Open Access

Expression and role of CaMKII and Cx43 in a rat model of post‑stroke depression

  • Authors:
    • Shuiliang Tao
    • Mengmeng Jia
    • Tao Qiu
  • View Affiliations

  • Published online on: July 17, 2019     https://doi.org/10.3892/etm.2019.7782
  • Pages: 2153-2159
  • Copyright: © Tao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Expression of Ca2+/CaM‑dependent protein kinase II (CaMKII) and connexin 43 (Cx43) in a rat model of post‑stroke depression (PSD) was investigated. Rats were separated into control group (10 rats underwent a sham operation and were not ligated after incision), PSD group (13 PSD rats) and KN93 group (12 rats were treated with KN93, an inhibitor of CaMKII, on the basis of the PSD group). After PSD modeling, Longa scoring was performed, and an open field test as well as a step‑through test were carried out to observe rat behavior. RT‑qPCR and western blot analysis were used to detect the expression of CaMKII and CX43 in the hippocampus tissue. On the 14th day, the Longa scores in the PSD and KN93 groups were higher than that in the control group (P<0.05), while on the 18th day, Longa score was higher in the PSD group than that in the control and KN93 groups, and higher in the KN93 group than that in the control group (both P<0.05). In the PSD group, the Longa score on the 18th day was significantly higher than that on the 14th day, whereas in the KN93 group, the Longa score on the 18th day was significantly lower than that on the 14th day (both P<0.05). Compared with the PSD group on the 18th day, the passive avoidance defects in the KN93 group were improved, and the frequency of activity in the open field test was significantly increased. On the 18th day, the expression levels of the mRNA and protein of CaMKII were higher in the PSD group than in the control group, whereas those of Cx43 were lower in the PSD group than those in the control group (P<0.05). The mRNA and protein expression levels of CaMKII in the KN93 group were lower than those in the PSD group, but higher than those in the control group. In PSD rats, CaMKII expression is upregulated, but Cx43 expression is downregulated, and both CaMKII and Cx43 may participate in PSD. The inhibitor of CaMKII, KN93, can improve the depression in PSD rats.

References

1 

Wei C, Gao J, Chen L, Zhang F, Ma X, Zhang N, Zhang W, Xue R, Luo L and Hao J: Factors associated with post-stroke depression and emotional incontinence: Lesion location and coping styles. Int J Neurosci. 126:623–629. 2016.PubMed/NCBI

2 

Valiengo L, Casati R, Bolognini N, Lotufo PA, Benseñor IM, Goulart AC and Brunoni AR: Transcranial direct current stimulation for the treatment of post-stroke depression in aphasic patients: A case series. Neurocase. 22:225–228. 2016. View Article : Google Scholar : PubMed/NCBI

3 

Quaranta D, Marra C and Gainotti G: Post-stroke depression: Main phenomenological clusters and their relationships with clinical measures. Behav Neurol. 25:303–310. 2012. View Article : Google Scholar : PubMed/NCBI

4 

Shen L, Piao L and Piao H: Clinical significance of SEP and plasma 5-HT in post stroke depression. J Apo Nerv Dis. 12:1122–1125. 2016.(In Chinese).

5 

Andersen G, Vestergaard K, Ingemann-Nielsen M and Lauritzen L: Risk factors for post-stroke depression. Acta Psychiatr Scand. 92:193–198. 1995. View Article : Google Scholar : PubMed/NCBI

6 

Cunha MP, Budni J, Pazini FL, Oliveira Á, Rosa JM, Lopes MW, Leal RB and Rodrigues AL: Involvement of PKA, PKC, CAMK-II and MEK1/2 in the acute antidepressant-like effect of creatine in mice. Pharmacol Rep. 66:653–659. 2014. View Article : Google Scholar : PubMed/NCBI

7 

Coultrap SJ and Bayer KU: CaMKII regulation in information processing and storage. Trends Neurosci. 35:607–618. 2012. View Article : Google Scholar : PubMed/NCBI

8 

Isobe T and Okuyama T: The amino-acid sequence of S-100 protein (PAP I-b protein) and its relation to the calcium-binding proteins. Eur J Biochem. 89:379–388. 1978. View Article : Google Scholar : PubMed/NCBI

9 

Yang X, Chu H, Tang Y and Dong Q: The role of connexin43 in hemorrhagic transformation after thrombolysis in vivo and in vitro. Neuroscience. 329:54–65. 2016. View Article : Google Scholar : PubMed/NCBI

10 

Najjar S, Pearlman DM, Mackenzie TA, Hernandez F Jr and Brown JR: Role of glial activation and BBB disruption in the pathophysiology of depression. Neurol Psychiatry Brain Res. 22:17–18. 2016. View Article : Google Scholar

11 

Major S, Friedman A and Dreier JP: Recurrent spreading depression (SD) causes early opening of the blood-brain barrier (BBB). J Cereb Blood Flow Metab. 25 (Suppl 1):S2602005. View Article : Google Scholar

12 

Li X, Rao F, Deng CY, Wei W, Liu FZ, Yang H, Wang ZY, Kuang SJ, Chen XY, Xue YM, et al: Involvement of ERK1/2 in Cx43 depression induced by macrophage migration inhibitory factor in atrial myocytes. Clin Exp Pharmacol Physiol. 44:771–778. 2017. View Article : Google Scholar : PubMed/NCBI

