| |
Record |
Links |
|
Author |
Fonken, L.K.; Bedrosian, T.A.; Zhang, N.; Weil, Z.M.; DeVries, A.C.; Nelson, R.J. |
|
| |
Title |
Dim light at night impairs recovery from global cerebral ischemia |
Type |
Journal Article |
| |
Year |
2019 |
Publication  |
Experimental Neurology |
Abbreviated Journal |
Exp Neurol |
|
| |
Volume |
317 |
Issue |
|
Pages |
100-109 |
|
| |
Keywords |
Animals; mouse models; cerebral ischemia |
|
| |
Abstract |
Nighttime lighting is one of the great conveniences of modernization; however, there is mounting evidence that inopportune light exposure can disrupt physiological and behavioral functions. Hospital patients may be particularly vulnerable to the consequences of light at night due to their compromised physiological state. Cardiac arrest/cardiopulmonary resuscitation (CA) was used to test the hypothesis in mice that exposure to dim light at night impairs central nervous system (CNS) recovery from a major pathological insult. Mice exposed to dim light at night (5lx) had higher mortality in the week following cardiac arrest compared to mice housed in dark nights (0lx). Neuronal damage was significantly greater in surviving mice exposed to dim light at night after CA versus those housed in dark nights. Dim light at night may have elevated neuronal damage by amplifying pro-inflammatory pathways in the CNS; Iba1 immunoreactivity (an indication of microglia activation) and pro-inflammatory cytokine expression were elevated in mice exposed to dim light at night post-CA. Furthermore, selective inhibition of IL-1beta or TNFalpha ameliorated damage in mice exposed to dim light at night. The effects of light at night on CA outcomes were also prevented by using a wavelength of nighttime light that has minimal impact on the endogenous circadian clock, suggesting that replacing broad-spectrum nighttime light with specific circadian-inert wavelengths could be protective. Together, these data indicate that exposure to dim light at night after global cerebral ischemia increases neuroinflammation, in turn exacerbating neurological damage and potential for mortality. |
|
| |
Address |
Department of Neuroscience, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA |
|
| |
Corporate Author |
|
Thesis |
|
|
| |
Publisher |
|
Place of Publication |
|
Editor |
|
|
| |
Language |
English |
Summary Language |
|
Original Title |
|
|
| |
Series Editor |
|
Series Title |
|
Abbreviated Series Title |
|
|
| |
Series Volume |
|
Series Issue |
|
Edition |
|
|
| |
ISSN |
0014-4886 |
ISBN |
|
Medium |
|
|
| |
Area |
|
Expedition |
|
Conference |
|
|
| |
Notes |
PMID:30822422 |
Approved |
no |
|
| |
Call Number |
GFZ @ kyba @ |
Serial |
2235 |
|
| Permanent link to this record |
