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Restoring Septohippocampal Cholinergic Signaling Rescues Surgery-Induced Neurogenesis and Memory Deficits in Aged

Lei Lei^1,2, Qingsheng Meng^3,4, Xiaoyu Hu¹

¹Department of Anesthesiology, Pain and Perioperative Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.

|June 5, 2026

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Surgery impairs memory and brain cell growth in aging mice due to reduced acetylcholine signaling. Restoring this signaling pathway in the hippocampus can reverse these effects, offering potential treatments for postoperative cognitive dysfunction.

Area of Science:

Neuroscience
Aging Research
Cognitive Science

Background:

Central cholinergic system dysfunction is implicated in postoperative cognitive dysfunction (POCD) in aged individuals.
Specific neural circuit mechanisms underlying surgery-induced cognitive deficits remain unclear.

Purpose of the Study:

To investigate the role of medial septum/vertical limb of the diagonal band (MS/vDB) cholinergic projections to the dentate gyrus (DG) in surgery-induced cognitive and neurogenic impairments in aged mice.
To explore the therapeutic potential of restoring MS/vDB projections for POCD.

Main Methods:

A laparotomy model was used in aged mice to induce surgery-related impairments.
In vivo fiber photometry monitored hippocampal acetylcholine release and neuronal activity.

Keywords:

adult hippocampal neurogenesis cholinergic signaling postoperative cognitive dysfunction septohippocampal pathway

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Chemogenetics and acetylcholinesterase inhibitors were employed to manipulate cholinergic signaling.

Main Results:

Surgery induced memory deficits and suppressed adult hippocampal neurogenesis (AHN).
Reduced hippocampal acetylcholine release and decreased MS/vDB cholinergic neuron activity were observed post-surgery.
Galantamine treatment rescued memory deficits and AHN.
Sustained chemogenetic activation of MS/vDB → DG projections restored memory and promoted neurogenesis.

Conclusions:

A causal link exists between the loss of MS/vDB → DG cholinergic signaling and POCD-related phenotypes.
Restoring this specific cholinergic pathway is a promising therapeutic strategy for rescuing neurogenesis and memory deficits in POCD.