alpha 1 antibodies immunoprecipitated > 90% of the binding activity. The variable amounts of staining and immunoprecipitation from the three brain areas by the four antisera demonstrate the presence of heterooligomeric receptor complexes with different alpha-subunit constituents in cortex, hippocampus, and cerebellum. The sum of cortical receptor activity precipitated individually by the four anti-alpha antisera was > 150%, indicating that some heterooligomers are likely to contain more than one class of alpha subtype, although most receptor complexes probably contain only one alpha subtype. These alpha-subunit subtype-specific antibodies should be useful in analyzing structure, function, and localization of GABAA/benzodiazepine receptors in mammalian brain.

Amino Acid Sequence↗

Immunochemical characterization of the beta 2 subunit of the GABAA receptor.

To date three beta subunits of the GABAA receptor have been identified in rat brain as a result of cDNA library screening. The beta 2 subunit has been reported to have a wide distribution in rat brain based on in situ hybridization studies quantifying beta 2 mRNA. To study the beta 2 subunit more directly, we have raised a polyclonal antibody to a synthetic peptide representing residues 315-334 of the intracellular loop of the beta 2 subunit. The antibody, which had been affinity-purified, recognized the beta 2 peptide but did not immunolabel homologous beta 1 and beta 3 subunit peptides, indicating that this antibody is specific for the beta 2 subunit of the receptor. In western blots of the purified receptor, the antibody recognized a major diffuse band of 54-58 kDa and exhibited minor labeling of lower-molecular-mass polypeptides. In western blots of cortex homogenate, the antibody exhibited nervous system-specific labeling of a 55-kDa band that comigrated with the 55-kDa band of the purified receptor. Quantitative immunolabeling of this 55-kDa polypeptide permitted direct determination of the relative amounts of the beta 2 subunit in different brain regions. The brainstem contained the highest relative specific activity of the beta 2 subunit, followed by the inferior colliculus, olfactory lobe, and cerebellum. Lower levels of immunolabeling were seen in hypothalamus, hippocampus, thalamus, and cortex.

Amino Acid Sequence↗

GABA alters GABAA receptor mRNAs and increases ligand binding.

In addition to its role as an inhibitory neurotransmitter, gamma-aminobutyric acid (GABA) influences the cytodifferentiation of developing neurons both in culture and in vivo. Here, we report some of the targets of GABA action and the mechanism through which GABA acts. In primary cultures of cerebellar granule cells, GABA specifically stimulates an increase in the levels of mRNAs for alpha 1 and beta 2 GABAA receptor subunits. The GABAA agonist 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) mimics this effect, and the GABAA antagonist bicuculline prevents it. In addition, GABA and THIP trigger an increase in the number of GABA binding sites. This increase parallels that seen in vivo, where the total number of GABAA receptor sites increases during postnatal cerebellar development. It is interesting that the period of the greatest increase in the number of receptor sites coincides with the development of the granule cells. Taken together, our data suggest that GABA may play an important role during maturation of cerebellar granule cells by influencing the number and composition of its own receptors.

Animals↗

GABAA receptor subtypes: ligand binding heterogeneity demonstrated by photoaffinity labeling and autoradiography.

Heterogeneity of binding affinities for a variety of ligands was observed for gamma-aminobutyric acid type A (GABAA) receptors in the rat CNS, at both GABA and benzodiazepine recognition sites. Photoaffinity labeling by [3H]flunitrazepam and [3H]muscimol to affinity column-purified receptor proteins was examined by gel electrophoresis in sodium dodecyl sulfate. Anesthetic barbiturates (pentobarbital) and steroids (alphaxalone) both differentially stimulated the incorporation of [3H]flunitrazepam more so into the 51-kDa alpha 1 subunit than into the 53-kDa alpha 2 polypeptide, and incorporation of [3H]muscimol into the 55-kDa beta 2 subunit more so than the 58-kDa beta 3 polypeptide. Binding to these polypeptides was also affected differentially by other allosteric modulators and competitive inhibitors, including the benzodiazepine "type 1" selective ligand CL218,872. Heterogeneity in affinity of this drug for the single 51-kDa alpha 1 polypeptide strongly suggests that type I receptors, like type II, are heterogeneous. In brain sections, the extent of enhancement of [3H]muscimol binding showed significant regional variation, similar for both steroids and barbiturates, and the GABA analogues THIP and taurine inhibited muscimol binding with regional variations in affinity that were almost opposites of each other. Modulation of [3H]flunitrazepam binding by steroids, barbiturates, and THIP significantly varied with regions. Taken together, ligand binding heterogeneity exhibited by photoaffinity labeling and autoradiography demonstrate the existence of multiple pharmacological-binding subtypes resulting from the combination of multiple polypeptide gene products into several oligomeric isoreceptors. Comparison of the regional distribution of binding subtypes with that of different subunit gene products allows the following conclusions about possible subunit compositions of native pharmacological receptor subtypes present in the brain: Benzodiazepine pharmacology of the oligomeric receptor isoforms is dependent on the nature of alpha and subunits other than alpha, GABA-benzodiazepine coupling is dependent on the nature of the alpha subunits, GABA site pharmacology is dependent on the nature of the beta subunits, and several subunits including alpha and beta contribute to the degree of sensitivity to steroids and barbiturates. Finally, the presence of discrete subunits may be necessary but is not sufficient to postulate a defined pharmacological property.

