Dorsal CA1 interneurons contribute to acute stress-induced sp

VGAT-Cre and DIO-hM4Di AAV were used to chemogenetically inactivate dorsal CA1 interneurons activity. (From BrainVTA)

The viruses used in this article from BrainVTA are in the table below

CRE Recombinase	PT-0346 rAAV-VGAT1-CRE-WPRE-hGH polyA
Chemogenetics	PT-0043 rAAV-EF1α-DIO-hM4D(Gi)-mCherry-WPREs
Control	PT-0013 rAAV-Ef1α-DIO-mCherry-WPRE-hGH polyA

Jing-Ying Yu, Ping Fang, Chi Wang, Xing-Xing Wang, Kun Li, Qian Gong, Ben-Yan Luo, Xiao-Dong Wang
Pub Date: 2018-04-05, DOI: 10.1016/j.neuropharm.2018.04.002, Email: sales@brainvta.com
Exposure to severely stressful experiences disrupts the activity of neuronal circuits and impairs declarative memory. GABAergic interneurons coordinate neuronal network activity, but their involvement in stress-evoked memory loss remains to be elucidated. Here, we provide evidence that interneurons in area CA1 of the dorsal hippocampus partially modulate acute stress-induced memory deficits. In adult male mice, both acute forced swim stress and restraint stress impaired hippocampus-dependent spatial memory and increased the density of c-fos-positive interneurons in the dorsal CA1. Selective activation of dorsal CA1 interneurons by chemogenetics disrupted memory performance in the spatial object recognition task. In comparison, anxiety-related behavior, spatial working memory and novel object recognition memory remained intact when dorsal CA1 interneurons were overactivated. Moreover, chemogenetic activation of dorsal CA1 interneurons suppressed the activity of adjacent pyramidal neurons, whereas a single exposure to forced swim stress but not restraint stress increased the activity of CA1 pyramidal neurons. However, chemogenetic inhibition of dorsal CA1 interneurons led to spatial memory impairments and failed to attenuate acute stress-induced memory loss. These findings suggest that acute stress may overactivate interneurons in the dorsal CA1, which reduces the activity of pyramidal neurons and in turn disrupts long-term memory.

Figure 1. Selective chemogenetic activation of interneurons in the dorsal CA1.

Here, we combined behavioral, molecular and chemogenetic approaches to investigate whether acute stress activates interneurons in the dorsal CA1 to impair hippocampus-dependent memory. This study may provide insight into the importance of CA1 interneurons in stress-induced cognitive deficits and suggest that acute stress may overactivate interneurons in the dorsal CA1, which reduces the activity of pyramidal neurons and in turn disrupts long-term memory.

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