↓ Skip to main content

Increased Synaptophysin Is Involved in Inflammation-Induced Heat Hyperalgesia Mediated by Cyclin-Dependent Kinase 5 in Rats

Overview of attention for article published in PLOS ONE, October 2012
Altmetric Badge

Mentioned by

twitter
1 X user

Citations

dimensions_citation
32 Dimensions

Readers on

mendeley
34 Mendeley
You are seeing a free-to-access but limited selection of the activity Altmetric has collected about this research output. Click here to find out more.
Title
Increased Synaptophysin Is Involved in Inflammation-Induced Heat Hyperalgesia Mediated by Cyclin-Dependent Kinase 5 in Rats
Published in
PLOS ONE, October 2012
DOI 10.1371/journal.pone.0046666
Pubmed ID
Authors

Hong-Hai Zhang, Xiao-Qin Zhang, Wen-Yuan Wang, Qing-Sheng Xue, Han Lu, Jin-Lu Huang, Ting Gui, Bu-Wei Yu

Abstract

Mechanisms associated with cyclin-dependent kinase 5 (Cdk5)-mediated heat hyperalgesia induced by inflammation remain undefined. This study was designed to examine whether Cdk5 mediates heat hyperalgesia resulting from peripheral injection of complete Freund's adjuvant (CFA) in the spinal dorsal horns of rats by interacting with synaptophysin, a well known membrane protein mediating the endocytosis-exocytosis cycle of synaptic vesicles as a molecular marker associated with presynaptic vesicle membranes. The role of Cdk5 in mediating synaptophysin was examined through the combined use of behavioral approaches, imaging studies, and immunoprecipitation following CFA-induced inflammatory pain. Results showed that Cdk5 colocalized with both synaptophysin and soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein receptors (SNAREs) consisting of VAMP-2, SNAP-25, and syntaxin 1A in spinal dorsal horn of rats. Increased synaptophysin expression of spinal cord horn neurons post intraplantar injection of CFA coincided with increased duration of heat hyperalgesia lasting from 6 h to 3 d. Intrathecal administration of roscovitine, a Cdk5 specific inhibitor, significantly depressed synaptophysin expression during peak heat hyperalgesia and heat hyperalgesia induced by peripheral injection of CFA. Data presented in this report indicated that calpain activity was transiently upregulated 6 h post CFA-treatment despite previous reports suggesting that calpain was capable of cleaving p35 into p25. Results from previous studies obtained by other laboratories demonstrated that significant changes in p35 expression levels within spinal cord horn neurons were not observed in the CFA-treated inflammatory pain model although significant upregulation of Cdk5 kinase was observed between 2 h to 7 d. Therefore, generation of p25 occurred in a calpain-independent fashion in a CFA-treated inflammatory pain model. Our results demonstrated that increased synaptophysin levels were involved in heat hyperalgesia mediated by Cdk5 in spinal cord dorsal horns of CFA-treated rats, suggesting that inhibiting abnormal activation of Cdk5-synaptophysin may present a novel target for diminishing inflammatory pain.

X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 34 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Spain 1 3%
United States 1 3%
Unknown 32 94%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 24%
Researcher 5 15%
Student > Bachelor 3 9%
Professor > Associate Professor 3 9%
Student > Master 3 9%
Other 7 21%
Unknown 5 15%
Readers by discipline Count As %
Agricultural and Biological Sciences 10 29%
Neuroscience 5 15%
Medicine and Dentistry 3 9%
Nursing and Health Professions 2 6%
Biochemistry, Genetics and Molecular Biology 2 6%
Other 6 18%
Unknown 6 18%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 October 2012.
All research outputs
#18,316,001
of 22,679,690 outputs
Outputs from PLOS ONE
#153,825
of 193,573 outputs
Outputs of similar age
#130,767
of 172,325 outputs
Outputs of similar age from PLOS ONE
#3,454
of 4,541 outputs
Altmetric has tracked 22,679,690 research outputs across all sources so far. This one is in the 11th percentile – i.e., 11% of other outputs scored the same or lower than it.
So far Altmetric has tracked 193,573 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 15.0. This one is in the 10th percentile – i.e., 10% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 172,325 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 11th percentile – i.e., 11% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 4,541 others from the same source and published within six weeks on either side of this one. This one is in the 11th percentile – i.e., 11% of its contemporaries scored the same or lower than it.