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Updated: Aug 11, 2026
Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
Published on: August 13, 2015
Histamine-induced microvascular leakage in pial venules: differences between the SJL/J and BALB/c inbred strains of
T Yong1, B F Bebo, B V Sapatino
1Department of Medical Physiology, Texas A&M University, College Station.
Abstract:
The actions of histamine on pial venule leaky site formation were measured intravitally in two inbred strains of mice (BALB/c and SJL/J). Pial venules were visualized using a cranial window microscopy technique, and microvascular leaky site formation was assessed visually using a fluorescein-dextran indicator. SJL/J mice were found to be sensitive to histamine-induced leakage, whereas the BALB/c strain was refractory. Exposure to pertussis toxin enhanced the sensitivity to histamine in the SJL/J strain, but little effect was observed for BALB/c mice. However, the employment of a polymerase chain reaction (PCR) technique for the detection of mRNA for histamine H1 receptor identified receptor-specific message in isolated cerebrovascular endothelium from both strains of mice. The lack of pial responsiveness in the BALB/c mice remains unexplained. Mast cells in the dura mater were found to be more numerous in SJL/J mice than in BALB/c mice. This observation supports previous observations of strain-specific differences in CNS inflammation. The results support the concept that genetically controlled differences in vascular sensitivity and localization of CNS-associated mast cells may play important roles in the generation of vasogenic edema and inflammation in CNS trauma and disease.
Insights
Histamine causes leakage in mouse brain venules, with SJL/J mice showing sensitivity and BALB/c mice showing resistance. Genetic factors and mast cells influence this histamine response, impacting central nervous system inflammation.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Histamine is a key mediator in inflammatory responses.
- Understanding strain-specific differences in vascular permeability is crucial for CNS disease research.
Purpose of the Study:
- To investigate histamine-induced pial venule leakage in different mouse strains.
- To explore the role of genetic factors and mast cells in central nervous system (CNS) inflammation.
Main Methods:
- Intravital microscopy of pial venules in BALB/c and SJL/J mice.
- Assessment of microvascular leakage using fluorescein-dextran.
- Polymerase chain reaction (PCR) for histamine H1 receptor mRNA detection.
- Mast cell quantification in dura mater.
Main Results:
- SJL/J mice exhibited significant histamine-induced leakage, while BALB/c mice were refractory.
- Pertussis toxin enhanced histamine sensitivity in SJL/J mice but not BALB/c mice.
- Histamine H1 receptor mRNA was detected in both strains, but BALB/c mice showed no pial response.
- SJL/J mice had more numerous dura mater mast cells than BALB/c mice.
Conclusions:
- Genetically controlled differences in vascular sensitivity and CNS-associated mast cell localization may influence vasogenic edema and inflammation.
- Strain-specific differences in mast cell populations contribute to variations in CNS inflammatory responses.
