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

We compared excitatory synaptic transmission between hippocampal pyramidal cells in dissociated hippocampal cell cultures and in area CA3 of hippocamp al slice cultures derived from wild-type mice and mice with a genetic delet ion of the presynaptic growth associated protein GAP-43. The basal frequenc y and amplitude of action potential-dependent and -independent spontaneous excitatory postsynaptic currents were similar in both groups. The probabili ty that any two CA3 pyramidal cells in wild-type or GAP-43 knockout (-/-) s lice cultures were synaptically connected was assessed with pal red recordi ngs and was not different. Furthermore, unitary synaptic responses were sim ilar in the two genotypes. Bath application of phorbol 12,13-diacetate (0.6 -3 mu M) elicited a comparable increase in the frequency of miniature excit atory synaptic currents in wild-type and GAP-43 (-/-) cultures. This effect was blocked by the protein kinase C inhibitor, bisindolylmaleimide I (1.2 mu M). Finally, 3 mu M 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 exc itatory synaptic transmission or the potentiation of presynaptic glutamate release mediated by activation of protein kinase C in the hippocampus.