Changes in calcium-binding protein expression in human cortical contusion tissue.
Traumatic brain injury (TBI) produces several cellular changes, such as gliosis, axonal and dendritic plasticity, and inhibition-excitation imbalance, as well as cell death, which can initiate epileptogenesis. It has been demonstrated that dysfunction of the inhibitory components of the cerebral cortex after injury may cause status epilepticus in experimental models; we proposed to analyze the response of cortical interneurons and astrocytes after TBI in humans. Twelve contusion samples were evaluated, identifying the expression of glial fibrillary acidic protein (GFAP) and calcium-binding proteins (CaBPs). The study was made in sectors with and without preserved cytoarchitecture evaluated with NeuN immunoreactivity (IR). In sectors with total loss of NeuN-IR the results showed a remarkable loss of CaBP-IR both in neuropil and somata. In sectors with conserved cytoarchitecture less drastic changes in CaBP-IR were detected. These changes include a decrease in the amount of parvalbumin (PV-IR) neurons in layer II, an increase of calbindin (CB-IR) neurons in layers III and V, and an increase in calretinin (CR-IR) neurons in layer II. We also observed glial fibrillary acidic protein immunoreactivity (GFAP-IR) in the white matter, in the gray-white matter transition, and around the sectors with NeuN-IR total loss. These findings may reflect dynamic activity as a consequence of the lesion that is associated with changes in the excitatory circuits of neighboring hyperactivated glutamatergic neurons, possibly due to the primary impact, or secondary events such as hypoxia-ischemia. Temporal evolution of these changes may be the substrate linking severe cortical contusion and the resulting epileptogenic activity observed in some patients.
Buriticá
Efraín
E
Centro de Estudios Cerebrales, Facultad de Salud, Universidad del Valle , Cali, Valle, Colombia.
Villamil
Liliana
L
Guzmán
Francisco
F
Escobar
Martha I
MI
García-Cairasco
Norberto
N
Pimienta
Hernán J
HJ
D000293:Adolescent; D000328:Adult; D000368:Aged; D034961:Antigens, Nuclear / Q000032:analysis / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins / Q000032:analysis / Q000378:metabolism*; D002540:Cerebral Cortex / Q000293:injuries / Q000378:metabolism* / Q000473:pathology*; D018450:Disease Progression; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000378:metabolism; D005911:Gliosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000032:analysis / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010320:Parvalbumins / Q000032:analysis / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000032:analysis / Q000378:metabolism; D055815:Young Adult
D034961:Antigens, Nuclear; D015415:Biomarkers; C576764:CALB2 protein, human; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; C506808:neuronal nuclear antigen NeuN, human; D018698:Glutamic Acid