Affinity Labels↗

The kindling model of alcohol dependence: similar persistent reduction in seizure threshold to pentylenetetrazol in animals receiving chronic ethanol or chronic pentylenetetrazol.

Rats on a chronic intermittent ethanol (CIE) regimen showed a persistent reduction in seizure threshold to the convulsant drug pentylenetetrazol (PTZ). CIE rats were given ethanol by intubation on an alternate day schedule and tested at selected intervals for seizure threshold with PTZ. A significant reduction in seizure threshold, a sign of withdrawal, was observed 20 hr after the first dose. The severity of withdrawal intensified on repetition of the ethanol administration and depression-hyperexcitability cycle, with the seizure threshold reaching a maximum decrease after 12 doses and remaining reduced up to 60 doses. The reduction in seizure threshold persisted for at least 40 days of no alcohol following the 60th dose. The long-lasting decrease in seizure threshold following CIE treatment resembled the "kindling" phenomenon produced by chronic administration of PTZ (25 mg/kg, 3 times/week). The CIE rats developed, in addition, a tolerance to the anticonvulsant action of ethanol, which occurred well after the decrease in PTZ seizure threshold, and a tolerance to the hypothermic effect of ethanol, which developed rapidly. PTZ kindled rats that had never been exposed to ethanol also exhibited tolerance to the hypothermic effect of ethanol. We propose that kindling contributes to the mechanism of the development of dependence on central nervous system depressants like benzodiazepines, barbiturates, and alcohol, drugs that act on the gamma-aminobutyric acid-A receptor chloride ion channel complex. Repeated episodes of depression and withdrawal hyperexcitability are postulated to produce kindling during the repeated withdrawal episodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Withdrawal Delirium↗

Enhancement of gamma-aminobutyric acidA receptor function and binding by the volatile anesthetic halothane.

The volatile general anesthetics halothane and enflurane increased muscimol-stimulated 36Cl- efflux via gamma-aminobutyric acid (GABA)A receptors in rat brain cortical slices and also increased basal 36Cl- efflux in the absence of GABA agonist. The effects occurred in the clinical range of anesthetic concentrations (0.56-1.7 mM halothane and 0.46-1.4 mM enflurane). Both anesthetics induced a slow onset increase in basal 36Cl- efflux rate when added alone with no exogenous GABA agonist. This direct effect of halothane had a biphasic dependence on anesthetic concentrations, with a maximal effect in the range 1.1 to 1.7 mM. Replacing extracellular calcium with magnesium or blocking voltage-gated calcium entry with cobalt (200 microM) altered the direct halothane effect, shifting the concentration-dependence curve to the right. Halothane direct potentiation of chloride flux in the absence of GABA agonist was blocked by the GABAA chloride channel antagonist picrotoxin but not by the GABAA receptor antagonist bicuculline. The halothane potentiation of the muscimol response was detectable at concentrations of 0.56 mM halothane in the assay buffer, and was linear with concentration up to 2.8 mM. The effect was more pronounced at low GABA agonist concentrations, apparently due to an increase in GABA affinity. Lowering the extracellular calcium concentration to micromolar levels did not affect halothane potentiation of muscimol responses. Halothane at similar concentrations increased the high-affinity binding of [3H]muscimol to GABAA receptor sites in rat brain cortical membranes in a calcium-independent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Expression of GABAA receptor polypeptides in clonal rat cell lines.

