English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

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 Ca 2+ -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 (DFC art /DFC ven ), mean maximum constriction (mMC art /mMC ven ), time to maximum constriction (tMC art /tMC ven ) after the flicker and reactive magnitude (RM art /RM ven ).   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 DFC art  ( p  = 0.100), DFC ven  ( p  = 0.100), mMD ven  ( p  = 0.075), and RM art  ( 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.

Retinal Vessel Responses to Flicker Stimulation Are Impaired in Cav2.3-Deficient Mice—An in-vivo Evaluation Using Retinal Vessel Analysis (RVA)