Present address: NIMS, 5 Gower Place, London WC1E 6BN, UK.
Excitatory synaptic transmission and its modulation by PKC is unchanged in the hippocampus of GAP-43- deficient mice
Version of Record online: 27 AUG 2008
© European Neuroscience Association
European Journal of Neuroscience
Volume 11, Issue 2, pages 433–440, February 1999
How to Cite
Capogna, M., Fankhauser, C., Gagliardini, V., Gähwiler, B. H. and Thompson, S. M. (1999), Excitatory synaptic transmission and its modulation by PKC is unchanged in the hippocampus of GAP-43- deficient mice. European Journal of Neuroscience, 11: 433–440. doi: 10.1046/j.1460-9568.1999.00450.x
- Issue online: 27 AUG 2008
- Version of Record online: 27 AUG 2008
- Received 8 June 1998, revised 29 August 1998, accepted 1 September 1998
- phorbol ester;
- transmitter release
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 μm) 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 μm). Finally, 3 μm 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.