Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Comparison of Two Superfusion Systems for Study of Neurotransmitter Release from Rat Cerebral Cortex Slices (1984)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 43 (1984), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Depolarization-induced release of [3H]γ-aminobutyric acid (GABA) and [3H]noradrenaline (NA) from rat cerebral cortex slices was studied in two superfusion systems: one with stationary and the other one with continuously shaken slice compartments. Calcium-dependent depolarization-induced release of GABA and NA could be demonstrated only with shaken slices. GABA, but not NA, could also be released by high K + media and veratridine from stationary slices. Synaptic transmitterreleasing mechanisms are apparently damaged in stationary slices, possibly due to impaired energy metabolism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1984.tb06701.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Hypotaurine Uptake by Brain Slices from Adult and 8-Day-Old Mice (1980)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 35 (1980), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Uptake of [35S]hypotaurine by brain slices prepared from adult and 8-day-old mice was studied at varying temperatures, under O2 and N2 atmospheres, and in the presence of metabolic inhibitors and varying concentrations of hypotaurine in the incubation medium. The tissue/medium concentration gradients generated were exceptionally high for an amino acid. Hypotaurine uptake was energy- and temperature-dependent, more strictly in adult mice. Uptake was saturable, containing a high-affinity and a low-affinity component. The estimated transport constants for the high-affinity uptake of hypotaurine (8-day-old mice, 17.2 μ mol/liter; adults, 35.3 μ mol/liter) were of the same order of magnitude as the reported transport constants of putative amino acid transmitters, but the total transport capacity appears to be greatest for hypotaurine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1980.tb09002.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Cation Dependence of Hypotaurine Uptake in Mouse Brain Slices (1981)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 37 (1981), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Mouse brain slices take up hypotaurine (2-aminoethanesulphinic acid) from medium by means of two concentrative low- and high-affinity transport systems. [35S]Hypotaurine uptake by the slices was significantly reduced in the absence of external potassium, calcium, or magnesium ions. An excess of potassium ions also inhibited hypotaurine uptake by one-half. Uptake was almost completely abolished on removal of sodium ions. The Km constants for both low- and high-affinity transport components increased in a low-sodium medium, suggesting that sodium ions are required when hypotaurine is attached to its possible carrier sites in plasma membranes. Sodium ions also mimicked allosteric effectors of hypotaurine transport, showing positive cooperativity. More than two sodium ions may be involved in the transport of one hypotaurine molecule across the cell membrane. The calculated activation energies of transport were fairly similar in normal and sodium-deficient media and thus sodium ions may not participate in the activation mechanisms of the transport. With respect to cation dependence, hypotaurine transport in brain slices exhibits features characteristic of neurotransmitter amino acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1981.tb00455.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Taurine release modified by GABAergic agents in hippocampal slices from adult and developing mice (2000)
    Springer
    Amino acids 18 (2000), S. 17-30 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids – Taurine release – GABA receptors – Hippocampal slices – Adult – Developing mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. In order to characterize the possible regulation of taurine release by GABAergic terminals, the effects of several agonists and antagonists of GABA receptors on the basal and K+-stimulated release of [3H]taurine were investigated in hippocampal slices from adult (3-month-old) and developing (7-day-old) mice using a superfusion system. Taurine release was concentration-dependently potentiated by GABA, which effect was reduced by phaclofen, saclofen and (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA) at both ages, suggesting regulation by both GABAB and GABAC receptors. The involvement of GABAA receptors could not be excluded since the antagonist bicuculline was able to affect both basal and K+-evoked taurine release. Furthermore, several GABAB receptor effectors were able to inhibit K+-stimulated taurine release in the adults, while the GABAC receptor agonists trans-4-aminocrotonic acid (TACA) and cis-4-aminocrotonic acid (CACA) potentiated this release. The potentiation of taurine release by agents acting on the three types of GABA receptors in both adult and developing hippocampus further indicates the involvement of transporters operating in an outward direction. This inference is corroborated by the moderate but significant inhibition of taurine uptake by the same compounds.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260050002
