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Published on: January 4, 2013
Cerebrovascular Gi Proteins Protect Against Brain Hypoperfusion and Collateral Failure in Cerebral Ischemia
Salvador Castaneda-Vega1,2, Sandra Beer-Hammer3,4, Veronika Leiss3
1Werner Siemens Imaging Center, Department of Preclinical Imaging and Radiopharmacy, Eberhard Karls University Tübingen and University Clinic, Tübingen, Germany.
Insights
Inhibitory G-protein-dependent receptor (GiPCR) signaling is crucial for maintaining brain blood flow. Disrupting this signaling causes hypoperfusion and microvascular collapse, leading to stroke-like symptoms.
Area of Science:
- Neuroscience
- Vascular Biology
- Pharmacology
Background:
- Cerebral hypoperfusion and vascular dysfunction are linked to stroke risk factors like hypertension, diabetes, and smoking.
- The role of inhibitory G-protein-dependent receptor (GiPCR) signaling in cerebrovascular regulation is not well understood.
Purpose of the Study:
- To investigate the significance of GiPCR signaling in maintaining cerebral blood flow (CBF) and its stability.
- To explore the impact of GiPCR signaling disruption on cerebrovascular function under ischemic conditions.
Main Methods:
- Utilized in vivo high-resolution magnetic resonance imaging (MRI) techniques.
- Induced a functional knockout of GiPCR signaling in brain vasculature using pertussis toxin (PTX).
- Assessed CBF and microvascular integrity following transient unilateral common carotid artery occlusion.
Main Results:
- PTX injection led to global brain hypoperfusion and microvascular collapse.
- Disruption of GiPCR signaling impaired CBF in the ipsilateral hemisphere after carotid artery occlusion.
- MRI and histological analyses revealed significant stroke features in affected brain regions.
Conclusions:
- Cerebrovascular GiPCR signaling plays a vital role in maintaining CBF.
- Targeting GiPCR signaling may offer novel therapeutic strategies for cerebrovascular dysfunction and stroke prevention/treatment.
Abstract:
Cerebral hypoperfusion and vascular dysfunction are closely related to common risk factors for ischemic stroke such as hypertension, dyslipidemia, diabetes, and smoking. The role of inhibitory G protein-dependent receptor (GiPCR) signaling in regulating cerebrovascular functions remains largely elusive. We examined the importance of GiPCR signaling in cerebral blood flow (CBF) and its stability after sudden interruption using various in vivo high-resolution magnetic resonance imaging techniques. To this end, we induced a functional knockout of GiPCR signaling in the brain vasculature by injection of pertussis toxin (PTX). Our results show that PTX induced global brain hypoperfusion and microvascular collapse. When PTX-pretreated animals underwent transient unilateral occlusion of one common carotid artery, CBF was disrupted in the ipsilateral hemisphere resulting in the collapse of the cortically penetrating microvessels. In addition, pronounced stroke features in the affected brain regions appeared in both MRI and histological examination. Our findings suggest an impact of cerebrovascular GiPCR signaling in the maintenance of CBF, which may be useful for novel pharmacotherapeutic approaches to prevent and treat cerebrovascular dysfunction and stroke.
