C&lt;i&gt;-fos&lt;/i&gt; Antisense Oligodeoxynucleotide Decreases Subcutaneous Bee Venom Injection-Induced Nociceptive Behavior and Fos Expression in the Rat

Wu, Sheng Xi; Wang, W.; Wang, Y.Y.; Ni, Tian-shu; Li, Y.Q.; Yew, D T-W

doi:10.1159/000065430

Cited by 16 publications

(11 citation statements)

References 20 publications

(31 reference statements)

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“…Decreased expression of Fos was confirmed by immunofluorescent evidence and was accompanied with decreased allodynia in the early stage. In agreement with our previous study [24], c- fos ASO could inhibit c- fos activation in parallel with the decreased allodynia induced by SNL. The most remarkable inhibitory effect of c- fos ASO on allodynia is at the early stage after SNL, which supports the above concept: c- fos activation contributes more to the induction of allodynia.…”

Section: Discussionsupporting

confidence: 93%

“…Fos protein is rapidly expressed in the spinal dorsal horn neurons following noxious peripheral nerve stimulation [21] and correlates well with nociceptive behaviors [19]. Thus, Fos expression is used to identify nociceptive input activated or excited population of neurons [22], [23], [24].…”

Section: Introductionmentioning

confidence: 99%

“…In the current study, L-α-aminoadipate (L-AA) was used to inactivate astrocytes based on the fact that its disruption of the astrocytic network in amygdala is confined to astrocytes [28], [29]. C- fos antisense oligodeoxynucleotides (ASO) was used in our previous studies and the corresponding nociceptive behavioral changes were observed as a consequence of knocking down its protein product [24], [30], [31], [32], thus, it was employed in this study to shut down activated neurons.…”

Section: Introductionmentioning

confidence: 99%

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Crosstalk between Spinal Astrocytes and Neurons in Nerve Injury-Induced Neuropathic Pain

et al. 2009

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Emerging research implicates the participation of spinal dorsal horn (SDH) neurons and astrocytes in nerve injury-induced neuropathic pain. However, the crosstalk between spinal astrocytes and neurons in neuropathic pain is not clear. Using a lumbar 5 (L5) spinal nerve ligation (SNL) pain model, we testified our hypothesis that SDH neurons and astrocytes reciprocally regulate each other to maintain the persistent neuropathic pain states. Glial fibrillary acidic protein (GFAP) was used as the astrocytic specific marker and Fos, protein of the protooncogene c-fos, was used as a marker for activated neurons. SNL induced a significant mechanical allodynia as well as activated SDH neurons indicated by the Fos expression at the early phase and activated astrocytes with the increased expression of GFAP during the late phase of pain, respectively. Intrathecal administration of c-fos antisense oligodeoxynucleotides (ASO) or astroglial toxin L-α-aminoadipate (L-AA) reversed the mechanical allodynia, respectively. Immunofluorescent histochemistry revealed that intrathecal administration of c-fos ASO significantly suppressed activation of not only neurons but also astrocytes induced by SNL. Meanwhile, L-AA shortened the duration of neuronal activation by SNL. Our data offers evidence that neuronal and astrocytic activations are closely related with the maintenance of neuropathic pain through a reciprocal “crosstalk”. The current study suggests that neuronal and non-neuronal elements should be taken integrally into consideration for nociceptive transmission, and that the intervention of such interaction may offer some novel pain therapeutic strategies.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Crosstalk between Spinal Astrocytes and Neurons in Nerve Injury-Induced Neuropathic Pain

et al. 2009

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“…Although intrathecal injections of c-Fos AS-ODNs can inhibit Fos protein expression after noxious stimuli [49,50,56-59], their effects on pain behavior are inconsistent. Several studies showed that c-Fos AS-ODNs decrease nociceptive behavior or hyperalgesia following formalin [60], bee venom [59], and adjuvant [58]. On the contrary, Hunter et al and Ibrahim et al reported that c-Fos AS-ODNs increase formalin-induced pain [49,50].…”

Section: The Role Of C-fos and Perk In Central Sensitizationmentioning

confidence: 99%

c-Fos or pERK, Which is a Better Marker for Neuronal Activation and Central Sensitization After Noxious Stimulation and Tissue Injury?

