Marco Capogna

Excitatory synaptic transmission and its modulation by PKC is unchanged in the hippocampus of GAP-43-deficient mice

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

  • M Capogna
  • C Fankhauser
  • ,
  • V Gagliardini
  • ,
  • B H Gähwiler
  • ,
  • S M Thompson

We compared excitatory synaptic transmission between hippocampal pyramidal cells in dissociated hippocampal cell cultures and in area CA3 of hippocampal slice cultures derived from wild-type mice and mice with a genetic deletion of the presynaptic growth associated protein GAP-43. The basal frequency and amplitude of action potential-dependent and -independent spontaneous excitatory postsynaptic currents were similar in both groups. The probability that any two CA3 pyramidal cells in wild-type or GAP-43 knockout (-/-) slice cultures were synaptically connected was assessed with paired recordings and was not different. Furthermore, unitary synaptic responses were similar in the two genotypes. Bath application of phorbol 12,13-diacetate (0.6-3 microM) elicited a comparable increase in the frequency of miniature excitatory synaptic currents in wild-type and GAP-43 (-/-) cultures. This effect was blocked by the protein kinase C inhibitor, bisindolylmaleimide I (1.2 microM). Finally, 3 microM phorbol 12,13-diacetate potentiated the amplitude of unitary synaptic currents to a comparable extent in wild-type and GAP-43 (-/-) slice cultures. We conclude that GAP-43 is not required for normal excitatory synaptic transmission or the potentiation of presynaptic glutamate release mediated by activation of protein kinase C in the hippocampus.

Original languageEnglish
JournalThe European journal of neuroscience
Volume11
Issue2
Pages (from-to)433-40
Number of pages8
ISSN0953-816X
Publication statusPublished - Feb 1999
Externally publishedYes

    Research areas

  • Animals, DNA Primers, Excitatory Postsynaptic Potentials/drug effects, GAP-43 Protein/genetics, Gene Deletion, Genotype, Glutamic Acid/metabolism, Hippocampus/chemistry, Mice, Mice, Inbred C57BL, Mice, Knockout, Phorbol Esters/pharmacology, Protein Kinase C/metabolism, Pyramidal Cells/chemistry, Synaptic Transmission/drug effects

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