Document Detail


Acetylcholine facilitates recovery of episodic memory after brain damage.
MedLine Citation:
PMID:  23035090     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Episodic memory depends on a network of interconnected brain structures including the inferior temporal cortex, hippocampus, fornix, and mammillary bodies. We have previously shown that a moderate episodic memory impairment in monkeys with transection of the fornix is exacerbated by prior depletion of acetylcholine from inferotemporal cortex, despite the fact that depletion of acetylcholine from inferotemporal cortex on its own has no effect on episodic memory. Here we show that this effect occurs because inferotemporal acetylcholine facilitates recovery of function following structural damage within the neural circuit for episodic memory. Episodic memory impairment caused by lesions of the mammillary bodies, like fornix transection, was exacerbated by prior removal of temporal cortical acetylcholine. However, removing temporal cortical acetylcholine after the lesion of the fornix or mammillary bodies did not increase the severity of the impairment. This lesion order effect suggests that acetylcholine within the inferior temporal cortex ordinarily facilitates functional recovery after structural lesions that impair episodic memory. In the absence of acetylcholine innervation to inferotemporal cortex, this recovery is impaired and the amnesia caused by the structural lesion is more severe. These results suggest that humans with loss of cortical acetylcholine function, for example in Alzheimer's disease, may be less able to adapt to memory impairments caused by structural neuronal damage to areas in the network important for episodic memory.
Authors:
Paula L Croxson; Philip G F Browning; David Gaffan; Mark G Baxter
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  32     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-04     Completed Date:  2013-01-17     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  13787-95     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acetylcholine / deficiency,  physiology*
Alzheimer Disease / psychology
Amnesia / etiology,  physiopathology*,  rehabilitation
Animals
Brain Damage, Chronic / complications*,  psychology
Cholinergic Fibers / physiology*
Disease Models, Animal
Female
Fornix, Brain / injuries*,  physiology
Macaca fascicularis
Macaca mulatta
Male
Mamillary Bodies / injuries*,  physiopathology
Memory, Episodic*
Neuronal Plasticity
Pattern Recognition, Visual
Psychomotor Performance / physiology
Reward
Temporal Lobe / physiopathology*
Grant Support
ID/Acronym/Agency:
071291//Wellcome Trust; MC_QA137504//Medical Research Council; //Wellcome Trust
Chemical
Reg. No./Substance:
E78ZFF4KQ0/Reward; N9YNS0M02X/Acetylcholine
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Analysis of synaptic growth and function in Drosophila with an extended larval stage.
Next Document:  Calcium-dependent isoforms of protein kinase C mediate glycine-induced synaptic enhancement at the c...