In urethane anaesthetized rats subcutaneous formalin injection in the right hind paw, a model of persistent pain, produced (i) a prolonged increase in the period of field rhythmic sinusoidal (or theta) activity, (ii) a depression of dorsal hippocampal field CA1 pyramidal cell synaptic excitability (mean peak depression of population spike amplitude being 50 +/- 6%) observed to the 60th min post injection, and (iii) a persistent decrease in extracellular activity of the majority of CA1 pyramidal cells (15/20 or 75%) with only a small percentage excited (5/20 or 25%). In contrast an intense noxious heat stimulus applied briefly to the distal end of the tail evoked a short duration increase in period of theta activation and suppression of pyramidal cell responses. With this acute stimulus the proportion of CA1 pyramidal cells excited (8/16) were similar to that suppressed (7/16). Finally, electrolytic lesions centred in the medial septal vertical limb of diagonal band of Broca (or septal region) prevented a noxious stimulus-induced theta and depression of CA1 pyramidal cell responses. Rather, in such lesioned animals noxious stimulation excited the majority CA1 complex spike cells studied (8/10). The above data are consistent with the notion that septohippocampal inputs are involved in noxious stimulus-induced CA1 pyramidal cell suppression. The formalin injection-induced selective activation of CA1 complex spike cells against a background of widespread pyramidal cell suppression might produce a "signal to noise" contributory to nociceptive processing in limbic structures. Such a processing might be involved in the affective motivational component of pain.