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Taurine and neural cell damage (2000)
    Springer
    Amino acids 19 (2000), S. 509-526 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids – Taurine – Cell-damaging conditions – Ischemia – Brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The inhibitory amino acid taurine is an osmoregulator and neuromodulator, also exerting neuroprotective actions in neural tissue. We review now the involvement of taurine in neuron-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress, and the presence of free radicals, metabolic poisons and an excess of ammonia. The brain concentration of taurine is increased in several models of ischemic injury in vivo. Cell-damaging conditions which perturb the oxidative metabolism needed for active transport across cell membranes generally reduce taurine uptake in vitro, immature brain tissue being more tolerant to the lack of oxygen. In ischemia nonsaturable diffusion increases considerably. Both basal and K+-stimulated release of taurine in the hippocampus in vitro is markedly enhanced under cell-damaging conditions, ischemia, free radicals and metabolic poisons being the most potent. Hypoxia, hypoglycemia, ischemia, free radicals and oxidative stress also increase the initial basal release of taurine in cerebellar granule neurons, while the release is only moderately enhanced in hypoxia and ischemia in cerebral cortical astrocytes. The taurine release induced by ischemia is for the most part Ca2+-independent, a Ca2+-dependent mechanism being discernible only in hippocampal slices from developing mice. Moreover, a considerable portion of hippocampal taurine release in ischemia is mediated by the reversal of Na+-dependent transporters. The enhanced release in adults may comprise a swelling-induced component through Cl− channels, which is not discernible in developing mice. Excitotoxic concentrations of glutamate also potentiate taurine release in mouse hippocampal slices. The ability of ionotropic glutamate receptor agonists to evoke taurine release varies under different cell-damaging conditions, the N-methyl-D-aspartate-evoked release being clearly receptor-mediated in ischemia. Neurotoxic ammonia has been shown to provoke taurine release from different brain preparations, indicating that the ammonia-induced release may modify neuronal excitability in hyperammonic conditions. Taurine released simultaneously with an excess of excitatory amino acids in the hippocampus under ischemic and other neuron-damaging conditions may constitute an important protective mechanism against excitotoxicity, counteracting the harmful effects which lead to neuronal death. The release of taurine may prevent excitation from reaching neurotoxic levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070003
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Uptake of leucine, lysine, aspartic acid, and glycine into isolated neurons and astrocytes (1981)
    Springer
    Neurochemical research 6 (1981), S. 873-884 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The uptake of tritium-labeledl-leucine,l-lysine,l-aspartic acid, and glycine by neurons and astrocytes isolated from the cerebral cortex of 3-week-old rats was followed for varying periods up to 40 min at amino acid concentrations from 1 to 2000 μmol/liter in medium. The effects of a low-sodium (15.5 mmol/liter) medium on the uptake were also studied. The influx of the amino acids was faster into astrocytes than into neurons. Leucine penetrated into the cells faster than the other amino acids. Amino acid transport was mainly saturable at the lowest amino acid concentrations studied, whereas nonsaturable penetration into the cells dominated in the millimolar concentration range. The saturable transport comprised only one transport system with relatively small transport constants, resembling in nature the so-called high-affinity transport. The maximal velocities of transport were about two times higher in astrocytes than in neurons. In neurons the partial substitution of sodium by choline in medium had the most effect in reducing the influx of glycine and aspartic acid. In astrocytes the effects were generally less pronounced. The results suggest that extracellular amino acids generally penetrate more readily into astrocytes than into neurons. Both cell types transport essential amino acids more effectively than other amino acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00965045
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Hypotaurine transport in brain slices (1981)
    Springer