The neuronal-like cell lines, B35, B65, B103, and B104, previously reported to possess high affinity GABA binding, were analyzed for various cellular properties. They possessed peripheral but lacked central benzodiazepine binding. Only B65 cells possessed [3H-]muscimol binding; none bound [35S]TBPS. None of the cells exhibited GABA-stimulated chloride conductance with patch clamp recordings. By Western blots the cells possessed alpha subunits. Northern blot and polymerase chain reaction analysis showed that out of alpha 1, alpha 4, beta 1 and gamma 2 subunits, only alpha 1 subunit mRNA was present. Thus, GABAA-receptor binding without associated central benzodiazepine receptor sites and without functional chloride channels appears to result from expression of an incomplete subunit composition.

Animals↗

Isolation and cloning of a voltage-dependent anion channel-like Mr 36,000 polypeptide from mammalian brain.

A polypeptide of M(r) 36,000 (36 kDa) was isolated from detergent-solubilized membrane fractions of mammalian brain on a benzodiazepine affinity column utilized for the purification of the gamma-aminobutyric acid/benzodiazepine receptor protein, followed by preparative gel electrophoresis. Partial protein sequence for two fragments of the 36-kDa polypeptide allowed the isolation of cDNA clones from a rat hippocampal library. An open reading frame coding a sequence of 295 amino acid residues containing the two probe peptide sequences with minor differences, and a putative N-terminal signal peptide of 25 residues was found. Hydropathy index revealed no regions of alpha-helix suitable for membrane spanning, but several areas of alternating hydrophilic and hydrophobic residues consistent with beta-strands. The sequence of this brain protein was 24% identical to that of a yeast mitochondrial protein, the voltage-dependent anion channel (VDAC), and over 70% identical with the VDAC from human B lymphocytes. The gamma-aminobutyric acid type A (GABAA) receptor/36-kDa preparation purified on benzodiazepine affinity column has channel-forming activity in lipid bilayer membranes that is virtually identical to VDAC isolated from mitochondria of various sources, indicating that the 36-kDa protein is a new member of the VDAC family of proteins. An antiserum raised against the purified 36-kDa polypeptide was able to precipitate [3H]muscimol binding activity, indicating a tight association with the GABAA receptor protein in vitro and copurification on the benzodiazepine affinity column due to this association. Further studies are needed to determine whether such an association occurs in vivo.

Amino Acid Sequence↗

Sex differences in sensitivity to pentylenetetrazol but not in GABAA receptor binding.

Female rats have a higher threshold than males for seizures induced by the convulsant pentylenetetrazol, a GABAA receptor-chloride channel complex blocker. No sex difference was observed for the anticonvulsant activities of ethanol or diazepam to protect against pentylenetetrazol seizures. Ovariectomy reduces the pentylenetetrazol seizure threshold of females to that of males. In contrast, females have a lower threshold than males to electroshock seizures. Pentylenetetrazol receptors were compared in males and females and gonadectomized animals by binding of several radioligands to the GABAA receptor complex. No differences were found for these four groups of animals in the binding of [3H]flunitrazepam to the benzodiazepine sites and [35S]t-butyl bicyclophosphorothionate ([35S]TBPS) to the chloride channel/convulsant sites in membrane homogenates, nor for allosteric modulation of binding by GABA, the steroid anesthetic alphaxalone, or the benzodiazepine Ro 5-4864. In tissue section autoradiography, no difference was observed for these same assays nor for the binding of [3H]muscimol in the presence and absence of alphaxalone in several major regions. We conclude that circulating female sex hormones, possibly neurosteroid metabolites of progesterone, known to interact directly with the GABAA receptor complex, are involved in the sex differences in pentylenetetrazol seizure susceptibility.

Anesthetics↗

Preparation of antibodies to beta subunits of gamma-aminobutyric acidA receptors.

Antisera were produced in rabbits against synthetic peptides based on two regions of the cDNA sequence of the beta 1 subunit of bovine gamma-aminobutyric acidA (GABAA) receptors. The deduced amino acid sequences were similar in other beta subunits of bovine, rat, and chick receptors, predicting cross-reactability with all beta subunits. One antiserum (anti-beta e) was raised against an extracellular moiety near the invariant disulfide loop thought to be located near the neurotransmitter binding domain; the other (anti-beta c) was raised against an intracellular moiety containing a consensus sequence for cyclic AMP-dependent protein kinase phosphorylation of a serine residue. Predicted secondary structures suggested high potential immunogenicity for the chosen antigen peptides. Both antisera at high dilutions recognized the same polypeptide bands on western blots of GABAA receptors purified from three regions of bovine brain (four bands at 57, 54, 53, and 52 kDa in cerebral cortex) but fewer bands (57, 54, and 52 kDa) in hippocampus and cerebellum (one major band at 54 kDa, traces at 57 and 53 kDa). This is consistent with the presence of multiple beta subunits whose expression varies with brain region, as shown by molecular cloning. The anti-beta c antibody was able to immunoprecipitate purified GABAA receptor [3H]-muscimol binding, 87% in bovine cortex and 75% in total rat brain; the anti-beta e was unable to immunoprecipitate any antigen. These antibodies indicate a region-dependent heterogeneity of beta subunits and should be useful for analyzing structure, function, and localization of GABAA receptor subtypes in brain.

