Extracellular alkaline transients mediated by glutamate receptors in the rat hippocampal slice are not due to a proton conductance

1994 ◽  
Vol 72 (4) ◽  
pp. 2031-2033 ◽  
Author(s):  
P. Paalasmaa ◽  
T. Taira ◽  
J. Voipio ◽  
K. Kaila
Keyword(s):  
Glutamate Receptors ◽  
Ampa Receptors ◽  
Hippocampal Slice ◽  
Aminobutyric Acid ◽  
Cation Channels ◽  
Ionic Mechanism ◽  
Synaptic Activation ◽  
Gamma Aminobutyric Acid ◽  
Proton Conductance ◽  
Ampa Receptor Channels

1. The ionic mechanism of extracellular alkaline transients mediated by alpha-amino-3-hydroxy-5-methylisoxazolate-4-propionic acid (AMPA) receptor channels was studied in the rat hippocampal slice (area CA1) by means of H(+)-, Ca(2+)- and Na(+)-selective microelectrodes. 2. Alkaline transients mediated by selective synaptic activation of AMPA receptors were coupled to a transient fall in extracellular Ca2+ ([Ca2+]o). 3. Removal of [Ca2+]o blocked the alkaline transient evoked by microinjection of AMPA, but had little effect on the simultaneous tetrodotoxin-resistant fall in extracellular Na+ ([Na+]o). 4. Alkaline transients evoked by microinjection of gamma-aminobutyric acid (GABA) were not affected by removal of [Ca2+]o. GABA had no effect on [Na+]o. 5. The present results indicate that activity-induced glutamatergic alkaline transients in the hippocampal slice are due to an influx of Ca2+, and not to a conductive movement of H+ ions across glutamate-gated cation channels.

scholarly journals Heterogeneity in expression of functional ionotropic glutamate and GABA receptors in astrocytes across brain regions: insights from the thalamus

2014 ◽  
Vol 369 (1654) ◽  
pp. 20130602 ◽  
Author(s):  
Simon Höft ◽  
Stephanie Griemsmann ◽  
Gerald Seifert ◽  
Christian Steinhäuser
Keyword(s):  
Ampa Receptors ◽  
Indirect Effects ◽  
Gaba Receptors ◽  
Brain Regions ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Functional Heterogeneity ◽  
Rt Pcr ◽  
Ventrobasal Thalamus ◽  
The Impact

Astrocytes may express ionotropic glutamate and gamma-aminobutyric acid (GABA) receptors, which allow them to sense and to respond to neuronal activity. However, so far the properties of astrocytes have been studied only in a few brain regions. Here, we provide the first detailed receptor analysis of astrocytes in the murine ventrobasal thalamus and compare the properties with those in other regions. To improve voltage-clamp control and avoid indirect effects during drug applications, freshly isolated astrocytes were employed. Two sub-populations of astrocytes were found, expressing or lacking α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. AMPA receptor-bearing astrocytes displayed a lower Kir current density than cells lacking the receptors. In contrast, all cells expressed GABA A receptors. Single-cell RT-PCR was employed to identify the receptor subunits in thalamic astrocytes. Our findings add to the emerging evidence of functional heterogeneity of astrocytes, the impact of which still remains to be defined.

Enflurane Directly Depresses Glutamate AMPA and NMDA Currents in Mouse Spinal Cord Motor Neurons Independent of Actions on GABAAor Glycine Receptors

2000 ◽  
Vol 93 (4) ◽  
pp. 1075-1084 ◽  
Author(s):  
Gong Cheng ◽  
Joan J. Kendig
Keyword(s):  
Spinal Cord ◽  
Nmda Receptor ◽  
Glutamate Receptors ◽  
Dorsal Horn ◽  
Motor Neurons ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Anesthetic Concentration

Background The spinal cord is an important anatomic site at which volatile agents act to prevent movement in response to a noxious stimulus. This study was designed to test the hypothesis that enflurane acts directly on motor neurons to inhibit excitatory synaptic transmission at glutamate receptors. Methods Whole-cell recordings were made in visually identified motor neurons in spinal cord slices from 1- to 4-day-old mice. Excitatory postsynaptic currents (EPSCs) or potentials (EPSPs) were evoked by electrical stimulation of the dorsal root entry area or dorsal horn. The EPSCs were isolated pharmacologically into glutamate N-methyl-d-aspartate (NMDA) receptor- and non-NMDA receptor-mediated components by using selective antagonists. Currents also were evoked by brief pulse pressure ejection of glutamate under various conditions of pharmacologic blockade. Enflurane was made up as a saturated stock solution and diluted in the superfusate; concentrations were measured using gas chromatography. Results Excitatory postsynaptic currents and EPSPs recorded from motor neurons by stimulation in the dorsal horn were mediated by glutamate receptors of both non-NMDA and NMDA subtypes. Enflurane at a general anesthetic concentration (one minimum alveolar anesthetic concentration) reversibly depressed EPSCs and EPSPs. Enflurane also depressed glutamate-evoked currents in the presence of tetrodotoxin (300 nm), showing that its actions are postsynaptic. Block of inhibitory gamma-aminobutyric acid A and glycine receptors by bicuculline (20 micrometer) or strychnine (2 micrometer) or both did not significantly reduce the effects of enflurane on glutamate-evoked currents. Enflurane also depressed glutamate-evoked currents if the inhibitory receptors were blocked and if either D,L-2-amino-5-phosphonopentanoic acid (50 micrometer) or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 micrometer) was applied to block NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptors respectively. Conclusions Enflurane exerts direct depressant effects on both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and NMDA glutamate currents in motor neurons. Enhancement of gamma-aminobutyric acid A and glycine inhibition is not needed for this effect. Direct depression of glutamatergic excitatory transmission by a postsynaptic action on motor neurons thus may contribute to general anesthesia as defined by immobility in response to a noxious stimulus.

