Prostaglandin E2 contributes to the synthesis of brain-derived neurotrophic factor in primary sensory neuron in ganglion explant cultures and in a neuropathic pain model

Duarte, P C; St-Jacques, Bruno; Ma, Weiya

doi:10.1016/j.expneurol.2012.01.021

Cited by 50 publications

(39 citation statements)

References 62 publications

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“…Among them, cAMP-response element-binding protein (CREB), a transcription factor, is one of the major downstream targets of PKA, which controls cellular functions via synthesis of a wide variety of proteins (Shaywitz and Greenberg, 1999). EP4-mediated CREB activation was reported in colon epithelial cells (Srivastava et al, 2012), dorsal root ganglion neurons (Cruz Duarte et al, 2012), Leydig tumor cells (Sirianni et al, 2009), and breast cancer cells (Subbaramaiah et al, 2008). Other signaling pathways in addition to CREB are activated via PKA.…”

Section: Signaling Pathwaysmentioning

confidence: 99%

The Prostanoid EP4 Receptor and Its Signaling Pathway

Yokoyama

Iwatsubo²,

Umemura³

et al. 2013

Pharmacol Rev

227

257

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Section: Signaling Pathwaysmentioning

confidence: 99%

The Prostanoid EP4 Receptor and Its Signaling Pathway

Yokoyama

Iwatsubo²,

Umemura³

et al. 2013

Pharmacol Rev

227

257

View full text Add to dashboard Cite

“…Binding of BDNF to postsynaptic TrkB induces increases in C-fiber activity and activation of PKC- and ERK- mediated signaling cascades (Kerr et al, 1999; Pezet et al, 2002; Yajima et al, 2005). Nerve injury can induce an ERK-mediated shift in BDNF expression from small/medium sized dorsal root ganglion (DRG) neurons to large DRG neurons thereby contributing to central sensitization at this first order synapse in the spinothalamaic tract (Cruz Duarte, St-Jacques, and Ma, 2012). Injury-associated activation of spinal microglia leads to the release of BDNF stores from microglia which disinhibits spinal projection neurons through GABA A and glycine receptors (Coull et al, 2005).…”

Section: Cellular and Synaptic Mechanismsmentioning

confidence: 99%

Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: Implications for pain and memory

Rahn

Guzman-Karlsson

Sweatt

2013

Neurobiology of Learning and Memory

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Sensitization is a form of non-associative conditioning in which amplification of behavioral responses can occur following presentation of an aversive or noxious stimulus. Understanding the cellular and molecular underpinnings of sensitization has been an overarching theme spanning the field of learning and memory as well as that of pain research. In this review we examine how sensitization, both in the context of learning as well as pain processing, shares evolutionarily conserved behavioral, cellular/synaptic, and epigenetic mechanisms across phyla. First, we characterize the behavioral phenomenon of sensitization both in invertebrates and vertebrates. Particular emphasis is placed on long-term sensitization (LTS) of withdrawal reflexes in Aplysia following aversive stimulation or injury, although additional invertebrate models are also covered. In the context of vertebrates, sensitization of mammalian hyperarousal in a model of post-traumatic stress disorder (PTSD), as well as mammalian models of inflammatory and neuropathic pain is characterized. Second, we investigate the cellular and synaptic mechanisms underlying these behaviors. We focus our discussion on serotonin-mediated long-term facilitation (LTF) and axotomy-mediated long-term hyperexcitability (LTH) in reduced Aplysia systems, as well as mammalian spinal plasticity mechanisms of central sensitization. Third, we explore recent evidence implicating epigenetic mechanisms in learning-and pain- related sensitization. This review illustrates the fundamental and functional overlay of the learning and memory field with the pain field which argues for homologous persistent plasticity mechanisms in response to sensitizing stimuli or injury across phyla.

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“…These results suggest that EP1 and EP4 receptor subtypes, PKA, ERK/MAPK, and CREB signaling pathways as well as NGF are involved in PGE 2 -induced BDNF synthesis in neurons. It has been suggested that injured nerve-derived PGE 2 contributes to BDNF up-regulation in dorsal root ganglion neurons following nerve injury [108]. Facilitating the synthesis of BDNF in primary sensory neurons appears to be one of the mechanisms underlying the role of PGE 2 in the genesis of neuropathic pain, repair of damaged neurons, and neuronal regeneration.…”

Section: Interaction Between Pufas and Bdnfmentioning

confidence: 99%

Autism as a disorder of deficiency of brain-derived neurotrophic factor and altered metabolism of polyunsaturated fatty acids

Das

2013

Nutrition

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Prostaglandin E2 contributes to the synthesis of brain-derived neurotrophic factor in primary sensory neuron in ganglion explant cultures and in a neuropathic pain model

Cited by 50 publications

References 62 publications

The Prostanoid EP4 Receptor and Its Signaling Pathway

The Prostanoid EP4 Receptor and Its Signaling Pathway

Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: Implications for pain and memory

Autism as a disorder of deficiency of brain-derived neurotrophic factor and altered metabolism of polyunsaturated fatty acids

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