PMID- 12020852
OWN - NLM
STAT- MEDLINE
DCOM- 20020828
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 939
IP  - 1-2
DP  - 2002 Jun 7
TI  - Evaluation of beta-amyloid peptide 25-35 on calcium homeostasis in cultured rat 
      dorsal root ganglion neurons.
PG  - 65-75
AB  - Accumulation of beta-amyloid (Abeta) protein in brain is an important 
      characteristic for the etiology of Alzheimer's disease. Of all the possible 
      processes generating the neurotoxic effects by Abeta, disruption of intracellular 
      Ca(2+) homeostasis is the primary event. In this process, various intracellular 
      Ca(2+) regulatory mechanisms are reported to be involved. Using patch-clamp 
      techniques, both low and high voltage activated Ca(2+) channel currents were 
      recorded in the cultured dorsal root ganglion (DRG) neurons. Application of Abeta 
      protein fragment, Abeta(25-35) (2 microM), for 30 s increased the amplitude in 
      both currents. The Abeta-triggered facilitation effect of Ca(2+) channel was 
      found in all the depolarized potentials tested, as shown in the current-voltage 
      relationship. Furthermore, after applying single cell Ca(2+) microfluorometric 
      method, it was found that Abeta(25-35) alone could trigger elevations of 
      intracellular Ca(2+) concentration ([Ca(2+)](i)) level in 90% of the cells 
      tested. The elevation diminished completely by cumulatively adding CdCl(2), 
      NiCl(2), thapsigargin (TG), FCCP and Zn(2+) in the normal bath solution. 
      Combining pharmacological approaches, we found that voltage-dependent Ca(2+) 
      channels, Ca(2+) stores and a putative Zn(2+)-sensitive extracellular Ca(2+) 
      entry, respectively, makes 61.0, 25.1, and 13.9% contribution to the [Ca(2+)](i) 
      increase caused by Abeta. When tested in a Ca(2+)-free buffer, mitochondria was 
      found to contribute 41.3% of Abeta produced [Ca(2+)](i) elevation and the 
      remaining 58.7% was attributed to endoplasmic reticulum (ER) release.
FAU - He, L-M
AU  - He LM
AD  - Institute of Biophysics and Biochemistry, Huazhong University of Science and 
      Technology, Wuhan 430074, PR China.
FAU - Chen, L-Y
AU  - Chen LY
FAU - Lou, X-L
AU  - Lou XL
FAU - Qu, A-L
AU  - Qu AL
FAU - Zhou, Z
AU  - Zhou Z
FAU - Xu, T
AU  - Xu T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Calcium Channels)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Peptide Fragments)
RN  - 0 (Uncoupling Agents)
RN  - 0 (amyloid beta-protein (25-35))
RN  - 370-86-5 (Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone)
RN  - 67526-95-8 (Thapsigargin)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Amyloid beta-Peptides/*metabolism/pharmacology
MH  - Animals
MH  - Calcium/*metabolism
MH  - Calcium Channels/drug effects/*metabolism
MH  - Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone/pharmacology
MH  - Cell Culture Techniques
MH  - Endoplasmic Reticulum/drug effects/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Ganglia, Spinal/*drug effects/*metabolism
MH  - Homeostasis/drug effects
MH  - Mitochondria/drug effects/metabolism
MH  - Neurons/*drug effects/*metabolism
MH  - Patch-Clamp Techniques
MH  - Peptide Fragments/*metabolism/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Thapsigargin/pharmacology
MH  - Uncoupling Agents/pharmacology
EDAT- 2002/05/22 10:00
MHDA- 2002/08/29 10:01
CRDT- 2002/05/22 10:00
PHST- 2002/05/22 10:00 [pubmed]
PHST- 2002/08/29 10:01 [medline]
PHST- 2002/05/22 10:00 [entrez]
AID - S0006899302025490 [pii]
AID - 10.1016/s0006-8993(02)02549-0 [doi]
PST - ppublish
SO  - Brain Res. 2002 Jun 7;939(1-2):65-75. doi: 10.1016/s0006-8993(02)02549-0.