Spinal γ-Aminobutyric Acid Interneuron Plasticity Is Involved in the Reduced Analgesic Effects of Morphine on Neuropathic Pain

Hiroki, Tadanao; Suto, Takashi; Ohta, Jo; Saito, Shigeru; Obata, Hideaki

doi:10.1016/j.jpain.2021.10.002

Cited by 8 publications

(3 citation statements)

References 48 publications

(57 reference statements)

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“…Administration of K252a successfully inhibits the increase of intracellular Ca2 + induced by BDNF in acute slices of the rat superficial dorsal horn [59]. Moreover, in vivo, it diminishes hypersensitivity in several pain models [152,[290][291][292][293][294][295][296][297][298]. Based on promising results from preclinical studies, various pharmaceutical companies have allocated significant resources toward developing and ameliorating kinase inhibitors.…”

Section: Implications For Pain Managementmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor, Nociception and Pain

Merighi

2024

Preprint

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This review article discusses the involvement of the Brain-Derived Neurotrophic Factor (BDNF) in the control of pain. BDNF, a neurotrophin known for its essential role in neuronal survival and plasticity, has garnered significant attention for its potential implications as a modulator of nociception and pain. This comprehensive review aims to provide insights into the multifaceted interactions between BDNF and pain pathways, encompassing both physiological and pathological pain conditions. I delve into the molecular mechanisms underlying BDNF's involvement in pain processing and discuss potential therapeutic applications of BDNF and its mimetics in managing pain. Furthermore, I highlight recent advancements and challenges in translating BDNF-related research into clinical practice.

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Section: Implications For Pain Managementmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor, Nociception and Pain

Merighi

2024

Preprint

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“…Systemic morphine administration increases 5‐hydroxytryptamine (5‐HT) levels in the spinal cord. 1 , 2 , 3 Intracerebroventricular (ICV) injection of morphine also induces 5‐HT release in the spinal cord, 4 , 5 and 5‐HT itself modifies pain transmission in the spinal cord. 6 However, the role of the 5‐HT induced by morphine is not yet fully understood.…”

Section: Introductionmentioning

confidence: 99%

Oral morphine induces spinal 5‐hydroxytryptamine (5‐HT) release using an opioid receptor‐independent mechanism

Nakamura

Komatsu

Yamada

et al. 2023

Pharmacology Res & Perspec

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Morphine induces spinal 5‐hydroxytryptamine (5‐HT) release, but the role and mechanism of the spinal 5‐HT release induced by morphine are not well understood. The purpose of this study was to define the role and mechanism of spinal 5‐HT release induced by oral morphine. We also examined whether persistent pain affected the spinal 5‐HT release induced by oral morphine. Spinal 5‐HT release was measured using microdialysis of lumbar cerebrospinal fluid (CSF). Two opioids, morphine and oxycodone, were orally administered and 5‐HT release was measured in awake rats. Naloxone and β‐funaltrexamine (β‐FNA) were used to determine whether the effect of morphine on 5‐HT release was mediated by opioid receptor activation. To study persistent pain, a formalin test was used. At 45 min after oral morphine administration, the formalin test was started and spinal 5‐HT release was measured. Oral morphine, but not oral oxycodone, increased 5‐HT release at the spinal cord to approximately 4000% of the baseline value. This effect of morphine was not antagonized by either naloxone or β‐FNA at a dose that antagonized the antinociceptive effect of morphine. Formalin‐induced persistent pain itself had no effect on spinal 5‐HT release but enhanced the oral morphine‐induced spinal 5‐HT release. Oral morphine‐induced spinal 5‐HT release was not mediated by opioid receptor activation. Spinal 5‐HT induced by oral morphine did not play a major role in the antinociceptive effect of morphine in the hot plate test. Persistent pain increased oral morphine‐induced spinal 5‐HT release.

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“…Morphine produces its analgesic effect via activation of the μ opioid receptor, and the analgesic effect of morphine is antagonised by naloxone, a μ opioid receptor antagonist. Systemic morphine administration increases 5-hydroxytryptamine (5-HT) levels in the spinal cord (Shimoi et al, 1978;Godefroy et al, 1098;Kimura et al, 2014), as does its intracerebroventricular (ICV) injection (Hiroki et al, 2022;Kawamata et al, 2002). 5-HT itself is known to modify pain transmission in the spinal cord (Stamford, 1995).…”

mentioning

confidence: 99%

Oral morphine induces spinal 5-hydroxytryptamine (5-HT) release using an opioid receptor-independent mechanism.

Nakamura

Komatsu

Yamada

et al. 2023

Preprint

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Background and Purpose Morphine induces spinal 5-hydroxytryptamine (5-HT) release, but the role and mechanism of this release is unclear. The purpose of this study was to define the role and mechanism of spinal 5-HT release induced by oral morphine. We also examined whether persistent pain affected the oral morphine-induced spinal release of 5-HT. Experimental Approach Spinal 5-HT release was measured using microdialysis in lumbar cerebrospinal fluid (CSF). Two opioids, morphine and oxycodone, were orally administered and 5-HT release was measured in awake rats. Naloxone was used to determine whether the effect of morphine on 5-HT release was mediated by opioid receptor activation. To study persistent pain, the formalin test was used. Forty-five minutes after oral morphine, the formalin test was started and spinal 5-HT release was measured. Key Results Oral morphine, but not oral oxycodone, increased 5-HT release in the spinal cord to approximately 4,000% of the baseline value, and this effect of morphine was not antagonised by naloxone at the dose that antagonised the analgesic effect of morphine. Formalin-induced persistent pain itself had no effect on spinal 5-HT release but enhanced the oral morphine-induced spinal 5-HT release. Conclusion and Implications Oral morphine-induced spinal 5-HT release is not mediated by opioid receptor activation. Spinal 5-HT release induced by oral morphine does not play an important role in the analgesic effect of morphine. Persistent pain increases oral morphine-induced spinal 5-HT release.

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Spinal γ-Aminobutyric Acid Interneuron Plasticity Is Involved in the Reduced Analgesic Effects of Morphine on Neuropathic Pain

Abstract: Spinal γ-aminobutyric acid interneuron plasticity is involved in the reduced analgesic effects of morphine on neuropathic pain,

Cited by 8 publications

References 48 publications

Brain-Derived Neurotrophic Factor, Nociception and Pain

Brain-Derived Neurotrophic Factor, Nociception and Pain

Oral morphine induces spinal 5‐hydroxytryptamine (5‐HT) release using an opioid receptor‐independent mechanism

Oral morphine induces spinal 5-hydroxytryptamine (5-HT) release using an opioid receptor-independent mechanism.

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