Microglia, astrocytes, and macrophages react differentially to central and peripheral lesions in the developing and mature rat whisker-to-barrel pathway: a study using immunohistochemistry for lipocortin1, phosphotyrosine, s100 beta, and mannose receptors.
Adult and neonatal rats were subjected to transection of the left infraorbital nerve or ablation of the left parietal cortex. The ensuing glial reaction in the whisker-to-barrel pathway was studied with immunohistochemistry for Lipocortin1- (LC1+), phosphotyrosine- (PY+), S100 beta- (S100 beta+), and mannose receptor- (MR+) immunoreactive microglia, astrocytes, and macrophages. Four days after infraorbital nerve transection in adult rats, LC1+ and PY+ microglia were prominently increased in the trigeminal sensory brain-stem nuclei on the deafferented side compared with the intact side. Changes were negligible at the second synapse of the pathway, i.e., the thalamic ventroposterior medial nucleus. Cortical ablation in adults led to an increase in microglia in the ipsilateral ventroposterior medial nucleus that reciprocally connects with the ablated cortex. Moreover, microglial reactions occurred in the contralateral trigeminal sensory brain-stem nuclei in which corticofugal projections from the ablated cortex terminate. S100 beta+ astrocytes, in contrast, appeared unaltered after both types of lesion in adults. In neonates, LC1+, PY+, and S100 beta+ cells did not have the adult morphology of microglia or astrocytes. Four days after nerve transection, LC1+ and PY+ cells were sparse and remained unchanged. In contrast, S100 beta+ cells substantially increased in the deafferented trigeminal brain-stem nuclei. Four days after cortical ablation in neonates, LC1+, PY+, and S100 beta+ cells had accumulated in the deprived thalamus. In contrast to adults, many of these cells were MR+ macrophages. In the deprived brain-stem, only S100 beta+ cells increased and none were macrophages. Therefore, macrophages do not appear to stem from microglia, and neonatal LC1+, PY+, and S100 beta+ cells may possess functions different from those in adults.
Melzer
P
P
Department of Cell Biology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.
Savchenko
V
V
McKanna
J A
JA
D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D017305:Annexin A1 / Q000032:analysis*; D001253:Astrocytes / Q000502:physiology*; D015415:Biomarkers; D001921:Brain / Q000166:cytology / Q000502:physiology*; D001933:Brain Stem / Q000502:physiology; D002135:Calcium-Binding Proteins / Q000032:analysis; D005260:Female; D007839:Functional Laterality; D007150:Immunohistochemistry; D037181:Lectins, C-Type; D008264:Macrophages / Q000502:physiology*; D008297:Male; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D008442:Maxillary Nerve / Q000502:physiology*; D017628:Microglia / Q000502:physiology*; D009414:Nerve Growth Factors; D019000:Phosphotyrosine / Q000032:analysis*; D051381:Rats; D020318:Rats, Long-Evans; D011956:Receptors, Cell Surface / Q000032:analysis*; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000032:analysis*; D013003:Somatosensory Cortex / Q000502:physiology*; D014738:Vibrissae / Q000294:innervation*
D017305:Annexin A1; D015415:Biomarkers; D002135:Calcium-Binding Proteins; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D009414:Nerve Growth Factors; D011956:Receptors, Cell Surface; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D019000:Phosphotyrosine