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. 1998 May 1;18(9):3147–3157. doi: 10.1523/JNEUROSCI.18-09-03147.1998

Fig. 1.

Fig. 1.

Inhibition of evoked acetylcholine release by recombinant GTPase-deficient Aplysia-Rab3.A, ACh release was evoked at identified synapses in the buccal ganglion of Aplysia californica. Postsynaptic response amplitude (%) is plotted against time (after injection). After the control recording was made, recombinantAplysia-Rab3 deficient in its GTPase activity (apRab3-Q80L, abbreviated as Q80L in the figure) was pressure-injected into one of the two presynaptic cholinergic neurons (see inset for a schematic drawing of the neuronal connections). The final concentration of apRab3-Q80L was ∼0.3–0.5 μm in the cell body; the other presynaptic neuron (○) was kept for internal control of release stability. B, Recordings of presynaptic action potentials (a) and postsynaptic responses (b), before and after injection of apRab3-Q80L. Note that amplitude of postsynaptic response is expressed as a change in postsynaptic conductance (nS). For further details see experimental procedures.