Optogenetic activation of parvalbumin and somatostatin interneurons selectively restores theta-nested gamma oscillations and oscillation-induced spike timing-dependent long-term potentiation impaired by amyloid β oligomers.

ABSTRACT:

Background

Abnormal accumulation of amyloid β_1-42 oligomers (AβO_1-42), a hallmark of Alzheimer's disease, impairs hippocampal theta-nested gamma oscillations and long-term potentiation (LTP) that are believed to underlie learning and memory. Parvalbumin-positive (PV) and somatostatin-positive (SST) interneurons are critically involved in theta-nested gamma oscillogenesis and LTP induction. However, how AβO_1-42 affects PV and SST interneuron circuits is unclear. Through optogenetic manipulation of PV and SST interneurons and computational modeling of the hippocampal neural circuits, we dissected the contributions of PV and SST interneuron circuit dysfunctions on AβO_1-42-induced impairments of hippocampal theta-nested gamma oscillations and

SUBMITTER: Park K 

PROVIDER: S-EPMC6961381 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature