Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis.
This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naive and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-, and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.
Kharlamov
Elena A
EA
Department of Neurology, Allegheny-Singer Research Institute, Allegheny General Hospital, Pittsburgh, PA, USA.
Kharlamov
Alexander
A
Kelly
Kevin M
KM
D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D020520:Brain Infarction / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D004268:DNA-Binding Proteins; D018891:Dentate Gyrus / Q000378:metabolism / Q000503:physiopathology; D004195:Disease Models, Animal; D004827:Epilepsy / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D005452:Fluoresceins; D005911:Gliosis / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D007150:Immunohistochemistry; D020767:Intracranial Thrombosis / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D008028:Light Coagulation / Q000009:adverse effects; D009410:Nerve Degeneration / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009478:Neuropeptide Y / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism; D009930:Organic Chemicals; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000378:metabolism / Q000503:physiopathology; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology
D004268:DNA-Binding Proteins; D005452:Fluoresceins; D009419:Nerve Tissue Proteins; C492380:NeuN protein, mouse; D009478:Neuropeptide Y; D009687:Nuclear Proteins; D009930:Organic Chemicals; C435731:fluoro jade