RESPONSES OF PRIMARY AFFERENTS AND SPINAL DORSAL HORN NEURONS TO THERMAL AND MECHANICAL STIMULI BEFORE AND DURING ZYMOSAN-INDUCED INFLAMMATION OF THE RAT HINDPAW
A. Randich et al., RESPONSES OF PRIMARY AFFERENTS AND SPINAL DORSAL HORN NEURONS TO THERMAL AND MECHANICAL STIMULI BEFORE AND DURING ZYMOSAN-INDUCED INFLAMMATION OF THE RAT HINDPAW, Brain research, 772(1-2), 1997, pp. 135-148
Intraplantar administration of zymosan produces inflammation and resul
ts in behavioral evidence of hyperalgesia to mechanical and thermal st
imuli in the rat. In the present studies, responses of primary afferen
ts and spinal dorsal horn neurons to mechanical and thermal stimuli we
re examined before and during zymosan-induced inflammation of the hind
paw. In tests of responses of primary afferents to mechanical stimuli,
group mean mechanical response thresholds of C-mechanonociceptor (CMN
) units significantly decreased after zymosan administration. The grou
p mean mechanical response thresholds of low threshold mechanoreceptor
(LTM) units, A-mechanoheat (AMH) units, high threshold mechanorecepto
r (HTM) units, and C-mechanoheat (CMH) units showed either no change o
r were increased significantly by intraplantar administration of zymos
an. The group mean total discharges evoked during the 10 s mechanical
stimulus were significantly increased after zymosan administration in
CMN units. The group mean total discharges were either significantly d
ecreased or unchanged in LTM, AMH, HTM, and CMH units. In tests of res
ponses of spinal dorsal horn neurons to mechanical stimuli, the group
mean mechanical response threshold of nociceptive specific (NS) units
decreased significantly 1 h following administration of zymosan, where
as no significant changes occurred in the mechanical response threshol
ds of wide dynamic range (WDR) neurons in zymosan-injected rats, WDR n
eurons in saline-injected rats, or NS neurons in saline-injected rats.
The group mean total discharges of only NS neurons were significantly
increased during the 10 s mechanical stimulus 3 and 4 h after zymosan
administration. In tests of responses of primary afferents to thermal
stimuli, intraplantar administration of zymosan resulted in significa
nt decreases in group mean response thresholds of CMH units and signif
icant increases in group mean response thresholds of AMH units. The gr
oup mean total discharges of CMH units was either unchanged or signifi
cantly increased during thermal stimuli depending on both the time of
testing and the temperature of the test stimulus. The group mean total
number of discharges of AMH units was significantly decreased during
tests of all thermal stimuli. In tests of responses of spinal dorsal h
orn neurons to thermal stimuli, intraplantar administration of zymosan
resulted in significant decreases in thermal response thresholds of b
oth WDR and NS units of zymosan-injected rats, but no changes in WDR a
nd NS units of saline-injected rats. The group mean total discharges e
voked by the 15 s thermal stimuli also increased significantly in both
WDR and NS units after zymosan administration. Zymosan administration
resulted in increased background activity only in CMH units. These in
creases occurred immediately following the injection and dissipated by
the first hourly test period. Significant changes in background disch
arges of both WDR and NS units occurred at some hourly test intervals
following administration of zymosan, but these changes were not consis
tent with respect to either unit type or modality of the test stimulus
. These data suggest that the zymosan-induced hyperalgesia to mechanic
al stimuli observed in behavioral studies reflects decreases in respon
se thresholds of peripheral CMN units and spinal NS neurons. Hyperalge
sia to thermal stimuli reflects decreases in response thresholds of pe
ripheral CMH units, spinal WDR neurons, and spinal NS neurons. These d
ata support the view that different physiological substrates mediate h
yperalgesia to either thermal or mechanical stimuli following intrapla
ntar administration of zymosan. (C) 1997 Elsevier Science B.V.