Our data show that different cell types recorded in vitro can be identified by their intrinsic membrane properties. One type of neuron, namely S-AHP cells, have the ability to fire single action potentials in a rhythmic fashion following sufficient membrane depolarization. The rate is apparently controlled by several voltage-dependent conductances. S-AHP cells are normally quiescent at their resting potentials but will discharge once threshold is reached (-55 to -60 mV). Importantly, S-AHP (or F-AHP) cells will not convert into burst-firing neurons merely with changes in membrane potential. On the other hand, burst-firing cells have the ability to switch to a repetitive-firing pattern following membrane depolarization. All of these data provide a first step in an understanding of the firing rates of basal forebrain neurons, however, our results must be consolidated with existing in vivo studies for a more general understanding of basal forebrain function. Comparing our data to an in vivo preparation of the MS/nDB with synaptic afferents surgically removed may be one approach to correlating in vitro and in vivo studies. Vinogradova et al. (1980) used single unit recording techniques in unanesthetized chronic rabbits and compared the firing rates of cells before and after deafferentation. These authors reported a preservation of burst-firing neurons (25% of the cells) after deafferentation but with a significant reduction in the mean frequency of bursts. In addition a higher percentage of regularly firing cells also occurred following deafferentation (Vinogradova et al., 1980). It is interesting to speculate that these regularly firing cells may correspond to S-AHP cells in our in vitro studies, and some of the burst-firing units may correspond to the burst-firing cells we record in slices. Nevertheless, the in vivo data strongly suggests that endogenous regular spiking as well as rhythmic burst capabilities are present in some MS/nDB cells, however, the firing rates of most MS/nDB neurons are strongly influenced by synaptic afferents (see also Vinogradova et al., 1980; 1987). The endogenous activity in vivo can be explained, in part, by the intrinsic properties elucidated in our in vitro studies. How the synaptic afferents control MS/nDB circuitry and integrative output is premature to speculate without a more thorough understanding of the synaptic mechanisms involved. It is possible that future in vitro studies will help define these mechanisms and again contribute to an understanding of basal forebrain function.