The membrane potential waveforms to be expected from many asynchronous inputs to CNS neurons are described, along with modes for repetitive firing through which the input waveforms are converted into spike trains. Area beneath a postsynaptic potential (PSP), rather than PSP peak height, is shown to be an important parameter susceptible to modification. Occasional crossings of threshold produce occasional spikes, but a sustained depolarizing waveform which attempts to hold the membrane potential above threshold elicits rhythmic firing. Firing rate is graded with the amount by which the synaptic depolarizing currents exceed the minimum current for rhythmic firing (approximately rheobase). A systematic sequence of alterations in the membrane potential trajectory between spikes, quite different from those of receptors and invertebrate neurons, may control the firing rate and give rise to sudden changes in the "gain" of this conversion of depolarizing current into firing rate. The different implications of synaptic location during the occasional spike mode and the rhythmic firing mode are discussed, as is the role of the antidromic invasion of the soma-dendritic region during rhythmic firing. Less frequently an"extra spike mode" is seen where depolarizing afterpotentials following a spike themselves cross threshold to elicit an extra spike, which may similarly elicit another extra spike, etc., in a regenerative cycle. The character of the underlying depolarizing afterpotentials (or "delayed depolarizations") is reviewed, along with theories for their origin from the antidromic invasion of the dendritic tree. The stereotyped burst firing patterns characteristic of the extra spike mode can also be seen in deafferented neurons and neurons studied in chronic syndromes such as epilepsy and central pain. This raises the question as to whether some disease states may augment extra spike firing, thus multiplying many-fold the response to a normal input.