Abstract
Substance P injected intrathecally or a conditioning stimulus (1 Hz, 20 s) at C-fiber strength, which releases substance P from intraspinal primary afferent terminals, each enhance the hamstring muscle flexor reflex elicited by electrical stimulation of the sural nerve in decerebrate, spinalized rats. This suggests a role for substance P in pain transmission. Since substance P N-terminal metabolites are biologically active, we examined the effect of the metabolite substance P-(1-7) on the flexor reflex and the enhancement of the flexor reflex following a conditioning stimulus of the sural nerve. In contrast to the excitatory effect of substance P, intrathecal injection of substance P-(1-7) had no effect on the flexor reflex. However, 10 and 30 min after injection, 0.6 or 6 μg of substance P-(1-7) attenuated the facilitation of the flexor reflex by the conditioning stimulus. These data indicate that substance P-(1-7) may modulate the expression of nociception involving repetitive firing of C-fibers while having no significant effect on acute or phasic responses.
Original language | English (US) |
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Pages (from-to) | 83-86 |
Number of pages | 4 |
Journal | European Journal of Pharmacology |
Volume | 259 |
Issue number | 1 |
DOIs | |
State | Published - Jun 23 1994 |
Bibliographical note
Funding Information:This work was supported by Grants for Research Abroad from the Univ. of Minn. Graduate Fellowship Office and ADAMHA training grant NIDA T32 DA07234-06 to V.M.G., the Swedish Medical Research Council (07913), Astra Pain Control AB, the Bank of Sweden Tercentenary Foundation and Marcus and Amalia Wal-lenberg Foundation to Z.W.-H. and U.S. Public Health Service Grant DA04090 to A.A.L. The authors thank Dr. Jingxia Hao for her technical assistance.
Keywords
- Antinociception
- Flexor reflex
- Pain
- Substance P, N-terminus