ArticlePain2012
Contribution of PKMζ-dependent and independent amplification to components of experimental neuropathic pain.
Article in Pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Article
- An assessor-blinded, randomized comparative trial of transcutaneous auricular vagus nerve stimulation (taVNS) combined with cranial electroacupuncture vs. citalopram for depression with chronic pain.Frontiers in psychiatry · 2022Article
- Neuronal Adenylyl Cyclase Targeting Central Plasticity for the Treatment of Chronic Pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Review
- Mechanisms Underlying Bone and Joint Pain.Current osteoporosis reports · 2018Review
- PKMζ in the nucleus accumbens acts to dampen cocaine seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Forebrain medial septum sustains experimental neuropathic pain.Scientific reports · 2018Article
- Brain-derived neurotrophic factor derived from sensory neurons plays a critical role in chronic pain.Brain : a journal of neurology · 2018Article
- PKMζ Is Not Required for Development of Postsurgical Pain.Molecular neurobiology · 2018Article
- Involvement of Spinal PKMζ Expression and Phosphorylation in Remifentanil-Induced Long-Term Hyperalgesia in Rats.Cellular and molecular neurobiology · 2017Article
- The TrkA receptor mediates experimental thermal hyperalgesia produced by nerve growth factor: Modulation by the p75 neurotrophin receptor.Neuroscience · 2017Article
- Cingulate Alpha-2A Adrenoceptors Mediate the Effects of Clonidine on Spontaneous Pain Induced by Peripheral Nerve Injury.Frontiers in molecular neuroscience · 2017Article
- The Effect of Electroacupuncture on PKMzeta in the ACC in Regulating Anxiety-Like Behaviors in Rats Experiencing Chronic Inflammatory Pain.Neural plasticity · 2017Article
- Consistent sex-dependent effects of PKMζ gene ablation and pharmacological inhibition on the maintenance of referred pain.Molecular pain · 2016Article
- Zeta Inhibitory Peptide as a Novel Therapy to Control Chronic Visceral Hypersensitivity in a Rat Model.PloS one · 2016Article
- Endogenous opioid activity in the anterior cingulate cortex is required for relief of pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- PKMζ knockdown disrupts post-ischemic long-term potentiation via inhibiting postsynaptic expression of aminomethyl phosphonic acid receptors.Journal of biomedical research · 2015Review
- Gabapentin prevents oxaliplatin-induced central sensitization in the dorsal horn neurons in rats.Iranian journal of basic medical sciences · 2015Article
- Involvement of protein kinase ζ in the maintenance of hippocampal long-term potentiation in rats with chronic visceral hypersensitivity.Journal of neurophysiology · 2015Article
- Plasticity-Related PKMζ Signaling in the Insular Cortex Is Involved in the Modulation of Neuropathic Pain after Nerve Injury.Neural plasticity · 2015Article
- Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Injuries can induce adaptations in pain processing that result in amplification of signaling. One mechanism may be analogous to long-term potentiation and involve the atypical protein kinase C, PKMζ. The possible contribution of PKMζ-dependent and independent amplification mechanisms to experimental neuropathic pain was explored in rats with spinal nerve ligation (SNL) injury. SNL increased p-PKMζ in the rostral anterior cingulate cortex (rACC), a site that mediates, in part, the unpleasant aspects of pain. Inhibition of PKMζ within the rACC by a single administration of ζ-pseudosubstrate inhibitory peptide (ZIP) reversed SNL-induced aversiveness within 24 hours, whereas N-methyl-d-aspartate receptor blockade with MK-801 had no effects. The SNL-induced aversive state (reflecting "spontaneous" pain), was re-established in a time-dependent manner, with full recovery observed 7 days post-ZIP administration. Neither rACC ZIP nor MK-801 altered evoked responses. In contrast, spinal ZIP or MK-801, but not scrambled peptide, transiently reversed evoked hypersensitivity, but had no effect on nerve injury-induced spontaneous pain. PKMζ phosphorylation was not altered by SNL in the spinal dorsal horn. These data suggest that amplification mechanisms contribute to different aspects of neuropathic pain at different levels of the neuraxis. Thus, PKMζ-dependent amplification contributes to nerve injury-induced aversiveness within the rACC. Moreover, unlike mechanisms maintaining memory, the consequences of PKMζ inhibition within the rACC are not permanent in neuropathic pain, possibly reflecting the re-establishment of amplification mechanisms by ongoing activity of injured nerves. In the spinal cord, however, both PKMζ-dependent and independent mechanisms contribute to amplification of evoked responses, but apparently not spontaneous pain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.