1. The electrical responses of nociceptive (N) lateral and N medial ne
urons of the leech segmental ganglion to mechanical, chemical, and the
rmal stimulation of the skin were studied in a superfused ganglion-bod
y wall preparation. 2. Mechanical indentation of the skin > 10 mN evok
ed in both types of cells a sustained discharge of impulses; afterdisc
harge was often observed with suprathreshold stimulations. 3. Applicat
ion to the cutaneous receptive area of 10-100 mM acetic acid or of NaC
l crystals and solutions also elicited a firing response in N medial a
nd N lateral cells. In contrast, capsaicin applied to the skin (3.3 x
10(-5) to 3.3 x 10(-2) M) excited N lateral but not N medial neurons.
Likewise, impulse discharges were obtained when capsaicin was applied
to the cell bodies of N lateral but not of N medial neurons. 4. In bot
h types of N neurons, heating of the skin above 39 degrees C evoked a
discharge of impulses whose frequency was roughly proportional to temp
erature values. 5. Application of repeated suprathreshold heating cycl
es at 10-min intervals enhanced the impulse frequency of the response
(sensitization). Shorter time intervals between heating cycles depress
ed the response to heat. Sensitization could not be obtained by equiva
lent soma depolarizations obtained by intracellular current injection.
6. Impulse discharges evoked by irritant agents were also augmented b
y previous application of noxious heat. 7. N lateral neurons fired in
response to low-pH solutions and capsaicin directly applied onto the g
anglion. N medial neurons responded inconsistently to acid and were in
sensitive to capsaicin. Action potentials evoked in N lateral cells by
capsaicin had a slow rise, a prominent hump, and a prolonged after hy
perpolarization 8. It is concluded that N neurons of the leech segment
al ganglion respond to different modalities of noxious stimuli applied
to their peripheral receptive fields and develop sensitization after
repeated noxious stimulation. These properties are typical of mammalia
n polymodal nociceptors; thus N neurons may be a simple model for anal
ysis of membrane mechanisms associated with poly-modality of nocicepti
ve neurons.