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Biomedical subjects

A Hamberger

Publications and source records attributed to A Hamberger.

At least 91 records · Page 5Linked to original sources
PubMed1987

Free amino acids in the pre-retinal vitreous space. Effect of high potassium and nipecotic acid.

The pre-retinal vitreous space of the eye of albino rabbits was perfused in vivo via a dialysis probe in order to measure the concentration of endogenous amino acids. Studies of isotope concentrations in the vitreal effluent following intracarotid injections of 3HOH and [14C]mannitol demonstrated that entrance of 3HOH into the dialysis probe occurred within a few minutes whereas [14C]mannitol was almost completely excluded. Among the amino acids, analysed with high-pressure liquid chromatography (HPLC), glutamine had a concentration similar to that in plasma and cerebrospinal fluid (CSF). Taurine was four times higher than in the CSF. Perfusion with 125 mM KCl media increased particularly the taurine and phosphoethanolamine content. Nipecotic acid, a potent inhibitor of gamma-aminobutyric acid (GABA) uptake, increased GABA concentration over 60 times. In addition, it increased taurine levels by almost 10 times.

Alanine↗
PubMed1987

In vivo microdialysis studies on the effects of decortication and excitotoxic lesions on kainic acid-induced calcium fluxes, and endogenous amino acid release, in the rat striatum.

The in vivo effects of kainate (1 mM) on fluxes of 45Ca2+, and endogenous amino acids, were examined in the rat striatum using the brain microdialysis technique. Kainate evoked a rapid decrease in dialysate 45Ca2+, and an increase in the concentration of amino acids in dialysates in Ca2+-free dialysates. Taurine was elevated six- to 10-fold, glutamate two- to threefold, and aspartate 1.5- to twofold. There was also a delayed increase in phosphoethanolamine, whereas nonneuroactive amino acids were increased only slightly. The kainic acid-evoked reduction in dialysate 45Ca2+ activity was attenuated in striata lesioned previously with kainate, suggesting the involvement of intrinsic striatal neurons in this response. The increase in taurine concentration induced by kainate was slightly smaller under these conditions. Decortication did not affect the kainate-evoked alterations in either dialysate 45Ca2+ or amino acids. These data suggest that kainate does not release acidic amino acids from their transmitter pools located in corticostriatal terminals.

Amino Acids↗
PubMed1987

In vivo studies on the extracellular, and veratrine-releasable, pools of endogenous amino acids in the rat striatum: effects of corticostriatal deafferentation and kainic acid lesion.

The effects of corticostriatal deafferentation (decortication) and destruction of intrinsic neurons (intrastriatal kainate injection) on the extracellular concentration, and veratrine-releasable pools, of endogenous amino acids in the rat striatum were examined using the in vivo brain dialysis technique. Intracellular amino acid content was also determined. Decortication reduced selectively intra- and extracellular levels of glutamate (Glu) and aspartate (Asp). Extracellular changes were more pronounced than those in tissue content. gamma-Aminobutyric acid (GABA), taurine (Tau), and phosphoethanolamine (PEA) levels were not affected, whereas nonneuroactive amino acids were increased at 1 week but not at 1 month post-lesion. The intracellular pool of Glu and Asp was also reduced in kainate-lesioned striata. However, extracellular levels of these compounds were not affected significantly by this treatment. The tissue content of all other amino acids was decreased, the most prominent change being in the concentration of GABA. Extracellular GABA concentration was also reduced dramatically, whereas the concentrations of noneuroactive amino acids were increased to varying degrees. These data suggest that transmitter pools of neuroactive amino acids are an important supply for their extracellular pools. Lesion-induced alterations in nonneuroactive amino acids are discussed with regard to the loss of metabolic pools, glial reactivity, and changes in blood-brain barrier transport. Veratrine induced a massive release of neuroactive amino acids such as Glu, Asp, GABA, and Tau into the extracellular fluid, and a delayed increase in PEA. Extracellular levels of neuroactive amino acids were raised slightly. Decortication reduced, selectively, the amounts of Glu and Asp released by veratrine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1987

Cellular origins of endogenous amino acids released into the extracellular fluid of the rat striatum during severe insulin-induced hypoglycemia.

