Blood—brain barrier breakdown in MBP-specific T cell induced experimental allergic encephalomyelitis

Brain ◽  
1993 ◽  
Vol 116 (1) ◽  
pp. 147-159 ◽  
Author(s):  
I. J. Namer ◽  
J. Steibel ◽  
P. Poulet ◽  
J. P. Armspach ◽  
M. Mohr ◽  
...  
Keyword(s):  
T Cell ◽  
Blood Brain Barrier ◽  
Experimental Allergic Encephalomyelitis ◽  
Brain Barrier ◽  
Allergic Encephalomyelitis ◽  
Blood Brain ◽  
Barrier Breakdown ◽  
Blood Brain Barrier Breakdown ◽  
Experimental Allergic

scholarly journals A Spatial Analysis of the Blood—Brain Barrier Damage in Experimental Allergic Encephalomyelitis

1985 ◽  
Vol 5 (4) ◽  
pp. 545-553 ◽  
Author(s):  
Marianne Juhler ◽  
Ronald G. Blasberg ◽  
Joseph D. Fenstermacher ◽  
Clifford S. Patlak ◽  
Olaf B. Paulson
Keyword(s):  
Blood Brain Barrier ◽  
Experimental Allergic Encephalomyelitis ◽  
Young Male ◽  
Lymphocytic Infiltration ◽  
Brain Barrier ◽  
Allergic Encephalomyelitis ◽  
Transfer Constant ◽  
Influx Rate ◽  
Blood Brain ◽  
Experimental Allergic

Experimental allergic encephalomyelitis was induced in young male Lewis rats. Following the development of neurological signs, the local distribution of perivascular inflammatory cellular infiltrates and the local blood-to-tissue transfer constants ( K1) of α-aminoisobutyric acid (AIB) were determined, and these results were compared. Perivascular infiltrative lesions were generally found near areas of the CNS that normally lack an effective blood–brain barrier (BBB) such as the choroid plexus and the entry zones of the cranial and spinal nerve roots. This distribution pattern indicates that the entry of the causative agent into CNS tissue may be by way of the permeable microvessels of these structures. In tissue around inflamed veins, the mean transfer constant was slightly but significantly increased (2.8 ± 1.5 μl g−1 min−1) compared with uninvolved regions (0.9 ± 0.2 μl g−1 min−1) and similar areas in control animals (0.9 ± 0.3 μl g−1 min−1). Analysis of the autoradiographic method of determining transfer constants suggested that the AIB influx rate in the lesion areas may actually be manyfold larger than measured, that BBB permeability may be greatly increased at such sites, and that the areas of lymphocytic infiltration and increased K values may be virtually identical.

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