Klinische Neurophysiologie 2011; 42(03): 172-176
DOI: 10.1055/s-0031-1285903
Nachwuchspreis Neurosonologie
Georg Thieme Verlag KG Stuttgart · New York

Ultraschall-induzierte Blut-Hirn-Schranken-Öffnung

Ultrasound-Induced Opening of the Blood-Brain Barrier
A. Alonso
1   Neurologische Klinik, Universitätsmedizin Mannheim
› Author Affiliations
Further Information

Publication History

Publication Date:
25 August 2011 (online)

Zusammenfassung

Einleitung:

Eine reversible Öffnung der Blut-Hirn-Schranke (BBB) mittels Ultraschall stellt einen neuen Therapieansatz zur Behandlung von ZNS-Erkrankungen dar. In der vorliegenden Studie wurden sekundär auftretende Bioeffekte der Ultraschall-induzierten BBB-Öffnung untersucht.

Methoden:

Wistar Ratten wurden mit 1 MHz-Ultraschall in Kombination mit intravenösen Mikrobläschen behandelt. Pathologische Stressantworten wurden mittels Immunfluoreszenz analysiert.

Ergebnisse und Diskussion:

In den beschallten Arealen zeigte sich eine Zunahme der Ubiquitinexpression in Neuronen, während Hsp 70 und Hsc 70 keine Expressionsänderung aufwiesen. Eine Apoptose konnte nur in wenigen Neuronen beobachtet werden. Nach Ultraschall-Applika­tion kam es vorwiegend in Astrozyten zu einer transienten Größenzunahme von gap junctional Plaques. Diese Umverteilung deutet auf einen Reaktionsmechanismus zur Erhaltung der Homöostase hin.

Abstract

Introduction:

Ultrasound-induced reversible blood-brain barrier (BBB) opening is a promising new strategy for the treatment of CNS diseases. In the present study, we examined secondary bioeffects following ultrasound-mediated opening of the BBB.

Methods:

Wistar rats were insonated with 1 MHz ultrasound in combination with microbubbles. Stress pathways were analysed by immunofluorescence.

Results and Discussion:

In insonated areas, we observed an increase in ubiquitin expression in neurons while no change in Hsp 70 and Hsc 70 expression could be demonstrated. Apoptosis occurred only in a few neuronal cells. Insonation led to an increase in gap junctional plaque sizes predominantly in astrocytes. This reorganisation may be a regulatory mechanism to maintain homeostasis.

 
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