Electrophysiological evidence for voltage-gated calcium channel 2 (Cav2) modulation of mechano- and thermosensitive spinal neuronal responses in a rat model of osteoarthritis

Rahman, Wahida; Patel, Ryan; Dickenson, Anthony H.

doi:10.1016/j.neuroscience.2015.07.073

Cited by 19 publications

(20 citation statements)

References 61 publications

(89 reference statements)

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“…Our finding correlates with earlier reports, where MIA‐placebo rats displayed a persistent decrease in the ipsilateral PWT to stimulation with von Frey filament. An important advance in operant behaviours is that these approaches may allow the detection and mechanistic investigation of spontaneous neuropathic or ongoing inflammatory/nociceptive (ie, non‐evoked) pain that is otherwise difficult to assess in nonverbal animals .…”

Section: Discussionsupporting

confidence: 93%

“…These results are in line with the fact that PGB medication has an analgesic effect by decreasing neuropeptides release as a primary mechanism of PGB drug action . It is recognized that MIA is able to induce massive calcium influx in rat peripheral nerve in vitro via inhibition of metabolism and in opposite, PGB may have roles in regulating vesicular neurotransmitter release in vivo by binding to the voltage‐dependent calcium channel . Moreover, nerve injury up‐regulated α 2 ‐δ‐1 expression in sensory neurons and the dorsal spinal cord that correlated with pain behaviours .…”

Section: Discussionsupporting

confidence: 76%

“…16,66 It is recognized that MIA is able to induce massive calcium influx in rat peripheral nerve in vitro via inhibition of metabolism 67 and in opposite, PGB may have roles in regulating vesicular neurotransmitter release in vivo by binding to the voltage-dependent calcium channel. 9 Moreover, nerve injury up-regulated α 2 -δ-1 expression in sensory neurons and the dorsal spinal cord that correlated with pain behaviours. 68 This sustains why gabapentinoids are preferentially active in states of facilitated nociceptive processing.…”

Section: Discussionmentioning

confidence: 99%

“…The chemical monosodium iodoacetate (MIA)‐induced joint degeneration in rats is one of the most used animal models to screen analgesic drugs to alleviate OA pain . Having established a high‐level sensitivity method for quantifying spinal neuropeptides, our group recently tested their reliability and validity as pain outcome in MIA‐induced OA: spinal nociceptive neuropeptides demonstrated face (high responsiveness to OA induction), construct (high specificity with lower concentration in naïve and sham rats), and criterion‐related validity (high sensitivity to detect analgesic response to punctual intra‐articular (IA) lidocaine administrations); their time‐response was also determined, demonstrating also repeatability and test‐retest reliability, as well as reproducibility in different chemical or surgical OA models in rats .…”

Section: Introductionmentioning

confidence: 99%

“…6,7 The chemical monosodium iodoacetate (MIA)-induced joint degeneration in rats is one of the most used animal models to screen analgesic drugs to alleviate OA pain. 8,9 Having established a high-level sensitivity method for quantifying spinal neuropeptides, 7,10,11 our group recently 6 tested their reliability and validity as pain outcome in MIA-induced OA:…”

Section: Introductionmentioning

confidence: 99%

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Sensitivity of functional targeted neuropeptide evaluation in testing pregabalin analgesic efficacy in a rat model of osteoarthritis pain

Otis

Guillot

Moreau

et al. 2019

Clin Exp Pharma Physio

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The monosodium iodoacetate (MIA)‐induced joint degeneration in rats is the most used animal model to screen analgesic drugs to alleviate osteoarthritis (OA) pain. This study aimed to evaluate the analgesic efficacy of pregabalin (PGB) in an MIA‐induced OA model in rodents by using functional and neuroproteomic pain assessment methods. Treatment group included PGB in curative intent over 9 days compared to gold standard therapy (positive controls) and placebo (negative control). Functional assessments of pain (quantitative sensory testing and operant test) were performed concomitantly with spinal neuropeptides quantification. At day 21 post‐OA induction, PGB in MIA rats reduced tactile allodynia (P = 0.028) and improved the place escape/avoidance behaviour (P = 0.04) compared to values recorded at last time‐point before initiating analgesic therapy. All spinal neuropeptide concentrations, such as substance P, calcitonin gene‐related peptide, bradykinin and somatostatin, came back to normal (non‐affected) rat values, compared to their increase observed in MIA rats receiving the placebo (P < 0.0001). Initiated 13 days after chemical OA induction, repeated medication with PGB provided analgesia according to quantitative sensory testing, operant test and targeted neuropeptides pain assessment methods. This report highlights the interest of using reliable and sensitive methods like targeted neuropeptide quantification to detect the analgesic effects of a test article with concomitant functional assessments of pain when studying OA pain components.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Sensitivity of functional targeted neuropeptide evaluation in testing pregabalin analgesic efficacy in a rat model of osteoarthritis pain

Otis

Guillot

Moreau

et al. 2019

Clin Exp Pharma Physio

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Challenges and opportunities in translational pain research – An opinion paper of the working group on translational pain research of the European pain federation (EFIC)

Mouraux¹,

Bannister

Becker

et al. 2021

European Journal of Pain

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For decades, basic research on the underlying mechanisms of nociception has held promise to translate into efficacious treatments for patients with pain. Despite great improvement in the understanding of pain physiology and pathophysiology, translation to novel, effective treatments for acute and chronic pain has however been limited, and they remain an unmet medical need. In this opinion paper bringing together pain researchers from very different disciplines, the opportunities and challenges of translational pain research are discussed. The many factors that may prevent the successful translation of bench observations into useful and effective clinical applications are reviewed, including interspecies differences, limited validity of currently available preclinical disease models of pain, and limitations of currently used methods to assess nociception and pain in non‐human and human models of pain. Many paths are explored to address these issues, including the backward translation of observations made in patients and human volunteers into new disease models that are more clinically relevant, improved generalization by taking into account age and sex differences, and the integration of psychobiology into translational pain research. Finally, it is argued that preclinical and clinical stages of developing new treatments for pain can be improved by better preclinical models of pathological pain conditions alongside revised methods to assess treatment‐induced effects on nociception in human and non‐human animals. Significance: For decades, basic research of the underlying mechanisms of nociception has held promise to translate into efficacious treatments for patients with pain. Despite great improvement in the understanding of pain physiology and pathophysiology, translation to novel, effective treatments for acute and chronic pain has however been limited, and they remain an unmet medical need.

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Voltage-Gated Calcium Channels in the Afferent Pain Pathway

Ferron

Zamponi²

2022

Voltage-Gated Calcium Channels

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Electrophysiological evidence for voltage-gated calcium channel 2 (Cav2) modulation of mechano- and thermosensitive spinal neuronal responses in a rat model of osteoarthritis

Abstract: HighlightsMIA-dependent antinociceptive effect of TROX-1 on neuronal activity.Alterations in Cav2.2 channel function contribute to osteoarthritic (OA) pain.Blocking Cav2.2 channels has therapeutic potential for treating OA pain.

Cited by 19 publications

References 61 publications

Sensitivity of functional targeted neuropeptide evaluation in testing pregabalin analgesic efficacy in a rat model of osteoarthritis pain

Sensitivity of functional targeted neuropeptide evaluation in testing pregabalin analgesic efficacy in a rat model of osteoarthritis pain

Challenges and opportunities in translational pain research – An opinion paper of the working group on translational pain research of the European pain federation (EFIC)

Voltage-Gated Calcium Channels in the Afferent Pain Pathway

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