Ischemic preconditioning inhibits expression of Na+/H+ exchanger 1 (NHE1) in the gerbil hippocampal CA1 region after transient forebrain ischemia

Content Provider	Semantic Scholar
Author	Lee, Jae-Chul Cho, Jeong-Hwi Ahn, Ji Hyeon Lee, Yun Lyul
Copyright Year	2015
Abstract	The participation of Na(+)/H(+) exchanger (NHE) in neuronal damage/death in the hippocampal CA1 region (CA1) induced by transient forebrain ischemia has not been well established, although acidosis may be involved in neuronal damage/death. In the present study, we examined the effect of ischemic preconditioning (IPC) on NHE1 immunoreactivity following a 5min of transient forebrain ischemia in gerbils. The animals used in the study were randomly assigned to four groups (sham-operated-group, ischemia-operated-group, IPC plus (+) sham-operated-group and IPC+ischemia-operated-group). IPC was induced by subjecting animals to 2min of ischemia followed by 1day of recovery. A significant neuronal loss was found in the stratum pyramidale (SP) of the CA1, not the CA2/3, of the ischemia-operated-group at 5days post-ischemia. However, in the IPC+ischemia-operated-group, neurons in the SP of the CA1 were well protected. NHE1 immunoreactivity was not detected in any regions of the CA1-3 of the sham- and IPC+sham-operated-groups. However, the immunoreactivity was apparently expressed in the SP of the CA1-3 after ischemia, and the NHE1immunoreactivity was very weak 5days after ischemia; however, at this point in time, strong NHE1immunoreactivity was found in astrocytes in the CA1. In the CA2/3, NHE1immunoreactivity was slightly changed, although NHE1immunoreactivity was expressed in the SP. In the IPC+ischemia-operated-groups, NHE1 immunoreactivity was also expressed in the SP of the CA1-3; however, the immunoreactivity was more slightly changed than that in the ischemia-operated-groups. In brief, our findings show that IPC dramatically protected CA1 pyramidal neurons and strongly inhibited NHE1 expression in the SP of the CA1 after ischemia-reperfusion. These findings suggest that the inhibition of NHE1 expression may be necessary for neuronal survival from transient ischemic damage.
Starting Page	146
Ending Page	153
Page Count	8
File Format	PDF HTM / HTML
DOI	10.1016/j.jns.2015.03.008
PubMed reference number	25783008
Journal	Medline
Volume Number	351
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/S0022510X15001392
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/S0022510X15001392?dgcid=api_sd_search-api-endpoint
Alternate Webpage(s)	https://doi.org/10.1016/j.jns.2015.03.008
Journal	Journal of the Neurological Sciences
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article