The effect of severe insulin-induced hypoglycemia on the extracellular levels of endogenous amino acids in the rat striatum was examined using the brain microdialysis technique. A characteristic pattern of alterations consisting of a 9-12-fold increase in aspartate (Asp), and more moderate increases in glutamate (Glu), taurine (Tau), and gamma-aminobutyric acid (GABA), was noted following cessation of electroencephalographic activity (isoelectricity). Glutamine (Gln) levels were reduced both during and after the isoelectric period and there was a delayed increase in extracellular phosphoethanolamine (PEA) content. The effects of decortication and excitotoxin lesions on the severe hypoglycemia-evoked efflux of endogenous amino acids in the striatum were also examined. Decortication reduced the release of Glu and Asp both 1 week and 1 month post-lesion. The efflux of other neuroactive amino acids was not affected significantly. In contrast, GABA, Tau, and PEA efflux was attenuated in kainate-lesioned striata. Glu and Asp release was also reduced under these conditions, and a smaller decrease in extracellular Gln was noted. These data suggest that GABA, Glu, and Asp are released primarily from their transmitter pools during severe hypoglycemia. The releasable pools of Tau and PEA appear to be located in kainate-sensitive striatal neurons. The significance of these results is discussed with regard to the excitotoxic theory of hypoglycemic cell death.

Amino Acids↗
PubMed1986

Effects of kynurenic acid on evoked extracellular field potentials in the rat olfactory bulb in vivo.

The effects of excitatory amino acid antagonists on extracellular field potentials in the olfactory bulb produced by lateral olfactory tract stimulation were analyzed in vivo. The two compounds tested, D-2-amino-5-phosphonovalerate and kynurenic acid, were administered by brain dialysis. Only kynurenic acid was able to effectively suppress the monosynaptic excitation of the major class of interneurons, the granule cells. This pharmacological profile suggests the involvement of non-NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1986

Blockade of N-methyl-D-aspartate-sensitive acidic amino acid receptors inhibits ischemia-induced accumulation of purine catabolites in the rat striatum.

The effect of blocking N-methyl-D-aspartate (NMDA)-sensitive excitatory amino acid (EAA) receptors during brain ischemia was studied in order to test a link between EAAs and neuronal energy metabolism. The receptors were blocked unilaterally in the rat striatum before, during and after an ischemic insult. The receptor blocker, D-2-amino-5-phosphonovalerate (D-APV) was administered by dialysis perfusion, which also allowed continuous sampling for analysis of adenosine triphosphate degradation products, i.e. purine catabolites, in control and D-APV-treated striata. Purine catabolites were analysed with reversed-phase liquid chromatography. Hypoxanthine, xanthine, inosine and adenosine increased dramatically in the striatum during ischemia and reached maximum levels during early reperfusion. D-APV reduced the extracellular accumulation of all measured purine catabolites during ischemia/reflow and improved to some extent the recovery of the striatal electroencephalographic activity in the majority of the animals. The results suggest that NMDA receptor blockade attenuates acute changes in energy metabolism during ischemia.

2-Amino-5-phosphonovalerate↗
PubMed1986

Ouabain-induced changes in extracellular aspartate, glutamate and GABA levels in the rabbit olfactory bulb in vivo.

The effect of ouabain on extracellular amino acid levels was investigated in the rabbit olfactory bulb using brain dialysis. Extracellular field potentials, elicited by stimulation of the lateral olfactory tract (LOT), were recorded simultaneously. Ouabain (100 microM) induced a rapid increase in extracellular aspartate, glutamate and gamma-aminobutyric acid. LOT-evoked potentials changed concomitantly, suggesting a neuronal depolarization.

Amino Acids↗
PubMed1986

Extracellular calcium in the hippocampus of unanesthetized rabbits monitored with dialysis-perfusion.

Extracellular levels of Ca2+ in the rabbit hippocampus were investigated in vivo with perfusion-dialysis. A thin semipermeable tubing was implanted and perfused at a constant rate with a Ca2+-free medium. Ca2+ levels in the dialysate were measured with an ion-specific electrode or as radioactivity after labeling of the endogenous pool with 45CaCl2. The system was characterized with model studies. The usefulness of the method is demonstrated for studies of, for example chemically evoked changes in Ca2+ concentrations extracellularly in CNS regions of non-anesthetized, freely moving rabbits. Moreover, measurements of Ca2+ changes are easily correlated with neurotransmitter levels in the same samples.

Animals↗
PubMed1986

An analysis of the effects of excitatory amino acid receptor antagonists on evoked field potentials in the olfactory bulb.