Gao¹,

Ji²

2009

TOPAINJ

348

280

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Abstractc-Fos, the protein of the protooncogene c-fos, has been extensively used as a marker for the activation of nociceptive neurons in the spinal cord for more than twenty years since Hunt et al. first reported that peripheral noxious stimulation to a hind paw of rats leads to a marked induction of c-Fos in superficial and deep dorsal horn neurons in 1987. In 1999, Ji et al. reported that phosphorylated extracellular signal-regulated kinase (pERK) is specifically induced by noxious stimulation in superficial dorsal horn neurons. Accumulating evidence indicates that pERK induction or ERK activation in dorsal horn neurons is essential for the development of central sensitization, increased sensitivity of dorsal horn neurons that is responsible for the generation of persistent pain. Further, molecular mechanisms underlying ERK-mediated central sensitization have been revealed. In contrast, direct evidence for c-Fos-mediated central sensitization is not sufficient. After a noxious stimulus (e.g., capsaicin injection) or tissue injury, c-Fos begins to be induced after 30-60 minutes, whereas pERK can be induced within a minute, which can correlate well with the development of pain hypersensitivity. While c-Fos is often induced in the nuclei of neurons, pERK can be induced in different subcellular structures of neurons such as nuclei, cytoplasma, axons, and dendrites. pERK can even be induced in spinal cord microglia and astrocytes after nerve injury. In summary, both cFos and pERK can be used as markers for neuronal activation following noxious stimulation and tissue injury, but pERK is much more dynamic and appears to be a better marker for central sensitization.

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“…The number of c-Fos-positive neurons began to decline in both superficial layers and deep layers at 4 h and completely disappeared at 96 h after bee venom insult. In comparison with the time course of behavioral nociceptive responses and hyperalgesia induced by bee venom, it is likely that c-Fos expression reflects establishment of a sensitized state at the spinal dorsal horn which requires at least 30 min of persistent primary afferent input to the central site (Wu et al, 2002). The sensitized state of the spinal dorsal horn that may be driven by peripheral nociceptor sensitization is responsible for the development and maintenance of hyperalgesia that disappears with the disappearance of spinal c-Fos expression (Luo et al, 1998; Chen et al, 1999b; Chen and Chen, 2000).…”

Section: Nociceptive and Inflammatory Effects Of Subcutaneous Bee mentioning

confidence: 99%

The nociceptive and anti-nociceptive effects of bee venom injection and therapy: A double-edged sword

Chen

Lariviere

2010

Progress in Neurobiology

166

121

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Bee venom injection as a therapy, like many other complementary and alternative medicine approaches, has been used for thousands of years to attempt to alleviate a range of diseases including arthritis. More recently, additional theraupeutic goals have been added to the list of diseases making this a critical time to evaluate the evidence for the beneficial and adverse effects of bee venom injection. Although reports of pain reduction (analgesic and antinociceptive) and anti-inflammatory effects of bee venom injection are accumulating in the literature, it is common knowledge that bee venom stings are painful and produce inflammation. In addition, a significant number of studies have been performed in the past decade highlighting that injection of bee venom and components of bee venom produce significant signs of pain or nociception, inflammation and many effects at multiple levels of immediate, acute and prolonged pain processes. This report reviews the extensive new data regarding the deleterious effects of bee venom injection in people and animals, our current understanding of the responsible underlying mechanisms and critical venom components, and provides a critical evaluation of reports of the beneficial effects of bee venom injection in people and animals and the proposed underlying mechanisms. Although further studies are required to make firm conclusions, therapeutic bee venom injection may be beneficial for some patients, but may also be harmful. This report highlights key patterns of results, critical shortcomings, and essential areas requiring further study.

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C<i>-fos</i> Antisense Oligodeoxynucleotide Decreases Subcutaneous Bee Venom Injection-Induced Nociceptive Behavior and Fos Expression in the Rat

Cited by 16 publications

References 20 publications

Crosstalk between Spinal Astrocytes and Neurons in Nerve Injury-Induced Neuropathic Pain

Crosstalk between Spinal Astrocytes and Neurons in Nerve Injury-Induced Neuropathic Pain

c-Fos or pERK, Which is a Better Marker for Neuronal Activation and Central Sensitization After Noxious Stimulation and Tissue Injury?

The nociceptive and anti-nociceptive effects of bee venom injection and therapy: A double-edged sword

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