Oxytocin may reverse amyloid beta-induced cognitive impairment

New research in Biochemical and Biophysical Research Communications probed the effect of oxytocin on synaptic plasticity using rodents.

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In prior studies, a number of researchers have focused on the peptide hormone oxytocin and its role in regulating learning and memory performance. But no study has delved into the effects of oxytocin on the amyloid β-induced impairment of synaptic plasticity, synonymous with cognitive disorders — that is, until now.

New research in Biochemical and Biophysical Research Communications probed the effect of oxytocin on synaptic plasticity using rodents.

“To investigate the effect of oxytocin on synaptic plasticity, we prepared acute hippocampal slices for extracellular recording and assessed long-term potentiation (LTP) with perfusion of the amyloid β (Aβ) active fragment (Aβ25-35) in the absence and presence of oxytocin,” a Japanese research team, led by Junpei Takahashi, stated in their article.

The team at the Tokyo University of Science initiated a set of experiments to demonstrate how Aβ triggers the signaling abilities of neurons in the slices to inhibit or impair their synaptic plasticity. They also noted that after increased perfusion with oxytocin, the signaling abilities surged, indicating that oxytocin could completely reverse the impairment of synaptic plasticity caused by Aβ.

“We found that oxytocin reversed the impairment of LTP induced by Aβ25-35 perfusion in the mouse hippocampus,” according to the findings. “These effects were blocked by pretreatment with the selective oxytocin receptor antagonist L-368,899. Furthermore, the treatment with the ERK inhibitor U0126 and selective Ca2+-permeable AMPA receptor antagonist NASPM completely antagonized the effects of oxytocin.”

“This is the first study in the world that has shown that oxytocin can reverse Aβ-induced impairments in the mouse hippocampus,” said Akiyoshi Saitoh, co-author of the study.

“This is the first report to demonstrate that oxytocin could reverse the effects of Aβ on hippocampal LTP in mice. We propose that ERK phosphorylation and Ca2+-permeable AMPA receptors are involved in this effect of oxytocin.”

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