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Figure 4


Fig. 4. Presynaptic overexpression of the non-phosphorylatable helSynALA9 mutant impairs PTP at C1-B2 synapses. (A) Sample electrophysiological recording of EPSPs recorded in B2 neurons before (pre) and 30 seconds after (post) a tetanus was applied to presynaptic C1 neurons that were either untreated (control) or overexpressing either GFP (GFP), GFP-tagged wild-type helSyn (helSyn-GFP) or the GFP-tagged helSyn phosphorylation mutant (helSynALA9-GFP). Bars: horizontal, 2 seconds; vertical, 5 mV control, 4 mV GFP, 5 mV helSyn, 2.5 mV helSynALA9. (B) Time-course of EPSP amplitude changes in PTP episodes evoked by presynaptic tetanization (arrowhead) in the various experimental groups. Values are normalized to the average amplitude of the last five pre-tetanic EPSPs. The peak amplitude and decay kinetics of PTP are nearly the same in the GFP and helSyn group with respect to controls. Conversely, helSynALA9 overexpression determines a conspicuous impairment of PTP. (C) Mean amplitudes of the peak PTP measured at 30 seconds after tetanus in the experimental groups shown in B. Values are normalized to the mean value of peak potentiation measured in the control group. helSynALA9 overexpression dramatically reduces PTP to below 30% of control levels. (D,E) Amplitudes (D) and rise times (E) of pre-tetanic EPSPs in the experimental groups shown in B and C. No significant differences were detectable as a consequence of presynaptic GFP, helSyn-GFP or helSynALA9 overexpression.





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