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1. The mechanism by which L-glutamic acid depolarizes hippocampal CA1 pyramidal neurones was investigated by using the in vitro slice and ionophoretic techniques. 2. Two types of responses were seen. One (in 85% of cells) consisted of spike discharges that outlasted the glutamate-induced depolarization. In the other (the rest of the cells), spikes were produced only during the rising phase of the depolarization. 3. The effect was highly localized; it disappeared when the ionophoretic electrode was moved vertically by as little as 20 micrometers. 4. The effect of glutamate persisted after synaptic transmission was blocked; this probably was due to a direct effect of glutamate on the cell membrane. 5. Small doses of glutamate produced either no change or an apparent increase in input resistance. With larger doses, the input resistance invariably decreased. The apparent increase in input resistance was not seen in cells treated with Mn2+ and TTX and is believed to be an effect of the depolarization rather than a direct effect of glutamate. 6. By extrapolation, the reversal potential for the glutamate response (EGlu) was found to -3.6 mV. 7. Following intracellular injection of Cs+, neurones could be depolarized to a range of +20 to +50 mV. The glutamate response could then be reversed. EGlu in these cells was -1.5 mV. 8. Using the Cs+-injection technique, it was also possible to reverse the e.p.s.p. E.e.p.s.p. was similar to EGlu. 9. When the external sodium concentration was reduced, the size of the glutamate response decreased, and EGlu became more negative.

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