EPSPs have been evoked in CA1 pyramidal cells by (1) activation of single CA3 neurons (unitary EPSPs), and (2) low-intensity stimuli to the CA1 stratum radiatum. Five unitary EPSPs were obtained; their mean peak amplitudes ranged from 85 to 275 microV and 3 of the 5 showed fluctuations in amplitude that were too great to be attributed to baseline noise. After subtraction of the variance due to the noise, these EPSPs had coefficients of variation much higher than those reported for variability in the quantal EPSP in other preparations. These results suggest that intermittent transmitter release is a major cause of EPSP amplitude fluctuation at this synapse. A noise deconvolution technique based on a nonrestrictive model of transmitter release was applied to the EPSPs obtained in this study. For 2 of the EPSPs evoked by stratum radiatum stimulation, the amplitudes fluctuated between discrete values that were sufficiently separated with respect to the noise to be resolved by the deconvolution procedure. Quantal increments of 224 and 193 microV were determined for the 2 EPSPs.

1. The effects of intracellular QX-314 on Ca2+ currents were examined in CA1 pyramidal cells acutely isolated from rat hippocampus. In neurons dialyzed with 10 mM QX-314 (bromide salt), the amplitude of the high-threshold Ca2+ current was on average 20% of that in control cells and the current-voltage relationships (I-Vs) were shifted in the positive voltage direction. 2. The positive shift in the I-Vs was due to the presence of intracellular Br-, because it was reproduced by 10 mM NaBr and was not present when the chloride salt of QX-314 was used. 3. Low-threshold (T-type) Ca2+ currents, at test voltages of -50 and -40 mV, were on average < 45% of control amplitude in cells containing 10 mM QX-314 (chloride salt) and < 10% of control amplitude in cells with 10 mM QX-314 (bromide salt). 4. In neurons dialyzed with 1 mM QX-314, high-threshold Ca2+ currents were still significantly different from control and Na+ currents were not completely blocked. 5. The proportions of high-threshold Ca2+ current blocked by omega-conotoxin GVIA, omega-agatoxin IVA, and nimodipine were similar in cells dialyzed with 10 mM QX-314 and control cells, indicating that the drug does not selectively inhibit any of the Ca2+ channel subtypes distinguished by these antagonists.

Spontaneous single-action potentials (units) were recorded extracellularly from explants of the rat organum vasculosum laminae terminalis in vitro. Increasing the osmotic pressure of the bathing solution by 15% by adding NaCl or mannitol increased frequency, whereas reducing the osmotic pressure by 15% by omitting NaCl reduced frequency. The mean frequency ratio (test/control) for 6 (of 13) units responding to a 15% increase was 2.2 +/- 0.5 (SE), and for 8 (of 11) units responding to a 15% decrease it was 0.6 +/- 0.1. These responding units all lay within 55 microns of the ventricular surface. Reduction of the calcium concentration from 2 to 0.75 mmol X l-1 increased the mean frequency of units by 55%. Putative transmitters were added to the bathing solution at 0.1 mol X l-1. The results were as follows: carbamylcholine (26 units), 27% excited and 19% inhibited; luteinizing hormone-releasing hormone (34 units), 38% excited and 12% inhibited; angiotensin II (ANG II) (34 units), 26% excited, and 6% inhibited; somatostatin (14 units), 36% excited and 43% inhibited; serotonin (15 units), 67% excited and none inhibited; and dopamine (13 units), 46% excited and none inhibited. Of the units tested, 86% lay less than 100 microns from the ventricular surface. Units responsive to ANG II lay deeper than units responding to serotonin (P less than 0.005), osmotic changes (P less than 0.001), or carbamylcholine (P less than 0.02).

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