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Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability
TLDR
This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability. Expand
Pleiotropic effect of histamine H4 receptor modulation in the central nervous system
TLDR
Results show the antinociceptive, antiamnesic, anxiolytic and anorexant effects induced by neuronal H4R agonism, suggesting that H4 modulators may have broader utility further the control of inflammatory and immune processes. Expand
Behavioural phenotype of histamine H4 receptor knockout mice: Focus on central neuronal functions
TLDR
It is illustrated that H 4R modulates various neurophysiological functions such as locomotor activity, anxiety, nociception and feeding behaviour, confirming the importance of the integrity and functionality of neuronal H4R in the histaminergic regulation of neuronal functions. Expand
Histamine H4 receptor activation alleviates neuropathic pain through differential regulation of ERK, JNK, and P38 MAPK phosphorylation
TLDR
Findings suggest a prevalent modulation of ERK activity after H4R stimulation and indicate the DRG as prominent site of action for H 4R-mediated antineuropathic activity. Expand
μ Opioid Receptor-Triggered Notch-1 Activation Contributes to Morphine Tolerance: Role of Neuron–Glia Communication
TLDR
The findings implicate the MOR-triggered Notch-1 signaling in promoting MOR internalization and morphine analgesic tolerance by epigenetic regulation mechanisms, and suggest that NotCh-1 inhibitors could represent an innovative therapeutic perspective for the management of opioid tolerance in chronic pain therapy. Expand
Histamine H4 receptor agonist‐induced relief from painful peripheral neuropathy is mediated by inhibition of spinal neuroinflammation and oxidative stress
TLDR
The contribution of neuroinflammation and oxidative stress in a model of peripheral neuropathy is studied to clarify the pathobiology of neuropathic pain and an innovative treatment is assessed by investigating the effects of histamine H4 receptor ligands in this model. Expand
The RNA-binding protein HuD promotes spinal GAP43 overexpression in antiretroviral-induced neuropathy
TLDR
Results indicated that HuD recruitment and GAP43 protein increase are mechanistically linked events involved in the response to antiretroviral-induced neurodegenerative processes. Expand
Inhibition of spinal ERK1/2-c-JUN signaling pathway counteracts the development of low doses morphine-induced hyperalgesia.
TLDR
The data suggest that ERK contributes to the morphine-induced hyperalgesia by regulating the activation of c-JUN, and double immunofluorescence studies revealed that p-ERK and p-c-jUN are localized on neurons of the spinal dorsal horn expressing µ receptors. Expand
The HDAC1/c‐JUN complex is essential in the promotion of nerve injury‐induced neuropathic pain through JNK signaling
TLDR
A role for histone deacetylase in the emergence of neuropathic pain is supported and co‐immunoprecipitation experiments showed the presence of a heterodimeric complex between HDAC1 and c‐Jun in SNI mice indicating that these transcription factors can act together to regulate transcription throughheterodimerization. Expand
ERK1/2 phosphorylation is involved in the antidepressant-like action of 2,5-diphenyl-3-(4-fluorophenylseleno)-selenophene in mice.
TLDR
Anti-immobility effect of F-DPS was completely blocked by pretreatment of animals with PD 98,059, an inhibitor of ERK phosphorylation, suggesting that ERK signalling activation is involved in its antidepressant-like action in mice. Expand
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