    Neurochemical research 6 (1981), S. 1179-1191 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hypotaurine uptake was compared to taurine and GABA uptakes in brain slices under identical experimental conditions. The slices effectively concentrated both hypotaurine and GABA from the medium, whereas taurine was taken up more slowly. The uptakes of these three structurally related amino acids were all saturable, consisting of one low-and one high-affinity transport component. The kinetic parameters of hypotaurine uptake were of the same order of magnitude as those of GABA uptake. All uptake systems were sensitive to temperature, metabolic poisons, and sodium omission. Hypotaurine uptake was inhibited by GABA,l-2,4-diaminobutyric acid (l-DABA), cysteic acid, and β-alanine, but not by taurine. Taurine uptake was strongly reduced by hypotaurine, β-alanine, andl-DABA, as well as by GABA, whereas GABA uptake was affected only by cystamine,l-DABA, and nipecotic acid. The uptake processes of hypotaurine, taurine, and GABA were thus fairly similar and showed properties characteristic for neurotransmitter uptake. Hypotaurine uptake resembled more GABA than taurine uptake. The present inhibition studies suggest that there may exist only one common two-component transport system for these three amino acids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00966676
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Mechanisms of L-Cysteine Neurotoxicity (2000)
    Springer
    Neurochemical research 25 (2000), S. 1397-1405 
    Details
    ISSN: 1573-6903
    Keywords: L-Cysteine ; neurotoxicity ; N-methyl-D-aspartate receptors ; free radicals ; catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We review here the possible mechanisms of neuronal degeneration caused by L-cysteine, an odd excitotoxin. L-Cysteine lacks the omega carboxyl group required for excitotoxic actions via excitatory amino acid receptors, yet it evokes N-methyl-D-aspartate (NMDA) -like excitotoxic neuronal death and potentiates the Ca2+ influx evoked by NMDA. Both actions are prevented by NMDA antagonists. One target for cysteine effects is thus the NMDA receptor. The following mechanisms are discussed now: (1) possible increase in extracellular glutamate via release or inhibition of uptake/degradation, (2) generation of cysteine α-carbamate, a toxic analog of NMDA, (3) generation of toxic oxidized cysteine derivatives, (4) chelation of Zn2+ which blocks the NMDA receptor-ionophore, (5) direct interaction with the NMDA receptor redox site(s), (6) generation of free radicals, and (7) formation of S-nitrosocysteine. In addition to these, we describe another new alternative for cytotoxicity: (8) generation of the neurotoxic catecholamine derivative, 5-S-cysteinyl-3,4-dihydroxyphenylacetate (cysdopac).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007616817499
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Mutual interactions in the transport of taurine, hypotaurine, and GABA in brain slices (1983)
    Springer
    Neurochemical research 8 (1983), S. 1377-1387 
    Details
    ISSN: 1573-6903
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mutual interactions and the effects of GABA on the saturable transport components of taurine and hypotaurine were investigated with mouse brain slices. The low-affinity taurine transport was competitively inhibited by both hypotaurine and GABA. Hypotaurine did not alter the kinetic parameters of high-affinity taurine uptake, whereas there occurred some stimulation with GABA, possibly by heteroexchange. Taurine had no significant effects on high-affinity hypotaurine uptake, whereas the low-affinity component was reduced by both taurine and GABA. GABA strongly interfered with the high-affinity hypotaurine uptake, being the preferred substrate in simultaneous uptake experiments. The results confirm that taurine, hypotaurine, and GABA are transported into brain slices by only one two-component system with affinities highest for GABA and lowest for taurine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964995
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Sodium-independent taurine binding to brain synaptic membranes (1983)
    Springer
    Cellular and molecular neurobiology 3 (1983), S. 183-187 
    Details
    ISSN: 1573-6830
    Keywords: taurine ; synaptic membranes ; sodium-independent binding ; postsynaptic receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Saturable sodium-independent taurine binding to mouse and rat brain synaptic membranes was exposed after two freezing-thawing cycles combined with Triton X-100 treatments. 2. The amount of saturable taurine binding was fairly low but was enhanced after depletion of brain taurine. 3. Saturable taurine binding was displaceable by some convulsants and anticonvulsants but its specificity still remains to be established.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00735281
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...