Estradiol Prevents A Beta(25-35) -Inhibited Long-Term Potentiation Induction Through Enhancing Survival Of Newborn Neurons In The Dentate Gyrus

Aim and Methods: Estradiol (E2) is reported to attenuate -amyloid (A) accumulation and slow the progression of Alzheimer's disease (AD). This study explored the beneficial effect of E2 in AD using histological examination and electrophysiological recording technique in AD model mice created by intracerebroventricular injection of -amyloid 25-35 (A(25-35)). Results: Infusion of A(25-35) reduced the number of newborn neurons in the 2nd week after birth, a critical period for neurite growth, and impaired high-frequency stimulation-dependent long-term potentiation (LTP) induction in perforant path-granular synapses of hippocampal dentate gyrus (DG). Administration of E2 from the 2nd to 4th week after cell birth in A(25-35)-mice ameliorated the impairment of newborn neurons and LTP induction in DG. Acute application of E2 failed to increase the newborn neurons and rescue LTP induction in the DG of A(25-35)-mice. Conclusions: The effect of E2 in A(25-35)-impaired LTP induction depends on its neuroprotection improvement.