Evidence Details for Creb1
PMID Title Journal Year Abstract
37548586 Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity. Brain Behav. 2023 Oct;13(10):e3177. doi: 10.1002/brb3.3177. Epub 2023 Aug 7. 2023 Oct BACKGROUND: Central sensitization is one of the important mechanisms underlying neuropathic and radicular pain due to cervical spondylotic radiculopathy (CSR). Recent studies have shown that the calmodulin-dependent protein kinase II (CaMKII)/cAMP-response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway mediates central sensitization through its involvement in spinal cord synaptic plasticity. Our group has previously found that electroacupuncture (EA) has a good analgesic effect on CSR. However, the central analgesic mechanism of EA for CSR is not yet clear. METHODS: The rats were randomly divided into Blank group, Sham-operated group, CSR group, and EA group. We prepared the CSR rat model using the fish wire extrusion method. The behavioral and mechanical pain thresholds of the rats in each group were measured 5 days after successful modeling and 7 days after the intervention. The first intervention was started 5 days after successful modeling, and the EA group was treated by acupuncture at the bilateral LI4 and LR3 points on the same side as one group, connected to a G6805-I electroacupuncture apparatus with continuous waves at 1.5 Hz. The remaining groups were not subjected to EA intervention. The treatment was administered once a day for 7 consecutive days and then executed. We used WB, immunofluorescence, and qRT-PCR to detect the expression of CaMKII/CREB/BDNF signaling pathway-related factors in the synaptic of rat spinal cord in each group. RESULTS: EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy. CONCLUSION: EA mediates central sensitization and exerts analgesic effects on CSR by modulating spinal synaptic plasticity, which may be related to the inhibition of CaMKII/CREB/BDNF signaling pathway."

Evidence Sentence: Recent studies have shown that the calmodulin-dependent protein kinase II (CaMKII)/cAMP-response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway mediates central sensitization through its involvement in spinal cord synaptic plasticity.
Evidence Sentence: The above suggests that EA inhibits CAMKII/CREB pathway transduction in the spinal cord tissue of CSR rats.
Evidence Sentence: Electroacupuncture regulated synaptic plasticity mediated by inhibiting CAMKII/CREB signaling pathway in the spinal cord of CSR rats
Evidence Sentence: We used WB, immunofluorescence, and qRT-PCR to detect the expression of CaMKII/CREB/BDNF signaling pathway-related factors in the synaptic of rat spinal cord in each group.
Evidence Sentence: EA mediates central sensitization and exerts analgesic effects on CSR by modulating spinal synaptic plasticity, which may be related to the inhibition of CaMKII/CREB/BDNF signaling pathway.
Evidence Sentence: Electroacupuncture mediates central sensitization and exerts analgesic effects on CSR by modulating spinal synaptic plasticity, which may be related to the inhibition of CaMKII/CREB/BDNF signaling pathway.
Evidence Sentence: Electroacupuncture ameliorates pain in cervical spondylotic radiculopathy rat by inhibiting the CaMKII/CREB/BDNF signaling pathway and regulating spinal synaptic plasticity
Evidence Sentence: EA improved pain threshold and motor function in CSR rats, inhibited the expression of BDNF, P-TrkB, CAMKII, and P-CREB in spinal cord synapses, reduced the expression of pain factor c-fos and postsynaptic membrane protein molecule neuroligin2, exerted a modulating effect on spinal cord synaptic plasticity in CSR rats, and suppressed the overactive synaptic efficacy.
Evidence Sentence: The expressions of CAMKII, CREB, and P-CREB in the spinal cord tissues were detected by WB, PCR, and immunohistochemistry.
Evidence Sentence: The results are presented in Figures 5, 7, and 8, there was no significant difference in the expression of CREB in the spinal cord tissues of the spinal cord among the four groups(p > .05).
Evidence Sentence: The expression of CAMKII, CAMKII mRNA, and P-CREB was increased in the spinal cord synaptic tissue of rats in the CSR group compared with the Sham group (p < .01).
Evidence Sentence: The expression of CAMKII, CAMKII mRNA, and P-CREB was reduced in the spinal cord tissue of rats in the EA group compared with the CSR group (p < .01).
Evidence Sentence: Immunofluorescence analysis showed that the staining density of CAMKII was weaker in the EA group compared with the CSR group, but no significant difference was seen in the staining density of CREB and P-CREB in each group.