Unitary EPSPs were evoked in CA1 pyramidal neurons by activation of single CA3 pyramidal neurons. Seventy-one EPSPs were recorded. The peak amplitudes of these EPSPs ranged from 30 to 665 microV with a mean of 131 microV. Rise times and half-widths were measured, the means +/- SD being 3.9 +/- 1.8 and 19.5 +/- 8.0 msec, respectively. The time courses of these EPSPs were consistent with a brief synaptic current at a localized electrotonic region of the dendritic tree followed by passive spread of current to the soma. EPSPs varied in amplitude from trial to trial. Sufficient records were collected for 12 EPSPs to demonstrate that this variation was greater than could be accounted for by baseline noise. The amplitude variations of one EPSP were reliably resolved from the background noise, and this EPSP fluctuated between 4 discrete amplitudes (including failures) separated by a quantal increment of 278 microV.

Long-term potentiation (LTP) was evaluated for small monosynaptic CA3-mediated EPSPs in CA1 neurons in the guinea pig hippocampal slice. Small EPSPs included those elicited by stimulation of Schaffer axon collaterals of several CA3 neurons (160-480 microV amplitude, n = 40 EPSPs in 40 neurons) and those elicited by stimulation of an individual CA3 neuron (89-563 microV amplitude, n = 14 EPSPs in 11 neurons). Various protocols were employed to induce LTP and were deemed successful as evaluated by recording sustained enhancement of the mean peak amplitude of conventionally elicited large compound EPSPs and extracellular field potentials. However, in 47 of 54 cases, tetanization did not lead to a potentiation of the small or unitary EPSPs. In 9 cases, it was possible to directly evaluate the compound EPSP (elicited by stimulating a group of CA3 neuron's axons) and the unitary EPSP (elicited by stimulating a single CA3 neuron) in the same CA1 neuron. The tetanization protocol was successful in inducing LTP in 7 of 9 of these CA1 neurons as evaluated by the compound EPSP but resulted in LTP for only 1 of 9 of the unitary EPSPs for the same neurons. One explanation for these results is a threshold mechanism controlling the expression of LTP. Although LTP induction occurred in most cases, it is proposed that a critical level of depolarization (achieved by the test activation of a sufficient number of CA3 neurons) is necessary so that the enhancement at the modified synapse is expressed.

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