DIFFERENCE IN LTP AT BASAL AND APICAL DENDRITES OF CA1 PYRAMIDAL NEURONS IN URETHANE-ANESTHETIZED RATS

In urethane-anesthetized rats, excitatory currents in hippocampal CA1 area following local stimulation were analyzed using the current source density technique. Systematic variation of stimulus depth revealed two dominant patterns of activation: basal versus apical dendritic excitation. The basal dendritic excitation (sink) was maximal after stimulation of stratum oriens; its onset latency was consistent with a monosynaptic excitation, and a late (presumed di- and polysynaptic) sink at the apical dendrites was observed. The apical dendritic excitation (sink) was maximal after stimulation of stratum radiatum; the early latency, presumed monosynaptic excitation was followed by a late, weak basal dendritic sink. Theta-frequency primed bursts of either high (400 mu A) or low intensity (40-70 mu A; 2 X threshold intensity) was delivered to either stratum oriens or radiatum, and long-term potentiation (LTP) was assessed. LTP was observed in both positive and negative components of the dipole field, as well as the (active) sink and (passive) source. Tetanus of stratum oriens resulted in a significant (P < 0.05) potentiation of the monosynaptic basal sink (at 2 ms from onset) following either high (135 +/- 11%, means +/- S.E.M., n = 7) or low intensity tetanus (178 +/- 21%, n = 7). Tetanus of stratum radiatum resulted in significant potentiation of the rise of the apical sink only for a high (173 +/- 51%, n = 6), but not for a low intensity tetanus (106 +/- 28%, n = 6). Significant LTP of the late apical sink was found following a high intensity tetanus of stratum oriens (155 +/- 15%, n = 7), but no significant change of the late basal sink was found following tetanization of stratum radiatum (118 +/- 20%, n = 6). LTP of either the apical and basal sinks was blocked by intraventricular infusion of +/-2-amino-5-phosphonovalerate, an N-methyl-D-aspartate antagonist. Thus, LTP has a lower threshold at the basal than apical synapses of CA1 cells.