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Regulation of glutamate and aspartate release from slices of the hippocampal CA1 area: effects of adenosine and baclofen.

Publication ,  Journal Article
Burke, SP; Nadler, JV
Published in: J Neurochem
November 1988

Glutamate and/or aspartate is the probable transmitter released from synaptic terminals of the CA3-derived Schaffer collateral, commissural, and ipsilateral associational fibers in area CA1 of the rat hippocampal formation. Slices of the CA1 area were employed to test the effects of adenosine- and gamma-aminobutyrate (GABA)-related compounds on the release of glutamate and aspartate from this projection. Under the conditions of these experiments, the release of glutamate and aspartate evoked by 50 mM K+ was more than 90% Ca2+-dependent and originated predominantly from the CA3-derived pathways. Adenosine reduced the K+-evoked release of glutamate and aspartate by a maximum of about 60%, but did not affect the release of GABA. This action was reversed by 1 microM 8-phenyltheophylline. The order of potency for adenosine analogues was as follows: L-N6-phenylisopropyladenosine greater than N6-cyclohexyladenosine greater than D-N6-phenylisopropyladenosine approximately equal to 2-chloroadenosine greater than adenosine much greater than 5'-N-ethylcarboxamidoadenosine. 8-Phenyltheophylline (10 microM) by itself enhanced glutamate/aspartate release, whereas dipyridamole alone depressed release. These results support the view that adenosine inhibits transmission at Schaffer collateral-commissural-ipsilateral associational synapses mainly by reducing transmitter release and that these effects involve the activation of an A1 receptor. Neither adenosine, L-N6-phenylisopropyladenosine, nor 8-phenyltheophylline affected the release of glutamate or aspartate evoked by 10 microM veratridine. The differing effects of adenosine compounds on release evoked by K+ and veratridine suggest that A1 receptor activation either inhibits Ca2+ influx through the voltage-sensitive channels or interferes with a step subsequent to Ca2+ entry that is coupled to the voltage-sensitive Ca2+ channels in an obligatory fashion. Neither baclofen nor any other agent active at GABAB or GABAA receptors affected glutamate or aspartate release evoked by elevated K+ or veratridine. Therefore, either baclofen does not inhibit transmission at these synapses by depressing transmitter release or else it does so in a way that cannot be detected when a chemical depolarizing agent is employed.

Duke Scholars

Published In

J Neurochem

DOI

ISSN

0022-3042

Publication Date

November 1988

Volume

51

Issue

5

Start / End Page

1541 / 1551

Location

England

Related Subject Headings

  • Veratridine
  • Synapses
  • Receptors, GABA-A
  • Rats, Inbred Strains
  • Rats
  • Potassium
  • Neurology & Neurosurgery
  • Kainic Acid
  • Hippocampus
  • Glutamic Acid
 

Citation

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Burke, S. P., & Nadler, J. V. (1988). Regulation of glutamate and aspartate release from slices of the hippocampal CA1 area: effects of adenosine and baclofen. J Neurochem, 51(5), 1541–1551. https://doi.org/10.1111/j.1471-4159.1988.tb01123.x
Burke, S. P., and J. V. Nadler. “Regulation of glutamate and aspartate release from slices of the hippocampal CA1 area: effects of adenosine and baclofen.J Neurochem 51, no. 5 (November 1988): 1541–51. https://doi.org/10.1111/j.1471-4159.1988.tb01123.x.
Burke, S. P., and J. V. Nadler. “Regulation of glutamate and aspartate release from slices of the hippocampal CA1 area: effects of adenosine and baclofen.J Neurochem, vol. 51, no. 5, Nov. 1988, pp. 1541–51. Pubmed, doi:10.1111/j.1471-4159.1988.tb01123.x.
Journal cover image

Published In

J Neurochem

DOI

ISSN

0022-3042

Publication Date

November 1988

Volume

51

Issue

5

Start / End Page

1541 / 1551

Location

England

Related Subject Headings

  • Veratridine
  • Synapses
  • Receptors, GABA-A
  • Rats, Inbred Strains
  • Rats
  • Potassium
  • Neurology & Neurosurgery
  • Kainic Acid
  • Hippocampus
  • Glutamic Acid