Chronological study of peripheral benzodiazepine binding sites in the rat brain stab wounds using [3H] PK-11195 as a marker for gliosis.
Chronological studies of the development of the peripheral benzodiazepine receptor sites were undertaken with the goal of evaluating the sensitivity of this marker for the study of the gliosis development in the injured brain. No significant increase in [3H] PK-11195 binding occurred in the rat brain stab wound one day following the puncture. A significant increase in the receptor density (Bmax) from the second day onward was observed. The Bmax reached its highest levels in the grey matter on the sixth day after a 23-gauge needle wound (8.75 +/- 0.09; pmol mg-tissue-1) and on the seventh day after an 18-gauge needle wound (8.98 +/- 0.31 pmol mg-tissue-1). In the white matter, the Bmax was greatest seven days after the wound (3.42 +/- 0.07; pmol mg-tissue-1; 23-gauge needle and 3.56 +/- 0.1 pmol mg-tissue-1 in the 18-gauge needle injury). Between 30 and 60 days after the wound, the Bmax was significantly lower than the Bmax observed between 6 and 14 days. The Bmax in the wound produced with needles was seven to eight times greater than the Bmax in the grey matter of the ipsilateral and contralateral cortices. Histological examination showed that there were no astrocytes or macrophages in the stab wound one day after the lesion. However, the glial fibrillary acidic protein positive cells and macrophages appeared on D3 after an injury. Gliosis, as measured by the PK-11195 binding, was also observed in the remote contralateral cortex. Data shows that PK-11195 binding is a very sensitive method of evaluating brain injury and could be of great value in studying progressive injuries in the living human brain in conjunction with positron emission tomography.
Miyazawa
N
N
Cone Laboratory for Neurosurgical Research, Montreal Neurological Institute, Quebec, Canada.
Diksic
M
M
Yamamoto
Y
Y
D000818:Animals; D001345:Autoradiography; D001921:Brain / Q000473:pathology; D001930:Brain Injuries / Q000473:pathology*; D004292:Dominance, Cerebral / Q000502:physiology; D005260:Female; D005911:Gliosis / Q000473:pathology*; D007546:Isoquinolines / Q000493:pharmacokinetics*; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism*; D014951:Wounds, Stab / Q000473:pathology*
D007546:Isoquinolines; D011963:Receptors, GABA-A; C037850:PK 11195