Postoperative pain impairs subsequent performance on a spatial memory task via effects on N-methyl-d-aspartate receptor in aged rats

Chi, Haidong; Kawano, Takashi; Tamura, Takahiko; Iwata, Hisato; Takahashi, Yasuhiro; Eguchi, Satoru; Yamazaki, Fumimoto; Kumagai, Naoya; Yokoyama, Masataka

doi:10.1016/j.lfs.2013.10.028

Cited by 59 publications

(47 citation statements)

References 32 publications

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“…Hippocampal NR2B protein levels significantly increase in irritable bowel syndrome-like rats, a model of chronic visceral pain (Chen Y. et al, 2014). Postoperative pain upregulates the levels of NMDAR2 subunits in the hippocampus (Chi et al, 2013). By contrast, the partial sciatic nerve ligation model of neuropathic pain reduces the expression of NR1 and NR2B in the hippocampus of injured rats (Wang et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Chronic Monoarthritis Pain Accelerates the Processes of Cognitive Impairment and Increases the NMDAR Subunits NR2B in CA3 of Hippocampus from 5-month-old Transgenic APP/PS1 Mice

Gong

Wang

Liu

et al. 2017

Front. Aging Neurosci.

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Many factors impact cognitive impairment; however, the effects of chronic pain and the mechanisms underlying these effects on cognitive impairment are currently unknown. Here we tested the hypothesis that chronic pain accelerates the transition from normal cognition to mild cognitive impairment (MCI) in 5-month-old transgenic APP/PS1 mice, an animal model of Alzheimer’s disease (AD), and that neurotoxicity induced by N-methyl-D-aspartic acid receptor (NMDAR) subunits may be involved in this process. Chronic monoarthritis pain was induced in transgenic APP/PS1 mice and 5-month-old wild-type (WT) mice by intra- and pre-articular injections of Freund’s complete adjuvant (FCA) into one knee joint. Pain behavior, learning and memory function, and the distribution and quantity of NMDAR subunits (NR1, NR2A and NR2B) in hippocampal CA1 and CA3 regions were assessed. Our results showed that although persistent and robust monoarthritis pain was induced by the FCA injections, only the transgenic APP/PS1 mice with chronic monoarthritis pain exhibited marked learning and memory impairments. This result suggested that chronic monoarthritis pain accelerated the cognitive impairment process. Furthermore, only transgenic APP/PS1 mice with chronic monoarthritis pain exhibited an overexpression of NR2B and an increased NR2B/NR2A ratio in the hippocampus CA3. These findings suggest that chronic pain is a risk factor for cognitive impairment and that increased neurotoxicity associated with NMDAR subunit activation may underpin the impairment. Thus, NMDARs may be a therapeutic target for the prevention of chronic pain-induced cognitive impairment.

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Section: Discussionmentioning

confidence: 99%

Chronic Monoarthritis Pain Accelerates the Processes of Cognitive Impairment and Increases the NMDAR Subunits NR2B in CA3 of Hippocampus from 5-month-old Transgenic APP/PS1 Mice

Gong

Wang

Liu

et al. 2017

Front. Aging Neurosci.

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“…Although spontaneous pain cannot be self-reported in animals, several observational methods have been developed to assess it, including evaluating facial expressions and/or grooming behavior, analgesic self-administration, and autotomy. 50,61 The Grimace Scale uses facial expression assessment to detect spontaneous pain across a variety of species, including in mice, 50,52,60 rats, 15,24,65,68,87 and cats, 35 and evaluates 4 different facial features that are rated on a severity scale of: 0 (not present), 1 (moderate), or 2 (present and severe) (FIGURE 2C). 50 The Grimace Scale has been reported to detect spontaneous pain in rodent models of neuropathic pain.…”

Section: Pain Symptomsmentioning

confidence: 99%

The Physiological Basis of Cervical Facet-Mediated Persistent Pain: Basic Science and Clinical Challenges

Ita¹,

Zhang²,

Holsgrove³

et al. 2017

Journal of Orthopaedic & Sports Physical Therapy

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FIGURE 1. Schematic illustrating the anatomy in the periphery of the facet joint and the relevant neuronal connections to the central nervous system. Afferents that innervate the facet joint and its capsular ligament have cell bodies in the DRG and synapse with neurons in the spinal dorsal horn. Nociceptive information is encoded by many types of afferents, including IB4-positive nonpeptidergic neurons and peptidergic fibers that produce neuropeptides, such as CGRP and substance P. Noxious stimuli are translated into electrical (eg, action potentials) and biochemical (eg, neurotransmitter) signals. In persistent pain, central sensitization occurs, with neuronal hyperexcitability and altered neurotransmitter production and release in the spinal dorsal horn. Abbreviations: CGRP, calcitonin gene-related peptide; DRG, dorsal root ganglion; IB4, isolectin B4.

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“…In fact, surgery induces peripheral immune challenges, leading to an exaggerated neuroinlammatory response. More recently, several studies have demo nstrated that neuroinlammation in the hippocampus is most likely to be involved in the pathogenesis of POCD [35,[44][45][46][47][48][49][50][51]. Neuroinlammation is a complex response to brain injury characterized by maladaptive microglial activation mainly involving the activation of glia and increased levels of pro-inlammatory cytokines, including interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) [52][53][54].…”

Section: Mechanisms Of Pocdmentioning

confidence: 99%

Postoperative Cognitive Dysfunction: Preclinical Highlights and Perspectives on Preventive Strategies

Locatelli¹,

Kawano²

2017

Current Topics in Anesthesiology

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One of the common complications associated with anaesthesia and surgery in geriatric patients is the postoperative cognitive dysfunction (POCD). This cognitive impairment afects the long-term prognosis and has been shown to be associated with long-term disability, higher health care costs, and even increased mortality. On the other hand, clinical research on POCD is in its infancy, the condition has not been clariied, and since no strategy for management is currently available, it is imperative to develop speciic methods for prevention and management. Although its pathogenesis involves various factors, accumulating evidence suggests that surgery elicits an inlammatory response in the hippocampus, a brain area closely related to cognitive function, playing a key role in the development of POCD. Several studies suggest that age-related phenotypic change of microglia is associated with pathogenic neuroinlammation, and more importantly it may be modiiable. In this chapter, we discuss the current overview and preclinical highlights regarding POCD. We further discuss some perspectives on preventive strategies for POCD, based on the indings of our preclinical research and the available literature.

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Postoperative pain impairs subsequent performance on a spatial memory task via effects on N-methyl-d-aspartate receptor in aged rats

Cited by 59 publications

References 32 publications

Chronic Monoarthritis Pain Accelerates the Processes of Cognitive Impairment and Increases the NMDAR Subunits NR2B in CA3 of Hippocampus from 5-month-old Transgenic APP/PS1 Mice

Chronic Monoarthritis Pain Accelerates the Processes of Cognitive Impairment and Increases the NMDAR Subunits NR2B in CA3 of Hippocampus from 5-month-old Transgenic APP/PS1 Mice

The Physiological Basis of Cervical Facet-Mediated Persistent Pain: Basic Science and Clinical Challenges

Postoperative Cognitive Dysfunction: Preclinical Highlights and Perspectives on Preventive Strategies

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