1. Intracellular recordings were used to examine the membrane properties and evoked responses of subicular neurons in horizontal and parasagittal slices from guinea pig brain as a step toward understanding excitatory transmission through the hippocampus. 2. Most cells (49/74) could fire a burst discharge, a portion of which was Ca2+ dependent, in response to direct depolarization or in response to orthodromic or antidromic activation. Other cells (23/74) could not be made to burst, but instead fired single repetitive spikes when directly depolarized or single spikes in response to orthodromic or antidromic activation. Two recorded cells appeared to be interneurons and differed from bursting and non-bursting cells in action-potential shape and response to extracellular stimulation. 3. Bursting cells differed from nonbursting cells in their membrane properties: 1) their time constants were typically shorter (averaging 7.4 ms for bursting cells and 11.5 ms for nonbursting cells), 2) they exhibited a pronounced "sag" in the potential response to hyperpolarizing current injection, and 3) they responded at the break of a hyperpolarizing stimulus with a depolarization (anodal break potential). The sag and the anodal break potential were not detected in recordings from nonbursting neurons. 4. A single-spiking mode could be induced in bursting cells by depolarization from resting potential to about -60 mV. Conversely, hyperpolarization of nonbursting cells did not convert them to bursting cells. 5. Both bursting and nonbursting cell types could be antidromically driven. Whereas both excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) were prominent in nonbursting cells, IPSPs were observed at a lower stimulus intensities than EPSPs in most cells. EPSPs were evident in bursting cells and they triggered burst discharges. IPSPs in bursting cells were detected only when these cells were depolarized, eliminating burst responses. 6. Spontaneous firing rates were low (averaging < 1 spike/s) for both cell types. Addition of picrotoxin produced spontaneous burst or EPSP responses in bursting cells, synchronous with different patterns of picrotoxin-induced population bursts originating in CA3 and/or entorhinal cortex. Individual subicular cells followed CA3 or entorhinal cortex or both. No such activity was recorded in nonbursting cells. No increases in activity in either cell type were seen after picrotoxin application to isolated pieces of subicular cortex.(ABSTRACT TRUNCATED AT 400 WORDS)