Age-related changes in membrane fluidity and fluorescence intensity by tachykinin neuropeptide NKB and Aβ (25-35) with 17β estradiol in female rat brain

Abstract

Changes in the fluidity of membrane lipids are known to occur during aging and by lipid peroxidation. It is well documented that the fluidity state of the lipid phase in a membrane is important for the activity of intrinsic membrane proteins. Oxidants and fluidity of membrane lipids play a significant role in aging and age related neurodegenerative diseases. The aim of the present study was to determine the effect of tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25-35) on 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. Aging brain functions were measured by membrane fluidity and fluorescent intensity with neuropeptides. An in-vitro incubation of Aβ (25-35) in E2 treated brain synaptosomes showed toxic effects on all the parameters. These effects of aging and Aβ (25–35) on membrane fluidity were restored by NKB and combined NKB and Aβ (25–35) with E2. Furthermore, we measured the Tryptophan (Trp) fluorescence to monitor changes in proteins and to make inferences regarding structure and dynamics. Trp is a sensitive marker of protein oxidation and its fluorescence significantly increased in E2 treated synaptosomes of aging rats. Furthermore, to evaluate the effect of oxidative stress on the membrane and protein conformation, fluorescent probe 1-Anilino-8-Naphthalenesulfonate (ANS) were used. An increase in ANS fluorescence in E2 treated synaptosomes of aging rats indicated that E2 is associated with significant conformational changes and surface hydrophobicity of membranes and proteins.

Keywords

• Aging, Neurokinin B, Amyloid Beta (25 - 35), Estradiol