Elsevier

Neuroscience

Volume 4, Issue 9, September 1979, Pages 1255-1263
Neuroscience

Calcium-dependent release of d-[3H]aspartate evoked by selective electrical stimulation of excitatory afferent fibres to hippocampal pyramidal cells in vitro

https://doi.org/10.1016/0306-4522(79)90155-6Get rights and content

Abstract

Selective electrical stimulation of CA1 excitatory afferent fibres in the stratum radiatum of a transverse slice of the hippocampus released d-[3H]aspartate in a stimulus dependent manner, d-aspartate being used to mimic endogenous l-glutamate. The release fulfilled several of the requirements for neurotransmitter identification in as much as it was Ca2+-dependent and specific. Neither [3H]γ-aminobutyrate nor l-[3H]leucine were released in response to stimulation. The stimulus dependent release of d-[3H]aspartate could also be demonstrated in an isolated preparation of the hippocampal slice containing the CA3/CA1 region, but devoid of the area dentata and subiculum. A cut carefully placed in the isolated CA3/CA1 slice dividing all CA1 afferents coursing through the stratum radiatum, without sectioning the pyramidal layer nor the stratum oriens/alveus, abolished the stimulus-evoked release of d-[3H]aspartate.

The results, together with previous work, favour l-glutamate as the neurotransmitter of the Schaffer collaterals of the CA3 pyramidal cells.

References (48)

  • SchwartzkroinP.A. et al.

    Cellular and field potential properties of epileptogenic hippocampal slices

    Brain Res.

    (1978)
  • SchwartzkroinP.A. et al.

    Long-lasting facilitation of a synaptic potential following tetanization in the in vitro hippocampal slice

    Brain Res.

    (1975)
  • SkredeK.K. et al.

    The transverse hippocampal slice: a well-defined cortical structure maintained in vitro

    Brain Res.

    (1971)
  • Storm-MathisenJ.

    Glutamic acid and excitatory nerve endings: reduction of glutamic acid uptake after axotomy

    Brain Res.

    (1977)
  • Storm-MathisenJ. et al.

    Uptake of [3H]glutamic acid in excitatory nerve endings. Light and electronmicroscopic observations in the hippocampal formation of the rat

    Neuroscience

    (1979)
  • Storm-MathisenJ. et al.

    Aspartate and/or glutamate may be transmitters in hippocampal efferents to septum and hypothalamus

    Neuroscience Letters

    (1978)
  • WalaasI. et al.

    The effects of surgical and chemical lesions on neurotransmitter candidates in the nucleus accumbens of the rat

    Neuroscience

    (1979)
  • AndersenP.

    Organization of hippocampal neurons and their interconnections

  • AndersenP.

    Long-lasting facilitation of synaptic transmission

  • AndersenP. et al.

    Organization of the hippocampal output

    Expl Brain Res.

    (1973)
  • AndersenP. et al.

    Unit analysis of hippocampal population spikes

    Expl Brain Res.

    (1971)
  • AndersenP. et al.

    Lamellar organization of hippocampal excitatory pathways

    Expl Brain Res.

    (1971)
  • BalcarV.J. et al.

    The structural specificity of the high affinity uptake ofl-glutamate andl-aspartate by rat brain slices

    J. Neurochem.

    (1972)
  • CotmanC.W. et al.

    Glutamate as a CNS neurotransmitter: properties of release, inactivation and biosynthesis

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