The effects of excitatory amino acid antagonists on extracellular field potentials in the olfactory bulb produced by lateral olfactory tract stimulation were analysed in vivo. The compounds tested D-2-amino-5-phosphonovalerate, L-(+)2-amino-4-phosphonobutyrate, gamma-D-glutamylglycine, L-glutamic acid diethylester and cis-2,3-piperidine dicarboxylic acid, were administered by brain dialysis. Of the compounds tested, only cis-2,3 piperidine-dicarboxylic acid and gamma-D-glutamylglycine were able to suppress the synaptic excitation of granule cells. This pharmacological profile suggests the involvement of non-N-methyl-D-aspartate receptors. However, the suppression was accompanied by a reduction in the amplitude of the presynaptic volley. A second finding was that D-2-amino-5-phosphono-valerate and gamma-D-glutamyl glycine attenuated granule cell mediated inhibition of mitral cells, suggesting the involvement of N-methyl-D-aspartate-sensitive receptors. The possibility that mitral cells and that either centrifugal fibres, or an intrinsic olfactory bulb feedback loop might use an excitatory amino acid as its neurotransmitter is therefore discussed.

2-Amino-5-phosphonovalerate↗
PubMed1986

Effects of kainic acid on brain calcium fluxes studied in vivo and in vitro.

The effect of in vivo administration of kainic acid into the rabbit hippocampus was studied with brain dialysis and subsequent determination of the Ca2+ concentration in the dialysate. When included in the perfusing medium, kainic acid as well as veratridine induced a decrease in extracellular Ca2+. The effect of kainic acid (but not of veratridine) was insensitive to tetrodotoxin. In vitro studies revealed no effect of kainic acid on 45Ca2+ uptake by isolated astrocytes, but showed an enhancement of synaptosomal 45Ca2+ accumulation. This was, however, only 25% of the stimulatory effect of high K+ depolarization. Glutamate activated synaptosomal Ca2+ uptake, whereas dihydrokainate had no effect. The uptake evoked by kainate and glutamate was independent of the K+ level in the medium which indicates the involvement of other than voltage-sensitive Ca2+ channels. The results confirm previous finding that kainic acid promotes the uptake of Ca2+ in brain cells. Kainate affects Ca2+ fluxes pre- and postsynaptically. Presynaptic Ca2+ influx may be mediated by chemically gated mechanisms.

Animals↗
PubMed1986

Chronic effects of dichloromethane on amino acids, glutathione and phosphoethanolamine in gerbil brain.

Mongolian gerbils were exposed to dichloromethane for three months by continuous inhalation at 210 ppm. Total free tissue amino acids, glutathione, and phosphoethanolamine were determined in the vermis posterior of the cerebellum and the frontal cerebral cortex. These two brain areas were chosen because humans occupationally exposed to dichloromethane have shown abnormalities in the electroencephalogram of the frontal part of the cerebral cortex. This study showed that long-term exposure of gerbils to dichloromethane (210 ppm) for three months leads to decreased levels of glutamate, gamma-aminobutyric acid, and phosphoethanolamine in the frontal cerebral cortex, while glutamine and gamma-aminobutyric acid are elevated in the posterior cerebellar vermis.

Amino Acids↗
PubMed1986

Chronic effects of perchloroethylene and trichloroethylene on the gerbil brain amino acids and glutathione.

Mongolian gerbils were exposed for 12 months to trichloroethylene (TCE) 50 or 150 ppm or perchloroethylene (PCE) 120 ppm. Vermis posterior of cerebellum and hippocampus were used for measurement of high-affinity uptake and release of 3H-gamma-aminobutyric acid (GABA) and 14C-glutamate, as well as for determination of total free tissue amino acids and glutathione. Glutathione was significantly elevated in the hippocampus of animals exposed to 150 ppm or TCE. Levels of amino acids were not appreciably affected. After PCE exposure, 120 ppm for 12 months, taurine significantly decreased in the hippocampus and even more in the posterior part of the cerebellar vermis. Glutamine was elevated in the hippocampus. No other significant changes in amino acids or glutathione were observed. After exposing the animals to TCE (50 and 150 ppm) for 12 months, the accumulation of glutamate by the posterior part of the cerebellar vermis increased in a dose-dependent manner, but no significant changes were observed in the hippocampus. The uptake of glutamate and GABA in cerebellum and hippocampus were unaffected after PCE exposure to 120 ppm for 12 months. The potassium-stimulated release of glutamate and GABA was unaffected in hippocampal tissue slices from gerbils exposed to 50 and 150 ppm TCE.

Amino Acids↗
PubMed1985

Effects of status epilepticus on extracellular amino acids in the hippocampus.

Extracellular amino acids were followed in the hippocampus during sustained seizures induced by systemic administration of kainic acid (KA) or bicuculline (BC). KA epilepsy was associated with marked increases in phosphoethanolamine (PEA) and taurine. Alanine and ethanolamine were moderately raised while other amino acids were unaffected. BC seizures encompassed a slightly different pattern of alterations. In contrast to KA seizures, BC epilepsy had no effect on taurine. Significant increments were observed for PEA and alanine while elevations of ethanolamine were subtle. In both types of seizures, glutamate and GABA remained unaffected extracellularly, probably due to efficient recapture mechanisms.

