Chronic dizocilpine or apomorphine and development of neuropathy in two animal models II: Effects on brain cytokines and neurotrophins

Al-Amin, Hassen; Sarkis, Rani A.; Atweh, Samir; Jabbur, Suhayl J.; Saadé, Nayef E.

doi:10.1016/j.expneurol.2010.11.005

Cited by 58 publications

(36 citation statements)

References 70 publications

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“…Whereas most studies have examined afferent nociceptors and spinal cord pathways, more recent investigations focus on brain circuitry. Various rodent models for persistent pain show morphological, functional, and molecular changes in limbic circuitry, including the hippocampus18192021, striatum222324, frontal cortex252627, and amygdala28. Based on these results and on recent human imaging data2930, we hypothesized that persistent neuropathic pain-like behavior in the rodent is primarily associated with functional reorganization of brain regions within the limbic system, including the hippocampus, amygdala, and striatum.…”

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confidence: 98%

Resting-state functional reorganization of the rat limbic system following neuropathic injury

Baliki

Chang

Baria

et al. 2014

Sci Rep

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Human brain imaging studies from various clinical cohorts show that chronic pain is associated with large-scale brain functional and morphological reorganization. However, how the rat whole-brain network is topologically reorganized to support persistent pain-like behavior following neuropathic injury remains unknown. Here we compare resting state fMRI functional connectivity-based whole-brain network properties between rats receiving spared nerve injury (SNI) vs. sham injury, at 5 days (n = 11 SNI; n = 12 sham) and 28 days (n = 11 SNI; n = 12 sham) post-injury. Similar to the human, the rat brain topological properties exhibited small world features and did not differ between SNI and sham. Local neural networks in SNI animals showed minimal disruption at day 5, and more extensive reorganization at day 28 post-injury. Twenty-eight days after SNI, functional connection changes were localized mainly to within the limbic system, as well as between the limbic and nociceptive systems. No connectivity changes were observed within the nociceptive network. Furthermore, these changes were lateralized and in proportion to the tactile allodynia exhibited by SNI animals. The findings establish that SNI is primarily associated with altered information transfer of limbic regions and provides a novel translational framework for understanding brain functional reorganization in response to a persistent neuropathic injury.

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confidence: 98%

Resting-state functional reorganization of the rat limbic system following neuropathic injury

Baliki

Chang

Baria

et al. 2014

Sci Rep

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“…Furthermore, depression-like behavior after maternal separation and exposure to corticosterone is associated with the alterations to BDNF-TrkB signaling in female but not male rats [35]. On the other hand, neuropathic pain decreased the levels of BDNF in the hippocampus [36]. The intracerebroventricular administration of 4-methylcatechol, a potent stimulator of BDNF synthesis, decreased the depression-like behavior induced by neuropathic pain [37].…”

Section: Discussionmentioning

confidence: 97%

Sex differences in depression-like behavior after nerve injury are associated with differential changes in brain-derived neurotrophic factor levels in mice subjected to early life stress

Nishinaka

Kinoshita

Nakamoto

et al. 2015

Neuroscience Letters

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“…Cytokines other than TNF, such IL-1β and IL-6, have been found to be have a role in neuropathic pain after peripheral nerve injury (Arruda et al, 2000; Balschun et al, 2004). Like TNF, IL-1β is a pro-inflammatory cytokine that has been implicated in the induction and maintenance of neuropathic pain (Honore et al, 2006; Ren et al, 2009; Bianchi et al, 1998; Hori et al, 1998) and has been found to be upregulated in the hippocampus after spared nerve injury or CCI (Al-Amin et al, 2011; del Rey et al 2011). Further, interfering with IL-1β signals in the brain reduces depressive-like symptoms observed during spared nerve injury (Norman et al, 2010), indicating that over-expression of IL-1β in the hippocampus may be relevant for these symptoms.…”

Section: Discussionmentioning

confidence: 99%

Neuropathic pain-induced depressive-like behavior and hippocampal neurogenesis and plasticity are dependent on TNFR1 signaling

Dellarole

Morton

Brambilla

et al. 2014

Brain, Behavior, and Immunity

134

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Patients suffering from neuropathic pain have a higher incidence of mood disorders such as depression. Increased expression of tumor necrosis factor (TNF) has been reported in neuropathic pain and depressive-like conditions and most of the pro-inflammatory effects of TNF are mediated by the TNF receptor 1 (TNFR1). Here we sought to investigate: 1) the occurrence of depressive-like behavior in chronic neuropathic pain and the associated forms of hippocampal plasticity, and 2) the involvement of TNFR1-mediated TNF signaling as a possible regulator of such events. Neuropathic pain was induced by chronic constriction injury of the sciatic nerve in wild-type and TNFR1−/− mice. Anhedonia, weight loss and physical state were measured as symptoms of depression. Hippocampal neurogenesis, neuroplasticity, myelin remodeling and TNF/TNFRs expression were analyzed by immunohistochemical analysis and western blot assay. We found that neuropathic pain resulted in the development of depressive symptoms in a time dependent manner and was associated with profound hippocampal alterations such as impaired neurogenesis, reduced expression of neuroplasticity markers and myelin proteins. The onset of depressive-like behavior also coincided with increased hippocampal levels of TNF, and decreased expression of TNF receptor 2 (TNFR2), which were all fully restored after mice spontaneously recovered from pain. Notably, TNFR1−/− mice did not develop depressive-like symptoms after injury, nor were there changes in hippocampal neurogenesis and plasticity. Our data show that neuropathic pain induces a cluster of depressive-like symptoms and profound hippocampal plasticity that are dependent on TNF signaling through TNFR1.

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Chronic dizocilpine or apomorphine and development of neuropathy in two animal models II: Effects on brain cytokines and neurotrophins

Cited by 58 publications

References 70 publications

Resting-state functional reorganization of the rat limbic system following neuropathic injury

Resting-state functional reorganization of the rat limbic system following neuropathic injury

Sex differences in depression-like behavior after nerve injury are associated with differential changes in brain-derived neurotrophic factor levels in mice subjected to early life stress

Neuropathic pain-induced depressive-like behavior and hippocampal neurogenesis and plasticity are dependent on TNFR1 signaling

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