Primary cortical glial reaction versus secondary thalamic glial response in the excitotoxically injured young brain: Microglial/macrophage response and major histocompatibility complex class I and II expression

The excitatory amino acid analog, N-methyl-D-aspartate, was injected intrac ortically into nine-day-old rats. Resulting axon-sparing lesions in the dev eloping sensorimotor cortex, which secondarily affect thalamic neurons that become deprived of cortical targets, provide an experimental model for the study of the glial response in distantly affected areas. The microglial/ma crophage response was studied using tomato lectin histochemistry and major histocompatibility complex I and II immunocytochemistry. Blood-brain barrie r integrity was evaluated. In the cortical lesion site, where blood-brain b arrier breakdown occurs, the rapid microglial response was restricted to th e degenerating area. Microglial changes were first seen at 4 h post-injecti on, peaking at days 3-5. Reactive microglia changed morphology, increased t omato lectin binding and expressed major histocompatibility complex I. Addi tionally, some cells expressed major histocompatibility complex II. In the secondarily affected thalamus, the microglial response was not as pronounce d as in the cortex, was first seen at 10 h post-injection and peaked at day s 3-5. Reactive microglia showed a bushy morphology, were intensely lectin positive and expressed major histocompatibility complex I. The exceptional response of the nine-day-old brain to cortical lesions make s this model an interesting tool for studying the implications of microglia l major histocompatibility factor expression in still enigmatic processes s uch as wound healing and plasticity. (C) 1998 IBRO. Published by Elsevier S cience Ltd.