Amino Acid Sequence↗

Regional variation in steroid anesthetic modulation of [35S]TBPS binding to gamma-aminobutyric acidA receptors in rat brain.

Steroids that enhance gamma-aminobutyric acid (GABA)A receptor function in the central nervous system allosterically modulate the binding of the convulsant chloride channel ligand [35S]-t-butyl bicyclophosphorothionate. When assayed in membrane homogenates and in tissue sections by autoradiography, concentration-dependence curves vary with respect to both brain region and the nature of the steroid. Alphaxalone and endogenous steroid hormone metabolites inhibit the binding of [35S]-t-butyl bicyclophosphorothionate in some regions, enhance it in others and give biphasic concentration-dependence in others, apparently the result of algebraic summation of two effects involving regional-dependent enhancement or inhibition. The alphaxalone effect is additive with that produced by adding GABA to the binding assays in some regions, but synergistic in other areas. Likewise, the effect of GABA is inhibited completely by saturating concentrations of the antagonist bicuculline methochloride in some areas but only partially in others, and completely or partially reversed by the convulsant benzodiazepine Ro5-4864, depending on region. The granule cell and molecular layers of cerebellum are particularly different in these allosteric interactions. The heterogeneity of binding behavior is consistent with the presence of multiple GABAA receptor subtypes in the brain. Regional variation in subunit gene expression apparently produces a family of hetero-oligomeric GABAA receptors with different biological and pharmacological properties, including qualitative and quantitative differences in modulation by neuroactive steroids.

Anesthetics↗

Immortalized hypothalamic GT1-7 neurons express functional gamma-aminobutyric acid type A receptors.

Neuronal cell lines provide a source of pure populations of neurons and allow the properties of many neurotransmitter receptors to be studied. However, none of these cells have been reported to express functional gamma-aminobutyric acid (GABA)A receptors. Indeed, there have been no reports of cell lines expressing functional amino acid receptors. Using biochemical and electrophysiological techniques, we have identified a neuronal cell line expressing functional GABAA receptors. Membranes from immortalized hypothalamic (GT1-7) neurons bound [3H]muscimol but not [3H]flunitrazepam. GABA-activated chloride currents, recorded from GT1-7 cells, were blocked by bicuculline and Zn2+ but were insensitive to diazepam. These results suggest that GABAA receptors on GT1-7 cells lack gamma subunits. The neurosteroid 5 alpha-pregnan-3 alpha-ol-20-one and pentobarbital both modulated GABAA receptors in these cells. Polymerase chain reaction analysis of the cells revealed the presence of mRNAs encoding alpha 1, beta 1, and beta 3 polypeptides. GT1-7 cells provide a useful model system for studying the regulation of GABAA receptor polypeptide expression.

Anesthetics↗

Taurine acts on a subclass of GABAA receptors in mammalian brain in vitro.

Taurine, an inhibitory amino acid, potently acts on a subclass of gamma-aminobutyric acid type A (GABAA) receptors. Taurine competitively inhibits [3H]muscimol binding to purified GABAA receptors with an average IC50 value of 50 microM, and enhances [3H]flunitrazepam binding to GABAA-linked benzodiazepine receptors with an EC50 of about 10 microM and with maximal extent lower than that for GABA. Taurine shows variable affinities (low micromolar to near millimolar) for muscimol binding sites in different brain regions as measured by autoradiography. The taurine-sensitive GABA sites are enriched in dentate gyrus, substantia nigra, cerebellum molecular layer, median thalamic nuclei, and hippocampal field CA3; these areas are also enriched in mRNA for the GABA-binding beta 2 subunit subtype. Taurine shows differential affinities for the multiple muscimol-GABA binding polypeptides present in purified GABAA receptors, notably a higher affinity for a beta 55 than a beta 58 polypeptide; these probably represent beta 2 and beta 3 clones, respectively. This work defines a significant target of taurine's inhibitory activity as some GABAA receptor GABA sites, lending support to the hypothesis that this endogenous substance may have a physiological action.

Affinity Labels↗