Neumaier, Felix ORCID: 0000-0002-6376-6391, Kotliar, Konstantin, Haeren, Roel Hubert Louis, Temel, Yasin, Lueke, Jan Niklas, Seyam, Osama, Lindauer, Ute, Clusmann, Hans, Hescheler, Juergen, Schubert, Gerrit Alexander, Schneider, Toni and Albanna, Walid (2021). Retinal Vessel Responses to Flicker Stimulation Are Impaired in Ca(v)2.3-Deficient Mice-An in-vivo Evaluation Using Retinal Vessel Analysis (RVA). Front. Neurol., 12. LAUSANNE: FRONTIERS MEDIA SA. ISSN 1664-2295

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Abstract

Objective: Metabolic demand increases with neuronal activity and adequate energy supply is ensured by neurovascular coupling (NVC). Impairments of NVC have been reported in the context of several diseases and may correlate with disease severity and outcome. Voltage-gated Ca2+-channels (VGCCs) are involved in the regulation of vasomotor tone. In the present study, we compared arterial and venous responses to flicker stimulation in Ca(v)2.3-competent (Ca(v)2.3([+/+])) and -deficient (Ca(v)2.3([-/-])) mice using retinal vessel analysis. Methods: The mice were anesthetized and the pupil of one eye was dilated by application of a mydriaticum. An adapted prototype of retinal vessel analyzer was used to perform dynamic retinal vessel analysis. Arterial and venous responses were quantified in terms of the area under the curve (AUC(art)/AUC(ven)) during flicker application, mean maximum dilation (mMD(art)/mMD(ven)) and time to maximum dilation (tMD(art)/tMD(ven)) during the flicker, dilation at flicker cessation (DFCart/DFCven), mean maximum constriction (mMC(art)/mMC(ven)), time to maximum constriction (tMC(art)/tMC(ven)) after the flicker and reactive magnitude (RMart/RMven). Results: A total of 33 retinal scans were conducted in 22 Ca(v)2.3([+/+]) and 11 Ca(v)2.3([-/-]) mice. Ca(v)2.3([-/-]) mice were characterized by attenuated and partially reversed arterial and venous responses, as reflected in significantly lower AUC(art) (p = 0.031) and AUC(ven) (p = 0.047), a trend toward reduced DFCart (p = 0.100), DFCven (p = 0.100), mMD(ven) (p = 0.075), and RMart (p = 0.090) and a trend toward increased tMD(art) (p = 0.096). Conclusion: To our knowledge, this is the first study using a novel, non-invasive analysis technique to document impairment of retinal vessel responses in VGCC-deficient mice. We propose that Ca(v)2.3 channels could be involved in NVC and may contribute to the impairment of vasomotor responses under pathophysiological conditions.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Neumaier, FelixUNSPECIFIEDorcid.org/0000-0002-6376-6391UNSPECIFIED
Kotliar, KonstantinUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Haeren, Roel Hubert LouisUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Temel, YasinUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Lueke, Jan NiklasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Seyam, OsamaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Lindauer, UteUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Clusmann, HansUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hescheler, JuergenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schubert, Gerrit AlexanderUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schneider, ToniUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Albanna, WalidUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-590581
DOI: 10.3389/fneur.2021.659890
Journal or Publication Title: Front. Neurol.
Volume: 12
Date: 2021
Publisher: FRONTIERS MEDIA SA
Place of Publication: LAUSANNE
ISSN: 1664-2295
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
B-WAVE AMPLITUDE; SUBARACHNOID HEMORRHAGE; NEUROVASCULAR UNIT; CALCIUM-CHANNELS; BLOOD-FLOW; AGE; CA(V)2.3; DIAMETER; LIGHT; RATMultiple languages
Clinical Neurology; NeurosciencesMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/59058

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