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The Journal of Neuroscience, January 15, 1999, 19(2):859-867
Peripheral Inflammation Facilitates A Fiber-Mediated Synaptic
Input to the Substantia Gelatinosa of the Adult Rat Spinal Cord
Hiroshi
Baba,
Timothy P.
Doubell, and
Clifford J.
Woolf
Neural Plasticity Research Group, Department of Anesthesia and
Critical Care, Massachusetts General Hospital and Harvard Medical
School, Boston, Massachusetts 02129
Whole-cell patch-clamp recordings were made from substantia
gelatinosa (SG) neurons in thick adult rat transverse spinal cord slices with attached dorsal roots to study changes in fast synaptic transmission induced by peripheral inflammation. In slices from naive
rats, primary afferent stimulation at A fiber intensity elicited
polysynaptic EPSCs in only 14 of 57 (25%) SG neurons. In
contrast, A fiber stimulation evoked polysynaptic EPSCs in 39 of 62 (63%) SG neurons recorded in slices from rats inflamed by an
intraplantar injection of complete Freund's adjuvant (CFA) 48 hr
earlier (p < 0.001). Although the
peripheral inflammation had no significant effect on the threshold and
conduction velocities of A, A , and C fibers recorded in dorsal
roots, the mean threshold intensity for eliciting EPSCs was
significantly lower in cells recorded from rats with inflammation
(naive: 33.2 ± 15.1 µA, n = 57; inflamed:
22.8 ± 11.3 µA, n = 62, p < 0.001), and the mean latency of EPSCs elicited
by A fiber stimulation in CFA-treated rats was significantly shorter
than that recorded from naive rats (3.3 ± 1.8 msec,
n = 36 vs 6.0 ± 3.5 msec,
n = 12; p = 0.010). A fiber
stimulation evoked polysynaptic IPSCs in 4 of 25 (16%) cells
recorded from naive rat preparations and 14 of 26 (54%) SG neurons
from CFA-treated rats (p < 0.001). The mean
threshold intensity for IPSCs was also significantly lower in
CFA-treated rats (naive: 32.5 ± 15.7 µA, n = 25; inflamed: 21.9 ± 9.9 µA, n = 26, p = 0.013). The facilitation of A fiber-mediated
input into the substantia gelatinosa after peripheral inflammation may contribute to altered sensory processing.
Key words:
inflammation; pain; dorsal horn; synaptic transmission; neural plasticity; substantia gelatinosa
Copyright © 1999 Society for Neuroscience 0270-6474/99/192859-09$05.00/0
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