Affiliations: Brain Research Laboratory, Department of Neurology,
Emory University School of Medicine, 575 Rollins Way, Atlanta, GA 30322,
USA
Note: [] Correspondence to: Donald G. Stein, Ph.D., The Graduate School,
Emory University, 202 Administration Bldg., Atlanta, GA 30322, USA. E-mail:
dgstein@grad.gsas.emory.edu
Abstract: Purpose: Ginkgo biloba extract (EGb 761) has been shown to
facilitate behavioral and neuro-morphological recovery from brain injury, but
less is known about its effects on glia. Since gliosis may be an important
component of the recovery process, we tested the hypothesis that EGb 761 alters
the time course and development of microglial activation and astrocytosis after
brain injury. Methods: Rats were treated with either saline or EGb 761 and
killed at 2 hrs, 1, 3, 7, and 14 days following unilateral entorhinal cortex
(EC) lesions. Microglia and their precursors were visualized with a silver
impregnation method, and astrocytes with GFAP. Results: Blood-borne
monocytes/macrophages were seen as early as 2 hrs after injury in all animals.
The side contralateral to the injury showed minimal microglial activation and
there were no significant effects of drug treatment. On the side ipsilateral to
the lesion EGb 761 enhanced microglial activation at 3, 7, and 14 days in the
molecular layer and the hilus of the dentate gyrus; the areas of most profound
deaf-ferentation after EC injury. Regions of the corpus callosum also showed
enhanced microglial activation over the same time course. Reactive astrocytes
were stained with GFAP and were found to be more numerous than activated
microglia, particularly in the ipsilateral corpus callo-sum. EGb 761 treatment
enhanced astrocytosis at 3 days in the molecular layer, the hilus, and the
corpus callosum on the ipsilateral side. Conclusions: Taken together our
results show that EGb 761 enhances, accelerates and prolongs the activation of
microglia and astrocytosis at the site of injury.
