Changes in extracellular K+ concentration ([K+]e) in dorsal horn were studied by means of double-barrel K+-sensitive microelectrodes in rats anesthetized with Nembutal. Acute nociceptive stimuli (pinch, press, heat) applied to the hind paw induced a transient increase in [K+]e of about 0.1-0.5 mM which persisted for 5-30 s. Regional variations in [K+]e were found in unstimulated rat spinal cords. The K+ level in the lower dorsal horn (laminae III-V) was by about 0.4 +/- 0.06 mM higher than that in more superficial laminae and in the ventral horn. Chemical or thermal injury was evoked by: s.c. injection of 0.1-0.5 ml formalin or turpentine into the hind paw, by application of mustard oil onto the skin, or by thermal injury of the hind paw. These produced a long-term increase in [K+]e in the lower dorsal horn by 0.3-3.0 mM in 75% of animals (n = 27). The increase in [K+]e began 5-15 min after injury and persisted for more than 2 h. In the rest of the animals, occasional elevation in [K+]e of 0.1-0.3 mM were observed. The K+ increases evoked by acute nociceptive stimuli as well as by injury were blocked by preinjecting the hind paw with 1% procaine. However, when procaine was applied 20 min or later after injury, the evoked long-term rise in [K+]e was not affected. This shows that the long-term K+ accumulation results from self-sustained abnormal neuronal firing induced in the dorsal horn by injury.(ABSTRACT TRUNCATED AT 250 WORDS)