Amino Acids↗
PubMed1985

Kainic acid-induced changes of extracellular amino acid levels, evoked potentials and EEG activity in the rabbit olfactory bulb.

The effect of kainic acid (KA) on the extracellular content of amino acids in the rabbit olfactory bulb was investigated, both in vivo with the brain dialysis technique and in vitro with a superfused tissue slice preparation. Olfactory bulb EEG activity and lateral olfactory tract (LOT)-evoked field potentials were monitored simultaneously during dialysis experiments. KA induced a rapid (within 5 min) increase of extracellular aspartate, glutamate, GABA, phosphoethanolamine and taurine in vivo. LOT-evoked potentials were altered concomitantly in a concentration- and time-dependent manner. The antidromic invasion of mitral/tufted cells was depressed and the synaptic activation of granule cells was abolished in the presence of KA. Olfactory bulb EEG activity was also affected. Oscillatory bursts in olfactory bulb EEG were abolished by 10 mM in most experiments, whereas sustained oscillations were induced by 1 mM KA. The effects of KA may partly be due to a blockade of amino acid reuptake since dihydrokainate (DKA) perfusion was found to increase extracellular aspartate and glutamate. However, DKA had no significant effect on EEG or evoked potentials. In vitro, aspartate and glutamate were selectively increased during KA perfusion.

Amino Acids↗
PubMed1985

Metabolically derived aspartate--elevated extracellular levels in vivo in lodoacetate poisoning.

Glycolysis was blocked in the hippocampus of the otherwise unaffected rabbit by perfusion of a previously implanted thin dialysis tube with a medium containing 0.1 mM iodoacetate. The perfusate from the dialysis tube was analyzed for free amino acids with liquid chromatographic separation of ortophthaldialdehyde derivatives. The data were used to calculate approximate levels of extracellular amino acids. Within 15 min after the beginning of iodoacetate perfusion, extracellular aspartate increased measurably, and the increase was tenfold within less than 2 hr. Although most other amino acids were unaffected, an elevation of taurine, phosphoethanolamine, and ethanolamine was observed with a delay of 30-40 min after the effect on aspartate.

Amino Acids↗
PubMed1985

Ischemia-induced shift of inhibitory and excitatory amino acids from intra- to extracellular compartments.

Brain ischemia was induced for 10 or 30 min by clamping the common carotid arteries in rabbits whose vertebral arteries had previously been electrocauterized. EEG and tissue content of high energy phosphates were used to verify the ischemic state and to evaluate the degree of postischemic recovery. Extracellular levels and total contents of amino acids were followed in the hippocampus during ischemia and 4 h of recirculation. At the end of a 30-min ischemic period, GABA had increased 250 times, glutamate 160 times, and aspartate and taurine 30 times in the extracellular phase. The levels returned to normal within 30 min of reflow. A delayed increase of extracellular phosphoethanolamine and ethanolamine peaked after 1-2 h of reflow. Ten minutes of ischemia elicited considerably smaller but similar effects. With respect to total amino acids in the hippocampus, glutamate and aspartate decreased to 30-50% of control while GABA appeared unaffected after 4 h of reflow. Alanine, valine, phenylalanine, leucine, and isoleucine increased severalfold. The importance of toxic extracellular levels of excitatory amino acids, as well as of high extracellular levels of inhibitory amino acids, are considered in relation to the pathophysiology of neuronal cell loss during cerebral ischemia.

Amino Acids↗
PubMed1985

In vivo studies on amino acid transmitters in the central auditory system of the guinea pig.

The extracellular concentrations of endogenous amino acids were measured in vivo in the guinea pig cochlear nucleus during sound stimulation. The purpose was to explore whether certain amino acids might be employed as neurotransmitters by the auditory nerve. A dialysis sampling probe was used to collect a dialysate of the cochlear nucleus. The amino acids were determined fluorometrically after precolumn derivation and high-performance liquid chromatography separation. A short pulse of p-chloromercuryphenylsulfonate (p-CMS) was used to reduce the reuptake of amino acids. The concentration of glutamic and aspartic acid increased twofold to threefold during sound stimulation, while gamma-aminobutyric acid was unaffected. The results support a role for glutamic and/or aspartic acids as neurotransmitters in the auditory nerve.

4-Chloromercuribenzenesulfonate↗