Journal
METABOLIC BRAIN DISEASE
Volume 30, Issue 1, Pages 151-156Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-014-9594-4
Keywords
Alzheimer disease; Amyloid beta-peptide; Borago Officinalis; Long-term potentiation; Hippocampus
Categories
Funding
- Hamadan University of Medical Sciences [9106142414]
Ask authors/readers for more resources
Alzheimer's disease (AD) begins with impairment in synaptic functions before developing into later neurodegeneration and neural loss. In the present study we have examined the protective effects of Borago Officinalis (borage) extract on amyloid beta (A beta)-Induced long term potentiation (LTP) disruption in hippocampal dentate gyrus (DG). Wistar male rats received intrahippocampal (IHP) injection of the A beta (25-35) and borage extract throughout gestation (100 mg/kg). LTP in perforant path- DG synapses was assessed using electrophysiology method and field excitatory post- synaptic potential (fEPSP) slope and population spike (PS) amplitude were measured by 400 Hz tetanization. Finally, the total thiol content of hippocampus was measured using colorimetric reaction based on the Ellman's method. The results showed that A beta (25-35) significantly decreased fEPSP slope and SP amplitude comparing with the control and sham group, whereas borage extract administration increased these parameters compared to the A beta group. A beta induced a remarkable decrease in total thiol content of hippocampus and borage prevented the decrease of the hippocampal total sulfhydryl (SH) groups. This data suggest that A beta (25-35) can effectively inhibit LTP in the granular cells of the DG in hippocampus, and borage supplementation reverse the synaptic plasticity in DG following A beta treatment and that borage consumption may lead to an improvement of AD-induced cognitive dysfunction.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available