Calcium-independent release of amino acid neurotransmitters: Fact or artifact?

https://doi.org/10.1016/0301-0082(92)90035-DGet rights and content

First page preview

First page preview
Click to open first page preview

References (508)

  • S. Barnes et al.

    The effects of calcium channel agonists and antagonists on the release of endogenous glutamate from cerebellar slices

    Neurosci. Lett.

    (1988)
  • S. Barnes et al.

    Effects of potassium channel blockade on endogenous glutamate release from cerebellar slices

    Brain Res.

    (1989)
  • B.A. Barres et al.

    Glial and neuronal forms of the voltage-dependent sodium channel: Characteristics and cell-type distribution

    Neuron

    (1989)
  • B.A. Barres et al.

    Ion channel expression by white matter glia: the O-2A glial progenitor cell

    Neuron

    (1990)
  • S. Bernath et al.

    Characterization of [3H]GABA release from striatal slices: Calcium-independent process via the GABA uptake system

    Neuroscience

    (1988)
  • S. Bernath et al.

    Dopamine may influence striatal GABA release via three separate mechanisms

    Brain Res.

    (1989)
  • S. Bernath et al.

    Calcium-independent release from rat striatal slices: the role of calcium channels

    Neuroscience

    (1990)
  • S. Bernath et al.

    Release of endogenous GABA can occur through CA2+-dependent and Ca2+-independent processes

    Neurochem. Int.

    (1989)
  • J.-L. Bossu et al.

    Patch-clamp study of the tetrodotoxin-resistant sodium current in group C sensory neurones

    Neurosci. Lett.

    (1984)
  • R.W. Brosemer

    Effects of inhibitors of Na+,K+-ATPase on the membrane potentials and neurotransmitter efflux in rat brain slices

    Brain Res.

    (1985)
  • P.M. Burger et al.

    Synaptic vesicles immunoisolated from rat cerebral cortex contain high levels of glutamate

    Neuron

    (1989)
  • S.P. Burke et al.

    Effects of glucose deficiency on glutamate/aspartate release and excitatory synaptic responses in the hippocampal CA1 area in vitro

    Brain Res.

    (1989)
  • P. Campochiaro et al.

    Excitatory amino acid analogs evoke release of endogenous amino acids and acetylcholine from chick retina in vitro

    Vision Res.

    (1985)
  • C.M. Carvalho et al.

    γ-Aminobutyric acid release from synaptosomes as influenced by Ca2+ and Ca2+ channel blockers

    Eur. J. Pharmac.

    (1986)
  • W.A. Catterall

    Activation of the action potential Na+ ionophore of cultured neuroblastoma cells by veratridine and batrachotoxin

    J. biol Chem.

    (1975)
  • H.H. Chang et al.

    Depolarization-induced release of g-glutamic acid from isolated-released synaptic membrane vesicles

    Biochim. biophys. Acta

    (1984)
  • M.P. Charlton et al.

    Modulation of transmitter release by intracellular sodium in squid giant synapse

    Brain Res.

    (1977)
  • M. Clark et al.

    Release of endogenous glutamate from rat cerebellar synaptosomes-interactions with adenosine and ethanol

    Life Sci.

    (1989)
  • J.R. Cunningham et al.

    GABA release from Xenopus retina does not correlate with horizontal cell membrane potential

    Neuroscience

    (1988)
  • A. Cupello et al.

    Evaluation of the electrophysiological consequences of GABA removal from the synaptic cleft by Na+ ion transport-coupled neuronal uptake

    Brain Res.

    (1985)
  • R.W.P. Cutler et al.

    Release of [3H]GABA and [14C]glutamic acid from rat cortex slices: the relationship between the tissue pool size and rates of spontaneous and electrically induced release

    Brain Res.

    (1975)
  • R.W.P. Cutler et al.

    Efflux of amino acid neurotransmitters from rat spinal cord slices. I. Factors influencing the spontaneous efflux of [14C]glycine and 3H-GABA

    Brain Res.

    (1971)
  • A.A. Abdel-Latif

    Calcium-mobilizing receptors, phosphoinositides and the generation of second messengers

    Pharmac. Rev.

    (1986)
  • M. Abe et al.

    On the existence of two GABA pools associated with newly synthesized GABA and with newly taken up GABA in nerve terminals

    Neurochem. Res.

    (1983)
  • R. Adair et al.

