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Substance P does not play a critical role in neurogenic inflammation in the rat masseter muscle
Jin Y Ro1, Youping Zhang, Michael Nies
1Department of Biomedical Sciences, University of Maryland Baltimore School of Dentistry, 666 W. Baltimore Street, Baltimore, MD 21201, USA. jyr001@dental.umaryland.edu
Abstract:
In this study, we performed a series of experiments to investigate whether substance P (SP) contributes to neurogenic inflammation in the skeletal muscle tissue. Intramuscular injection of an inflammatory irritant, mustard oil (MO), induces significant edema formation in the rat masseter muscle. In order to study the contribution of endogenous SP in the MO-induced edema, groups of rats were pretreated with two different doses (100 nmol; 1 microl) of either peptidergic (Sendide) or non-peptidergic (L703, 606) neurokinin 1 (NK1) receptor antagonist in one masseter muscle 15 min prior to the MO injection in the same muscle. The extent of edema was assessed as the percent weight difference of the injected muscle compared to the non-injected muscle. Neither Sendide nor L703,606 pretreatment resulted in a significant inhibition of the MO-induced edema in the masseter muscle. Exogenous application of SP also produced a significant swelling of the muscle, which was blocked by L703,606 (1 microl) pretreatment, suggesting that evoked release of SP following MO injection is not sufficient to induce significant edema formation. Capsaicin (1% in 25 microl), which is known to cause neurogenic inflammation, failed to produce edema formation in the masseter muscle. The same concentration of capsaicin injected into the hindpaw produced significant swelling of the injected paw. Taken together, these results provide compelling evidence that, unlike cutaneous or joint tissue, SP does not play a critical role in inducing neurogenic inflammation in the skeletal muscle tissue.
Insights
Substance P (SP) does not significantly contribute to neurogenic inflammation in skeletal muscle. Experiments showed that blocking SP receptors did not inhibit mustard oil-induced swelling, indicating SP is not critical for this response in muscle tissue.
Area of Science:
- Neuroscience
- Inflammation Research
- Skeletal Muscle Physiology
Background:
- Neurogenic inflammation is a complex process involving the nervous system.
- Substance P (SP) is a neuropeptide implicated in inflammatory responses in various tissues.
- The role of SP in skeletal muscle neurogenic inflammation remains unclear.
Purpose of the Study:
- To investigate the contribution of substance P (SP) to neurogenic inflammation in rat masseter muscle.
- To determine if SP is essential for edema formation induced by inflammatory irritants in skeletal muscle.
Main Methods:
- Rats were pretreated with neurokinin 1 (NK1) receptor antagonists (Sendide or L703,606) before mustard oil (MO) injection into the masseter muscle.
- Edema was quantified by comparing the weight of injected versus non-injected muscles.
- Exogenous SP and capsaicin were used to assess their direct effects on muscle swelling.
Main Results:
- Pretreatment with NK1 receptor antagonists did not significantly inhibit MO-induced edema in the masseter muscle.
- Exogenous SP induced swelling, but this was blocked by L703,606, suggesting endogenous SP release was insufficient.
- Capsaicin, a known neurogenic inflammation agent, failed to induce edema in the masseter muscle, unlike in the hindpaw.
Conclusions:
- Substance P (SP) does not play a critical role in inducing neurogenic inflammation in skeletal muscle tissue.
- Unlike in cutaneous or joint tissues, SP-mediated pathways are not the primary drivers of inflammation in skeletal muscle.
- These findings differentiate the inflammatory mechanisms in skeletal muscle from other tissue types.
