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 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.
Min
Sun Seek
SS
Department of Physiology and Biophysics, Eulji University School of Medicine, Daejeon, South Korea.
Quan
Hui Yan
HY
Ma
Jinhua
J
Lee
Ki Ho
KH
Back
Seung Keun
SK
Na
Heung Seek
HS
Han
Seung Ho
SH
Yee
Jae-Yong
JY
Kim
Chan
C
Han
Jung-Soo
JS
Seol
Geun Hee
GH