Hemodynamic correlation imaging of the mouse brain for application in unilateral neurodegenerative diseases.
Journal
Biomedical optics express
ISSN: 2156-7085
Titre abrégé: Biomed Opt Express
Pays: United States
ID NLM: 101540630
Informations de publication
Date de publication:
01 Apr 2019
01 Apr 2019
Historique:
received:
05
12
2018
revised:
25
02
2019
accepted:
27
02
2019
entrez:
16
5
2019
pubmed:
16
5
2019
medline:
16
5
2019
Statut:
epublish
Résumé
We developed a single-camera two-channel hemodynamic imaging system that uses near-infrared light to monitor the mouse brain in vivo with an exposed, un-thinned, and intact skull to explore the effect of Parkinson's disease on the resting state functional connectivity of the brain. To demonstrate our system's ability to monitor cerebral hemodynamics, we first performed direct electrical stimulation of an anesthetized healthy mouse brain and detected hemodynamic changes localized to the stimulated area. Subsequently, we developed a unilaterally lesioned 6-hydroxydopamine (hemi-parkinsonian) mouse model and detected the differences in functional connectivity between the normal and hemi-parkinsonian mouse brains by comparing the hemispheric hemodynamic correlations during the resting state. Seed-based correlation for the oxy-hemoglobin channel from the left and right hemispheres of healthy mice was much higher and more symmetric than in hemi-parkinsonian mice. Through a k-means clustering of the hemodynamic signals, the healthy mouse brains were segmented according to brain region, but the hemi-parkinsonian mice did not show a similar segmentation. Overall, this study highlights the development of a spatial multiplexing hemodynamic imaging system that reveals the resting state hemodynamic connectivity in healthy and hemi-parkinsonian mice.
Identifiants
pubmed: 31086700
doi: 10.1364/BOE.10.001736
pii: 349727
pmc: PMC6485007
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1736-1749Déclaration de conflit d'intérêts
The authors declare that there are no conflicts of interest related to this article.
Références
Pharmacol Biochem Behav. 1999 Jun;63(2):313-8
pubmed: 10371661
J Cereb Blood Flow Metab. 2004 Jan;24(1):1-6
pubmed: 14688611
Proc Natl Acad Sci U S A. 2005 Jul 5;102(27):9673-8
pubmed: 15976020
Clin Neuropsychol. 2007 Jan;21(1):9-37
pubmed: 17366276
Neuroimage. 2009 Aug 1;47(1):148-56
pubmed: 19344773
Neurosci Lett. 2009 Aug 21;460(1):6-10
pubmed: 19463891
J Biomed Opt. 2009 Sep-Oct;14(5):054032
pubmed: 19895134
Opt Express. 2010 Mar 15;18(6):5730-9
pubmed: 20389589
Eur Neuropsychopharmacol. 2010 Aug;20(8):519-34
pubmed: 20471808
Hum Brain Mapp. 2011 Sep;32(9):1443-57
pubmed: 20740649
Neuroimage. 2011 Mar 1;55(1):8-23
pubmed: 21111053
PLoS One. 2011 Jan 20;6(1):e16322
pubmed: 21283729
Magn Reson Med. 2011 Sep;66(3):644-57
pubmed: 21394769
Brain Connect. 2011;1(1):13-36
pubmed: 22432952
Opt Express. 2012 Mar 26;20(7):6932-43
pubmed: 22453371
Parkinsonism Relat Disord. 2012 Jul;18(6):781-7
pubmed: 22510204
J Neurosci Methods. 2013 Apr 15;214(2):144-8
pubmed: 23376497
Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):6169-74
pubmed: 23530246
Neurobiol Aging. 2014 Feb;35(2):431-41
pubmed: 24074808
Biomed Opt Express. 2013 Oct 04;4(11):2332-46
pubmed: 24298398
Behav Brain Res. 2015 May 1;284:153-7
pubmed: 25698596
Biomed Opt Express. 2015 Jan 28;6(2):615-30
pubmed: 25780751
J Cereb Blood Flow Metab. 2017 Feb;37(2):471-484
pubmed: 26868180
Prog Brain Res. 2016;225:153-79
pubmed: 27130415
Open Med (Wars). 2017 Mar 6;12:5-11
pubmed: 28401194
J Neurosci. 2017 Aug 2;37(31):7513-7533
pubmed: 28674167
Nat Commun. 2018 Jan 26;9(1):395
pubmed: 29374172
Physiol Behav. 1972 Jan;8(1):139-42
pubmed: 4579152
Trends Neurosci. 1997 Oct;20(10):435-42
pubmed: 9347608