FAST PRESYNAPTIC GABA(A) RECEPTOR-MEDIATED CL- CONDUCTANCE IN CULTURED RAT HIPPOCAMPAL-NEURONS

1. Hippocampal neurones cultured from the 18-day-old embryonic rat for 3 days to 3 weeks were recorded with Cl--filled patch pipettes. Spont aneous synaptic currents, which reversed at the equilibrium potential for Cl- ions (E(Cl)) and were blocked by the GABA(A) (gamma-aminobutyr ic acid) receptor antagonists bicuculline or picrotoxin, were recorded in every culture. At 25 degrees C and -80 mV they decayed with a time constant greater than or equal to 20 ms that invariably increased at positive potentials. After 2 weeks, 50-75 % of all neurones were GABA immunoreactive. 2. In pairs-recordings, coincident synaptic currents i n both cells were either spontaneous or evoked by stimulation of one c ell, In the presence of tetrodotoxin and using pipettes containing lid ocaine (lignocaine) N-ethyl bromide, coincident spontaneous Cl- transi ents still occurred in both neurones far more frequently than expected by chance. 3. Holding the potential of one neurone at a positive valu e reversed the synaptic transients in that cell and, in half of the ce lls, increased the frequency of coincident events in both cells. 4. In neurones where depolarization increased the frequency of coinciding e vents and all regenerative current apparent at the soma was abolished, short depolarizing pulses occasionally evoked all-or-none, pre- and p ostsynaptic currents with matching transmission failures and identical delays in transmission. 5. The results suggest that the same pulse of GABA simultaneously activates GABA(A) receptor-coupled Cl- channels o n both sides of the same synaptic cleft, producing immediate auto-tran smission in the absence of collaterals or interneurones.