Home › Research › Drug development
Val⁸-GLP-1 remodels synaptic activity and intracellular calcium homeostasis impaired by amyloid β peptide in rats
Wang XH, Yang W, Hölscher C, Wang ZJ, Cai HY, Li QS, Qi JS.. Journal of neuroscience research, 2013-01-18
Topic: Brain proteins, microglia and lab models
Type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer's disease (AD) in the elderly. Glucagon-like peptide-1 (GLP-1), a modulator in T2DM therapy, has been shown to have neuroprotective properties. However, the native GLP-1 can be rapidly degraded by the enzyme dipeptidyl peptidase IV (DPP IV); the neuroprotective mechanism of GLP-1 in the central nervous system is still an open question, and whether GLP-1 can prevent amyloid β (Aβ)-induced synaptic dysfunction and calcium disorder is still unclear. The present study, by using patch clamp and calcium imaging techniques, investigated the effects of Val⁸-GLP-1(7-36), a GLP-1 analogue with profound resistance to DPP IV, on the excitatory and inhibitory synaptic transmission and intracellular calcium concentration ([Ca²⁺](i) ) in the absence or presence of Aβ1-40. The results showed that 1) Aβ1-40 significantly reduced the frequency of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) in CA1 pyramidal neurons of rat brain slices; 2) Val⁸-GLP-1(7-36) did not affect the activity of miniature postsynaptic currents but effectively protected against the Aβ1-40-induced decrease in mEPSC and mIPSC frequency; 3) Aβ1-40 significantly increased [Ca²⁺](i) in primary neuronal cultures; and 4) Val⁸-GLP-1(7-36) alone did not change the intracellular calcium level but prevented Aβ1-40-induced persistent elevation of [Ca²⁺](i). These findings demonstrate for the first time that central application of Val⁸-GLP-1(7-36) could protect against Aβ-induced synaptic dysfunction and intracellular calcium overloading, suggesting that the neuroprotection of GLP-1 may be involved in the remodeling of synaptic activity and intracellular calcium homeostasis in the brain.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wang, X. H., Yang, W., Hölscher, C., Wang, Z. J., Cai, H. Y., Li, Q. S., et al. (2013). Val⁸-GLP-1 remodels synaptic activity and intracellular calcium homeostasis impaired by amyloid β peptide in rats. Journal of neuroscience research. https://doi.org/10.1002/jnr.23181
Vancouver
Wang XH, Yang W, Hölscher C, Wang ZJ, Cai HY, Li QS, et al. Val⁸-GLP-1 remodels synaptic activity and intracellular calcium homeostasis impaired by amyloid β peptide in rats. Journal of neuroscience research. 2013. doi:10.1002/jnr.23181. PMID: 23335292.
BibTeX
@article{wang2013-23335292,
author = {Wang, X. H. and Yang, W. and Hölscher, C. and Wang, Z. J. and Cai, H. Y. and Li, Q. S. and Qi, J. S.},
title = {{Val⁸-GLP-1 remodels synaptic activity and intracellular calcium homeostasis impaired by amyloid β peptide in rats}},
journal = {Journal of neuroscience research},
year = {2013},
doi = {10.1002/jnr.23181},
pmid = {23335292},
url = {https://doi.org/10.1002/jnr.23181}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- The results showed that 1) Aβ1-40 significantly reduced the frequency of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) in CA1 pyramidal neurons of rat brain slices; 2) Val⁸-GLP-1(7-36) did not affect the activity of miniature postsynaptic currents but effectively protected against the Aβ1-40-induced decrease in mEPSC and mIPSC frequency; 3) Aβ1-40 significantly increased [Ca²⁺](i) in primary neuronal cultures; and 4) Val⁸-GLP-1(7-36) alone did not change the intracellular calcium level but prevented Aβ1-40-induced persistent elevation of [Ca²⁺](i).
- These findings demonstrate for the first time that central application of Val⁸-GLP-1(7-36) could protect against Aβ-induced synaptic dysfunction and intracellular calcium overloading, suggesting that the neuroprotection of GLP-1 may be involved in the remodeling of synaptic activity and intracellular calcium homeostasis in the brain.
New to this subject? Start with our plain-English guide: Treatments →
Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuroscience research) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2013 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “rats”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23335292) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related
Studies in the library that share something with this one. The line above each title says what.