ArticleMolecular pain2016
Consistent sex-dependent effects of PKMζ gene ablation and pharmacological inhibition on the maintenance of referred pain.
Article in Molecular pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 41 citations in OpenAlex.
- PKMζ is necessary for long-term depression and long-term potentiation in the medial prefrontal cortex.The Journal of physiology · 2026Article
- Sex differences in the transition to chronic pain.The Journal of clinical investigation · 2025Review
- Peripheral macrophages contribute to nociceptor priming in mice with chronic intermittent hypoxia.Science signaling · 2024Article
- Neuroendocrine Mechanisms Governing Sex Differences in Hyperalgesic Priming Involve Prolactin Receptor Sensory Neuron Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Qualitative sex differences in pain processing: emerging evidence of a biased literature.Nature reviews. Neuroscience · 2020Review
- Recent advances toward understanding the mysteries of the acute to chronic pain transition.Current opinion in physiology · 2019Article
- aPKC in neuronal differentiation, maturation and function.Neuronal signaling · 2019Review
- PKMζ in the nucleus accumbens acts to dampen cocaine seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Sex differences in the role of atypical PKC within the basolateral nucleus of the amygdala in a mouse hyperalgesic priming model.Neurobiology of pain (Cambridge, Mass.)Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPersistently active PKMζ has been implicated in maintaining spinal nociceptive sensitization that underlies pain hypersensitivity. However, evidence for PKMζ in the maintenance of pain hypersensitivity comes exclusively from short-term studies in males using pharmacological agents of questionable selectivity. The present study examines the contribution of PKMζ to long-lasting allodynia associated with neuropathic, inflammatory, or referred visceral and muscle pain in males and females using pharmacological inhibition or genetic ablation.
resultsPharmacological inhibition or genetic ablation of PKMζ reduced mild formalin pain and slowly developing contralateral allodynia in nerve-injured rats, but not moderate formalin pain or ipsilateral allodynia in models of neuropathic and inflammatory pain. Pharmacological inhibition or genetic ablation of PKMζ also effectively reduced referred visceral and muscle pain in male, but not in female mice and rats.
conclusionWe show pharmacological inhibition and genetic ablation of PKMζ consistently attenuate long-lasting pain hypersensitivity. However, differential effects in models of referred versus inflammatory and neuropathic pain, and in males versus females, highlight the roles of afferent input-dependent masking and sex differences in the maintenance of pain hypersensitivity.
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