Document Detail

Anterior thalamic lesions stop synaptic plasticity in retrosplenial cortex slices: expanding the pathology of diencephalic amnesia.
MedLine Citation:
PMID:  19403787     Owner:  NLM     Status:  MEDLINE    
Recent, convergent evidence places the anterior thalamic nuclei at the heart of diencephalic amnesia. However, the reasons for the severe memory loss in diencephalic amnesia remain unknown. A potential clue comes from the dense, reciprocal connections between the anterior thalamic nuclei and retrosplenial cortex, another region vital for memory. We now report a loss of synaptic plasticity [long-term depression (LTD)] in rat retrosplenial cortex slices months following an anterior thalamic lesion. The loss of LTD was lamina-specific, occurring only in superficial layers of the cortex and was associated with a decrease in GABA(A)-mediated inhibitory transmission. As retrosplenial cortex is itself vital for memory, this distal lesion effect will amplify the impact of anterior thalamic lesions. These findings not only provide novel insights into the functional pathology of diencephalic amnesia and have implications for the aetiology of the posterior cingulate hypoactivity in Alzheimer's disease, but also show how distal changes in plasticity could contribute to diaschisis.
Derek L F Garden; Peter V Massey; Douglas A Caruana; Ben Johnson; E Clea Warburton; John P Aggleton; Zafar I Bashir
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-04-29
Journal Detail:
Title:  Brain : a journal of neurology     Volume:  132     ISSN:  1460-2156     ISO Abbreviation:  Brain     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-25     Completed Date:  2009-09-09     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0372537     Medline TA:  Brain     Country:  England    
Other Details:
Languages:  eng     Pagination:  1847-57     Citation Subset:  AIM; IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Amnesia / metabolism,  pathology*,  physiopathology
Anterior Thalamic Nuclei / metabolism,  pathology*,  physiopathology
Gyrus Cinguli / pathology*,  physiopathology
N-Methylaspartate / metabolism
Neuronal Plasticity*
Patch-Clamp Techniques
Receptors, N-Methyl-D-Aspartate / physiology
Synapses / physiology*
Synaptic Transmission / physiology
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid / metabolism
gamma-Aminobutyric Acid / metabolism
Grant Support
G0401403//Medical Research Council; G9713086//Medical Research Council; //Biotechnology and Biological Sciences Research Council; //Medical Research Council
Reg. No./Substance:
0/Receptors, N-Methyl-D-Aspartate; 56-12-2/gamma-Aminobutyric Acid; 6384-92-5/N-Methylaspartate; 77521-29-0/alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Comment In:
Brain. 2009 Dec;132(Pt 12):e133; author reply e134   [PMID:  19858081 ]

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

Previous Document:  Is depression associated with health risk-related behaviour clusters in adults?
Next Document:  In vivo measurement of axon diameter distribution in the corpus callosum of rat brain.