    Studies of the uptake and release of [3H]β-alanine by frog spinal slices

    J. Neurochem.

    (1977)
  • C.-D. Agardh et al.

    Severe hypoglycemia leads to accumulation of arachidonic acid in brain tissue

    Acta physiol. scand.

    (1980)
  • E. Agardh et al.

    The release of [3H]GABA from the rabbit retina

    Acta physiol. scand.

    (1984)
  • J. Albrecht et al.

    Enhanced potassium-stimulated γ-aminobutyric acid release by astrocytes derived from rats with early hepatogenic encephalopathy

    J. Neurochem.

    (1987)
  • J. Albrecht et al.

    The Na+/K+ ATPase activity and GABA uptake in astroglial cell-enriched fractions and synaptosomes derived from rats in the early stage of experimental hepatogenic encephalopathy

    Acta neurol. scand.

    (1985)
  • W. Almers et al.

    Non-selective conductance in calcium channels of frog muscle: Calcium selectivity in a single-file pore

    J. Physiol., Lond.

    (1984)
  • W. Almers et al.

    A non-selective cation conductance in frog muscle membrane blocked by micromolar external calcium ions

    J. Physiol., Lond.

    (1984)
  • M.C. Aragón et al.

    Depolarization-induced release of glycine and β-alanine from plasma membrane vesicles derived from rat brain synaptosomes

    Biochim. biophys. Acta

    (1988)
  • J.T. Archibald et al.

    Rapid reversal of internal Na+ and K+ of synaptosomes by ouabain

    Nature

    (1974)
  • C. Arias et al.

    Differential calcium dependence of γaminobutyric acid and acetylcholine release in mouse brain synaptosomes

    J. Neurochem.

    (1986)
  • C. Arias et al.

    Stimulation of [3H]γ-aminobutyric acid release by calcium chelators in synaptosomes

    J. Neurochem.

    (1984)
  • C.K. Atterwill et al.

    Characterization of Na+, K+-ATPase in cultured and separated neuronal and glial cells from rat cerebellum

    J. Neurochem.

    (1984)
  • G.S. Ayoub et al.

    The release of γ-aminobutyric acid from horizontal cells of the goldfish (Carassius auratio) retina

    J. Physiol., Lond.

    (1984)
  • P.F. Baker et al.

    A note on the mechanism by which inhibitors of the sodium pump accelerate spontaneous release of transmitter from motor nerve terminals

    J. Physiol., Lond.

    (1975)
  • V.J. Balcar et al.

    The structural specificity of the high affinity uptake of l-glutamate and l-spartate by rat brain slices

    J. Neurochem.

    (1972)
  • V.J. Balcar et al.

    High affinity uptake of l-glutamate and l-aspartate by glial cells

    J. Neurochem.

    (1977)
  • Cited by (174)

    • Presynaptic CaMKIIα modulates dopamine D3 receptor activation in striatonigral terminals of the rat brain in a Ca<sup>2+</sup> dependent manner

      2013, Neuropharmacology
      Citation Excerpt :

      In this study we evaluated whether procedures that markedly enhance cytoplasmic Ca2+ modify the effects of activating D3Rs in the striatal projections to the SNr via a CaMKIIα-mediated process. We concentrated, mostly, on the effects of K+-induced depolarization because this procedure triggers Ca2+-dependent transmitter release that is akin to the naturally occurring process (Bernath, 1992). Furthermore, K+ depolarization of neuronal cultures leads to CaMKIIα accumulation near active zones (AZs) (Tao-Cheng et al., 2006).

    • GABA<inf>B</inf> receptors modulate depolarization-stimulated [<sup>3</sup>H]glutamate release in slices of the pars reticulata of the rat substantia nigra

      2010, European Journal of Pharmacology
      Citation Excerpt :

      The depolarization caused by the high K+ concentration releases glutamate from the nerve terminals and glial cells (Bernath, 1992). Because the release of the glutamate from the glial cells is not Ca2+-dependent (Bernath, 1992), the strong Ca2+ dependency (Fig. 1) suggests that, under the present conditions, the [3H]glutamate was released mainly from the nerve terminals. The presence of dihydrokainic acid during incubation of the slices would have reduced the uptake of the [3H]glutamate into the glial cells (Kawahara et al., 2002; Bernardinelli and Chatton, 2008), thereby reducing the release from glial cells caused by the high K+ solution.

    View all citing articles on Scopus
    View full text