Time-Dependent Cross Talk between Spinal Serotonin 5-HT<sub>2A</sub>Receptor and mGluR1 Subserves Spinal Hyperexcitability and Neuropathic Pain after Nerve Injury

Aira, Zigor; Buesa, Itsaso; Gallego, Mónica; Caño, Gontzal Garcı́a del; Mendiable, Nahia; Mingo, Janire; Rada, Diego; Bilbao, Juan; Zimmermann, M.; Azkue, Jon Jatsu

doi:10.1523/jneurosci.1364-12.2012

Cited by 35 publications

(26 citation statements)

References 95 publications

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“…identified upregulation of serotonin receptors (5‐HT 2A Receptor) and impairment of μ‐opioid receptors in neuropathic pain subjects . Moreover, Aira et al . observed that 5‐HT 2A receptor agonists increased the potentials of pain‐transmitting C fibers in the dorsal horn.…”

Section: Autonomic Modulation Of Painmentioning

confidence: 99%

“…In response to these findings, Klintschar concluded that serotonin is particularly important in the process of endogenous analgesia . Aira et al . identified upregulation of serotonin receptors (5‐HT 2A Receptor) and impairment of μ‐opioid receptors in neuropathic pain subjects .…”

Section: Autonomic Modulation Of Painmentioning

confidence: 99%

“…Specific serotonin receptors mediate analgesia (5‐HT 1A , 5‐HT 1B , 5‐HT 1D , and 5‐HT 7 ), while others are pronociceptive (5‐HT 2A and 5‐HT 3 ) . Interventions that specifically agonized antinociceptive receptors or antagonized pro‐nociceptive receptors (or both) could produce analgesic results . Antagonists for central CCK receptors could potentially increase the viability of placebo analgesia and other analgesic interventions .…”

Section: Expert Commentary and 5‐year Reviewmentioning

confidence: 99%

“…32,33 In response to these findings, Klintschar 35 concluded that serotonin is particularly important in the process of endogenous analgesia. 36 Aira et al 37 identified upregulation of serotonin receptors (5-HT 2A Receptor) and impairment of μ-opioid receptors in neuropathic pain subjects. 34 Moreover, Aira et al 37 observed that 5-HT 2A receptor agonists increased the potentials of pain-transmitting C fibers in the dorsal horn.…”

Section: Serotonergic Modulation Of Painmentioning

confidence: 99%

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Therapeutic Basis of Clinical Pain Modulation

Kirkpatrick

McEntire

Hambsch

et al. 2015

Clinical Translational Sci

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Pain is a hallmark of almost all bodily ailments and can be modulated by agents, including analgesics and anesthetics that suppress pain signals in the central nervous system. Defects in the modulatory systems, including the endogenous pain-inhibitory pathways, are a major factor in the initiation and chronicity of pain. Thus, pain modulation is particularly applicable to the practice of medicine. This review summarizes the existing literature on pain modulation. Here, we critically reviewed the literature from PubMed on pain modulation published primarily within last 5 years in high impact journals. Specifically, we have discussed important anatomical landmarks of pain modulation and outlined the endogenous networks and underlying mechanisms of clinically relevant pain modulatory methods. The Gate Control Theory is briefly presented with discussion on the capacity of pain modulation to cause both hyper- and hypoalgesia. An emphasis has been given to highlight key areas in pain research that, because of unanswered questions or therapeutic potential, merit additional scientific scrutiny. The information presented in this article would be helpful in developing novel therapies, metrics, and interventions for improved patient management.

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Section: Autonomic Modulation Of Painmentioning

confidence: 99%

Section: Autonomic Modulation Of Painmentioning

confidence: 99%

Section: Expert Commentary and 5‐year Reviewmentioning

confidence: 99%

Section: Serotonergic Modulation Of Painmentioning

confidence: 99%

See 2 more Smart Citations

Therapeutic Basis of Clinical Pain Modulation

Kirkpatrick

McEntire

Hambsch

et al. 2015

Clinical Translational Sci

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“…With regard to the (bilateral) spreading of CRPS signs, it was suggested that centrally mediated crosstalk of commissural interneurons between the spinal cord, brainstem and trans-synaptic changes in the spinal cord dorsal horn contralateral to the affected side may underlie this spreading [21]. This clinical bilaterality also corresponds to the finding of bilateral maladaptive cortical changes (see below), which are inconclusively understood [18][19][20]22].…”

Section: Review Reinersmann Maier Schwenkreis and Lenzmentioning

confidence: 99%

Complex Regional Pain Syndrome: More Than a Peripheral Disease

et al. 2013

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SUMMARY At early stages, complex regional pain syndrome (CRPS) is clinically characterized by damage of peripheral tissues and nerves (edema, activation of osteoblasts, hyperalgesia to blunt pressure). These signs are the result of a dysbalance of pro- and anti-inflammatory cytokines, which normalizes approximately 6 months after the beginning of the disease, independent from clinical outcome. At the same time, evolving clinical signs such as allodynia, cold hyperalgesia, reduced tactile acuity or symptoms of disrupted body representation (e.g., neglect-like syndrome, impaired hand laterality recognition or shift of the body midline) suggest a crucial role of the CNS in the pathophysiology of this pain syndrome. Imaging studies have found a severe but reversible reduction of the cortical hand representation (primary and secondary somatosensory cortices and primary motor cortices). Interestingly however, complex multisensory integration in central association areas are unaffected in CRPS, as patients are capable of integrating artificial body parts or recognize 2D forms despite tactile dysfunction. Furthermore, despite its unilateral clinical manifestation, it has been shown that in CRPS but not in other unilateral neuropathic pain syndromes, alterations in cortical excitability occur bilaterally, both in sensory and motor regions. In conclusion, a more widespread and bilateral pattern of CNS reorganization appears to characterize CRPS, which might be related to dysfunctions in the basal ganglia or in thalamo-cortical structures. Consequently, CRPS treatment should involve not only anti-inflammatory measures and pain therapy, but also the integration of neurorehabilitative training programs.

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Raphe and ventrolateral medulla proteomics in sudden unexplained death in childhood with febrile seizure history

Leitner,

William,

Faustin

et al. 2024

Acta Neuropathol

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Time-Dependent Cross Talk between Spinal Serotonin 5-HT_2AReceptor and mGluR1 Subserves Spinal Hyperexcitability and Neuropathic Pain after Nerve Injury

Cited by 35 publications

References 95 publications

Therapeutic Basis of Clinical Pain Modulation

Therapeutic Basis of Clinical Pain Modulation

Complex Regional Pain Syndrome: More Than a Peripheral Disease

Raphe and ventrolateral medulla proteomics in sudden unexplained death in childhood with febrile seizure history

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Time-Dependent Cross Talk between Spinal Serotonin 5-HT2AReceptor and mGluR1 Subserves Spinal Hyperexcitability and Neuropathic Pain after Nerve Injury

Cited by 35 publications

References 95 publications

Therapeutic Basis of Clinical Pain Modulation

Therapeutic Basis of Clinical Pain Modulation

Complex Regional Pain Syndrome: More Than a Peripheral Disease

Raphe and ventrolateral medulla proteomics in sudden unexplained death in childhood with febrile seizure history

Contact Info

Product

Resources

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Time-Dependent Cross Talk between Spinal Serotonin 5-HT_2AReceptor and mGluR1 Subserves Spinal Hyperexcitability and Neuropathic Pain after Nerve Injury