Glutamate is the major excitatory transmitter in CNS although it causes severe brain damage by pathologic excitotoxicity. Central to effi cient neurotransmission is a powerful protection afforded by specifi c high-affi nity glutamate transporters in neurons and glia, clearing synaptic glutamate. In whole-cell patch clamp experiments the infl uence of neuronal glutamate transporters on spontaneous (sEPSC) and evoked postsynaptic currents (eEPSC) in hippocampal CA1 neurons was examined by manipulating the content of intracellular solution. With Cs+- based internal solution the defi cient of presynaptic glutamate transporters affected the occurrence of synaptic event and thus involved in the regulation of transmitter release. eEPSCs were generally suppressed both in amplitude (to 48.73 % vs. control ) and in success rate (Rsuc ) by TBOA (10 μM) (from 91.1 % in control to 79.57%). In contrast, with K+ -based internal solution (all GluT are intact), amplitude of eEPSC was substantially potentiated by pre-treatment with TBOA (up to 150%), whereas (Rsuc) was reduced to 79.8% in average. The identical reduction of event success rate as well as increased PPF ratio for eEPSC in both cases is indicative for TBOA effect on presynaptic uptake site. In conclusion, presynaptic transporters are suggested to act mainly as negative feedback signal on presynaptic release and/ or referred to vesicle refi lling processes, when postsynapticaly located transporters are supposed to shape postsynaptic events.
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