13 

Fu Y, Zhang SS, Xiao S, Basheer WA, Baum R, Epifantseva I, Hong T and Shaw RM: Cx43 isoform GJA1-20k promotes microtubule dependent mitochondrial transport. Front Physiol. 8:9052017. View Article : Google Scholar : PubMed/NCBI

14 

Wu X, Balesar R, Lu J, Farajnia S, Zhu Q, Huang M, Bao AM and Swaab DF: Erratum to: Increased glutamic acid decarboxylase expression in the hypothalamic suprachiasmatic nucleus in depression. Brain Struct Funct. 222:38632017. View Article : Google Scholar : PubMed/NCBI

15 

Overstreet DH: Modeling depression in animal models. Methods Mol Biol. 829:125–144. 2012. View Article : Google Scholar : PubMed/NCBI

16 

Longa EZ, Weinstein PR, Carlson S and Cummins R: Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke. 20:84–91. 1989. View Article : Google Scholar : PubMed/NCBI

17 

Livak KJ and Schmittgen TD: Analysis of relative geneexpression data using real time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods. 25:402–408. 2001. View Article : Google Scholar : PubMed/NCBI

18 

No authors listed, . Correction to: In-hospital risk prediction for post-stroke depression: Development and validation of the post-stroke depression prediction scale. Stroke. 48:e1512017.PubMed/NCBI

19 

Swartz RH, Bayley M, Lanctôt KL, Murray BJ, Cayley ML, Lien K, Sicard MN, Thorpe KE, Dowlatshahi D, Mandzia JL, et al: Post-stroke depression, obstructive sleep apnea, and cognitive impairment: Rationale for, and barriers to, routine screening. Int J Stroke. 11:509–518. 2016. View Article : Google Scholar : PubMed/NCBI

20 

Li W, Ling S, Yang Y, Hu Z, Davies H and Fang M: Systematic hypothesis for post-stroke depression caused inflammation and neurotransmission and resultant on possible treatments. Neuro Endocrinol Lett. 35:104–109. 2014.PubMed/NCBI

21 

Freitas-Andrade M, She J, Bechberger J, Naus CC and Sin WC: Acute connexin43 temporal and spatial expression in response to ischemic stroke. J Cell Commun Signal. 12:193–204. 2018. View Article : Google Scholar : PubMed/NCBI

22 

Zhang Z, Fei P, Mu J, Wang H, Li W and Song J: Decreased expression of neuronal Per-Arnt-Sim domain protein 4 gene in the hippocampus of a post-stroke depression rat model. Exp Ther Med. 7:1045–1049. 2014. View Article : Google Scholar : PubMed/NCBI

23 

Zhang L, Zhao M and Sui RB: Cerebellar fastigial nucleus electrical stimulation alleviates depressive-like behaviors in post-stroke depression rat model and potential mechanisms. Cell Physiol Biochem. 41:1403–1412. 2017. View Article : Google Scholar : PubMed/NCBI

24 

Wu C, Zhang J and Chen Y: Study on the behavioral changes of a post-stroke depression rat model. Exp Ther Med. 10:159–163. 2015. View Article : Google Scholar : PubMed/NCBI

25 

Kozoriz MG, Bechberger JF, Bechberger GR, Suen MW, Moreno AP, Maass K, Willecke K and Naus CC: The connexin43 C-terminal region mediates neuroprotection during stroke. J Neuropathol Exp Neurol. 69:196–206. 2010. View Article : Google Scholar : PubMed/NCBI

26 

Margrie TW, Rostas JA and Sah P: Presynaptic long-term depression at a central glutamatergic synapse: A role for CaMKII. Nat Neurosci. 1:378–383. 1998. View Article : Google Scholar : PubMed/NCBI

27 

Feigin VL, Krishnamurthi RV, Parmar P, Norrving B, Mensah GA, Bennett DA, Barker-Collo S, Moran AE, Sacco RL, Truelsen T, et al GBD 2013 Writing Group; GBD 2013 stroke panel experts group, : Update on the global burden of ischemic and hemorrhagic stroke in 1990–2013: The GBD 2013 Study. Neuroepidemiology. 45:161–176. 2015. View Article : Google Scholar : PubMed/NCBI

28 

Sacco RL, Adams R, Albers G, Alberts MJ, Benavente O, Furie K, Goldstein LB, Gorelick P, Halperin J, Harbaugh R, et al American Heart Association; American Stroke Association Council on Stroke; Council on Cardiovascular Radiology and Intervention; American Academy of Neurology, : Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: A statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: Co-sponsored by the Council on Cardiovascular Radiology and Intervention: The American Academy of Neurology affirms the value of this guideline. Stroke. 37:577–617. 2006. View Article : Google Scholar : PubMed/NCBI

Related Articles

Journal Cover

September 2019
Volume 18 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
APA
Tao, S., Jia, M., & Qiu, T. (2019). Expression and role of CaMKII and Cx43 in a rat model of post‑stroke depression. Experimental and Therapeutic Medicine, 18, 2153-2159. https://doi.org/10.3892/etm.2019.7782
MLA
Tao, S., Jia, M., Qiu, T."Expression and role of CaMKII and Cx43 in a rat model of post‑stroke depression". Experimental and Therapeutic Medicine 18.3 (2019): 2153-2159.
Chicago
Tao, S., Jia, M., Qiu, T."Expression and role of CaMKII and Cx43 in a rat model of post‑stroke depression". Experimental and Therapeutic Medicine 18, no. 3 (2019): 2153-2159. https://doi.org/10.3892/etm.2019.7782