MK-801 affects the potassium-induced increase of glial fibrillary acidic protein immunoreactivity in rat brain.
Exposure of a limited brain surface to a high potassium (K+) concentration produces an injury limited to the underlying cortex, without apparently affecting other brain areas. Such a treatment produces an increased expression of glial fibrillary acidic protein (GFAP) in astrocytes, as assessed by immunohistochemical techniques, throughout the cortex ipsilateral to K+ exposure. This effect is evident 2 days after treatment and persists up to, at least, day 7. Thirty days after K+ exposure GFAP immunostaining is similar in both hemispheres. Administration of the non-competitive NMDA antagonist MK-801 (4 mg/kg i.p.) prior to the injury prevented the rise in GFAP immunoreactivity (IR) at 2 but not 7 days after the treatment. Administration of MK-801 after the injury appeared to have no effect on GFAP expression. This work confirms that brain injury, associated with spreading depression, can induce a glial response far from the lesion site. Furthermore, the fact that this phenomenon can be modified by an NMDA receptor antagonist suggests that glutamate may play a role, in vivo, in the regulation of astrocytic response to injury and introduces the possibility that brain injury-induced gliosis may be pharmacologically manipulated.
Department of Pharmacology and Therapeutics, McGill University, Montreal, Que., Canada.
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DG
Herrera
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Cuello
D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000187:drug effects*; D005971:Glutamates / Q000502:physiology; D018698:Glutamic Acid; D007091:Image Processing, Computer-Assisted; D008297:Male; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D005904:Glial Fibrillary Acidic Protein; D005971:Glutamates; D018698:Glutamic Acid; D016291:Dizocilpine Maleate; D011188:Potassium