Endomorphin-1 reduces carrageenan-induced Fos expression in the rat spinal dorsal horn

Jin, Sen; Lei, Liugen; Wang, Y.; Da, Dreiling; Zhao, Zhi‐Qi

doi:10.1054/npep.1999.0040

Cited by 24 publications

(8 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[146][147][148] However, it has been reported that capsaicin-induced SP release is reduced by opioids. 149,150 Additionally, it has been reported that opioids inhibit neurogenic inflammation by reducing SP released from peripheral afferent terminals. 149,150 Prolonged morphine usage enhances the release of CGRP induced by capsaicin.…”

Section: Sp and Cgrpmentioning

confidence: 99%

“…149,150 Additionally, it has been reported that opioids inhibit neurogenic inflammation by reducing SP released from peripheral afferent terminals. 149,150 Prolonged morphine usage enhances the release of CGRP induced by capsaicin. 135 Neurotransmitter modulation through chronic opioid exposure activates TRPV1 and causes opioid associated tolerance and thermal hyperalgesia.…”

Section: Sp and Cgrpmentioning

confidence: 99%

See 1 more Smart Citation

The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence

et al. 2015

View full text Add to dashboard Cite

Initiated by the activation of various nociceptors, pain is a reaction to specific stimulus modalities. The μ-opioid receptor (MOR) agonists, including morphine, remain the most potent analgesics to treat patients with moderate to severe pain. However, the utility of MOR agonists is limited by the adverse effects associated with the use of these drugs, including analgesic tolerance and physical dependence. A strong connection has been suggested between the expression of the transient receptor potential vanilloid type 1 (TRPV1) ion channel and the development of inflammatory hyperalgesia. TRPV1 is important for thermal nociception induction, and is mainly expressed on sensory neurons. Recent reports suggest that opioid or TRPV1 receptor agonist exposure has contrasting consequences for anti-nociception, tolerance and dependence. Chronic morphine exposure modulates TRPV1 activation and induces the anti-nociception effects of morphine. The regulation of many downstream targets of TRPV1 plays a critical role in this process, including calcitonin gene-related peptide (CGRP) and substance P (SP). Additional factors also include capsaicin treatment blocking the anti-nociception effects of morphine in rats, as well as opioid modulation of TRPV1 responses through the cAMP-dependent PKA pathway and MAPK signaling pathways. Here, we review new insights concerning the mechanism underlying MOR-TRPV1 crosstalk and signaling pathways and discuss the potential mechanisms of morphine-induced anti-nociception, tolerance and dependence associated with the TRPV1 signaling pathway and highlight how understanding these mechanisms might help find therapeutic targets for the treatment of morphine induced antinociception, tolerance and dependence.

show abstract

Section: Sp and Cgrpmentioning

confidence: 99%

Section: Sp and Cgrpmentioning

confidence: 99%

The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Furthermore, opioids can reduce proinflammatory cytokines and adhesion molecules (Belkowski et al, 1995;Wilson et al, 1998;Walker et al, 2000;Philippe et al, 2003), edema and plasma extravasation (Jin et al, 1999;Khalil et al, 1999;Romero et al, 2005;Jiménez et al, 2006;Börzsei et al, 2008), and radiological and histological parameters (Binder et al, 2000(Binder et al, , 2001Walker, 2003). In human tissue sample, opioids have been shown to reduce proinflammatory cytokines, matrix metalloproteinase, and synovial leukocyte counts (Raap et al, 2000;Takeba et al, 2001;Straub et al, 2008).…”

Section: Opioid Effects On Inflammation and Wound Healingmentioning

confidence: 99%

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

2011

View full text Add to dashboard Cite

“…Opioid receptor agonists exhibit anti-inflammatory effects [11, 12]. Activation of opioid receptors on primary afferent neurons reduces the excitability of these neurons suppressing the antidromic release of pro-inflammatory neuropeptides such as substance P (SP) and neurokinin-A (NKA) [1, 13, 14].…”

Section: Introductionmentioning

confidence: 99%

Morphine-induced early delays in wound closure: Involvement of sensory neuropeptides and modification of neurokinin receptor expression

Rook

Hasan

McCarson

2009

Biochemical Pharmacology

View full text Add to dashboard Cite

Dose-limiting side effects of centrally-acting opioid drugs have led to the use of topical opioids to reduce the pain associated with chronic cutaneous wounds. However, previous studies indicate that topical morphine application impairs wound healing. This study was designed to elucidate the mechanisms by which morphine delays wound closure. Rats were depleted of sensory neuropeptides by treatment with capsaicin, and full-thickness 4 mm diameter wounds were excised from the intrascapular region. Wounds were treated topically twice daily with 5 mM morphine sulfate, 1 mM substance P, 1 mM neurokinin A, or 5 mM morphine combined with 1 m M substance P or neurokinin A and wound areas assessed. During closure, wound tissue was taken 1, 3, 5, and 8 days post-wounding from control and morphine-treated rats and immunostained for neurokinin receptors and markers for macrophages, myofibroblasts, and vasculature. Results obtained from capsaicin-treated animals demonstrated a significant delay in the early stages of wound contraction that was reversed by neuropeptide application. Treatment of capsaicin-treated rats with topical morphine did not further delay wound closure, suggesting that topical opioids impair wound closure via the inhibition of peripheral neuropeptide release into the healing wound. Morphine application altered neurokinin-1 and neurokinin-2 receptor expression in inflammatory and parenchymal cells essential for wound healing in a cell-specific manner, demonstrating a direct effect of morphine on neurokinin receptor regulation within an array of cells involved in wound healing. These data provide evidence indicating a potentially detrimental effect of topical morphine application on the dynamic wound healing process.

show abstract

Endomorphin-1 reduces carrageenan-induced Fos expression in the rat spinal dorsal horn

Cited by 24 publications

References 19 publications

The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence

The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

Morphine-induced early delays in wound closure: Involvement of sensory neuropeptides and modification of neurokinin receptor expression

Contact Info

Product

Resources

About