Nov 7, 2018

Optogenetic activation of SST-positive interneurons restores hippocampal theta oscillation impairment induced by soluble amyloid beta oligomers in vivo

BioRxiv : the Preprint Server for Biology
Hyowon ChungJeehyun Kwag


Abnormal accumulation of amyloid β oligomers (AβO) is a hallmark of Alzheimer's disease (AD), which leads to learning and memory deficits. Hippocampal theta oscillations that are critical in spatial navigation, learning and memory are impaired in AD. Since GABAergic interneurons, such as somatostatin-positive (SST+) and parvalbumin-positive (PV+) interneurons, are believed to play key roles in the hippocampal oscillogenesis, we asked whether AβO selectively impairs these SST+ and PV+ interneurons. To selectively manipulate SST+ or PV+ interneuron activity in mice with AβO pathology in vivo , we co-injected AβO and adeno-associated virus (AAV) for expressing floxed channelrhodopsin-2 (ChR2) into the hippocampus of SST-Cre or PV-Cre mice. Local field potential (LFP) recordings in vivo in these AβO-injected mice showed a reduction in the peak power of theta oscillations and desynchronization of spikes from CA1 pyramidal neurons relative to theta oscillations compared to those in control mice. Optogenetic activation of SST+ but not PV+ interneurons in AβO-injected mice fully restored the peak power of theta oscillations and resynchronized the theta spike phases to a level observed in control mice. In vitro whole-cell voltage-clamp ...Continue Reading

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Mentioned in this Paper

In Vivo
Ca1 antibody
Injection Product
GABRQ gene
APP protein, human
Adeno-Associated Virus
Memory Impairment
Spatial Distribution
PDZK1 gene

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