Substance P N-terminus inhibits C-fiber-dependent facilitation of the rat flexor reflex

Virginia M. Goettl; Xiao Jun Xu; Alice A. Larson; Zsuzsanna Wiesenfeld-Hallin

doi:10.1016/0014-2999(94)90162-7

Substance P N-terminus inhibits C-fiber-dependent facilitation of the rat flexor reflex

Virginia M. Goettl, Xiao Jun Xu, Alice A. Larson, Zsuzsanna Wiesenfeld-Hallin

Veterinary and Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

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)
Pages (from-to)	83-86
Number of pages	4
Journal	European Journal of Pharmacology
Volume	259
Issue number	1
DOIs	https://doi.org/10.1016/0014-2999(94)90162-7
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

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10.1016/0014-2999(94)90162-7

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title = "Substance P N-terminus inhibits C-fiber-dependent facilitation of the rat flexor reflex",

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.",

keywords = "Antinociception, Flexor reflex, Pain, Substance P, N-terminus",

author = "Goettl, {Virginia M.} and Xu, {Xiao Jun} and Larson, {Alice A.} and Zsuzsanna Wiesenfeld-Hallin",

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.",

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AU - Goettl, Virginia M.

AU - Xu, Xiao Jun

AU - Larson, Alice A.

AU - Wiesenfeld-Hallin, Zsuzsanna

N1 - 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.

PY - 1994/6/23

Y1 - 1994/6/23

N2 - 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.

AB - 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.

KW - Antinociception

KW - Flexor reflex

KW - Pain

KW - Substance P, N-terminus

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Substance P N-terminus inhibits C-fiber-dependent facilitation of the rat flexor reflex

Abstract

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Keywords

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