Impairment of long-term depression induced by chronic brain inflammation in rats

Although deficits in synaptic plasticity have been identified in aged or neuroinflamed animals with memory impairments, few studies have examined the cellular basis of plasticity in such animals. Here, we examined whether chronic neuroinflammation altered long-term depression (LTD) and studied the u...

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Published in:Biochemical and biophysical research communications 2009-05, Vol.383 (1), p.93-97
Main Authors: Min, Sun Seek, Quan, Hui Yan, Ma, Jinhua, Lee, Ki Ho, Back, Seung Keun, Na, Heung Seek, Han, Seung Ho, Yee, Jae-Yong, Kim, Chan, Han, Jung-Soo, Seol, Geun Hee
Format: Article
Language:English
Subjects:
Alzheimer Disease - physiopathology
Animals
Chronic Disease
Dementia
Encephalitis - physiopathology
Hippocampus
Long-term depression
Long-Term Synaptic Depression
Male
Memory
Neuroinflammation
NMDAR-dependent LTD
NMDAR-independent LTD
Rats
Rats, Inbred F344
Receptors, Glutamate - physiology
Receptors, N-Methyl-D-Aspartate - physiology
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Summary:Although deficits in synaptic plasticity have been identified in aged or neuroinflamed animals with memory impairments, few studies have examined the cellular basis of plasticity in such animals. Here, we examined whether chronic neuroinflammation altered long-term depression (LTD) and studied the underlying mechanism of LTD impairment by neuroinflammation. Chronic neuroinflammation was induced by administration of lipopolysaccharide (LPS) to the fourth ventricle. Excitatory postsynaptic potentials were recorded extracellularly in the rat hippocampal CA1 area to examine alterations in synaptic plasticity. Chronic administration of LPS induced remarkable memory impairment in the Morris water maze test. N-methyl-d-aspartate receptor (NMDAR)-dependent LTD was almost absent in LPS-infused animals. The AMPA receptor (AMPAR)-mediated synaptic response was reduced in the LPS-infused group. These results suggest that reduction in NMDAR-dependent LTD might arise because of alterations in postsynaptic AMPARs as well as NMDARs and that such changes may be present in mild and early forms of Alzheimer-type dementia.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2009.03.133