Purification of Antihemophilic Factor (Factor VIII) by Amino Acid Precipitation*

1964 ◽  
Vol 11 (01) ◽  
pp. 064-074 ◽  
Author(s):  
Robert H Wagner ◽  
William D McLester ◽  
Marion Smith ◽  
K. M Brinkhous
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Factor Viii ◽  
Plasma Protein ◽  
Acid Precipitation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Specific Procedure ◽  
Beta Alanine ◽  
Antihemophilic Factor

Summary1. The use of several amino acids, glycine, alpha-aminobutyric acid, alanine, beta-alanine, and gamma-aminobutyric acid, as plasma protein precipitants is described.2. A specific procedure is detailed for the preparation of canine antihemophilic factor (AHF, Factor VIII) in which glycine, beta-alanine, and gammaaminobutyric acid serve as the protein precipitants.3. Preliminary results are reported for the precipitation of bovine and human AHF with amino acids.

A Simple Method for Preparing Fibrinogen

1966 ◽  
Vol 16 (01/02) ◽  
pp. 198-206 ◽  
Author(s):  
W Straughn ◽  
R. H Wagner
Keyword(s):  
Barium Sulfate ◽  
Caproic Acid ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Human Fibrinogen ◽  
Simple Method ◽  
High Yields ◽  
Marked Stability

SummaryA simple new procedure is reported for the isolation of canine, bovine, porcine, and human fibrinogen. Two molar β-alanine is used to precipitate fibrinogen from barium sulfate adsorbed plasma. The procedure is characterized by dependability and high yields. The material is 95% to 98% clottable protein but still contains impurities such as plasminogen and fibrin-stabilizing factor. Plasminogen may be removed by adsorption with charcoal. The fibrinogen preparations exhibit marked stability to freezing, lyophilization, and dialysis. Epsilon-amino-n-caproic acid and gamma-aminobutyric acid which were also studied have the property of precipitating proteins from plasma but lack the specificity for fibrinogen found with β-alanine.

Understanding Schizophrenia: Genetic Causes and Treatment

2019 ◽  
Vol 1 (1) ◽  
pp. 6-12
Author(s):  
Fatima Javeria ◽  
Shazma Altaf ◽  
Alishah Zair ◽  
Rana Khalid Iqbal
Keyword(s):  
Copy Number ◽  
Drug Targets ◽  
Disease Risk ◽  
Mental Disease ◽  
Copy Number Variants ◽  
Aminobutyric Acid ◽  
Epigenetic Mechanisms ◽  
Gamma Aminobutyric Acid ◽  
Wide Range ◽  
Severe Mental Disease

Schizophrenia is a severe mental disease. The word schizophrenia literally means split mind. There are three major categories of symptoms which include positive, negative and cognitive symptoms. The disease is characterized by symptoms of hallucination, delusions, disorganized thinking and speech. Schizophrenia is related to many other mental and psychological problems like suicide, depression, hallucinations. Including these, it is also a problem for the patient’s family and the caregiver. There is no clear reason for the disease, but with the advances in molecular genetics; certain epigenetic mechanisms are involved in the pathophysiology of the disease. Epigenetic mechanisms that are mainly involved are the DNA methylation, copy number variants. With the advent of GWAS, a wide range of SNPs is found linked with the etiology of schizophrenia. These SNPs serve as ‘hubs’; because these all are integrating with each other in causing of schizophrenia risk. Until recently, there is no treatment available to cure the disease; but anti-psychotics can reduce the disease risk by minimizing its symptoms. Dopamine, serotonin, gamma-aminobutyric acid, are the neurotransmitters which serve as drug targets in the treatment of schizophrenia. Due to the involvement of genetic and epigenetic mechanisms, drugs available are already targeting certain genes involved in the etiology of the disease.

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