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A Transmission Electron Microscopic Study of Microglia/macrophages in the Hippocampal Cortex and Neocortex Following Chronic Exposure to Valproate

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Publisher Wiley
Specialty Pathology
Date 2005 Apr 7
PMID 15810980
Citations 4
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Abstract

In chronic administration of sodium valproate to rats, significant disorders of structural integrity of the hippocampal gyrus and the neocortex of the temporal lobe, observed in the last two stages of the experiment (after 9 and 12 months), coexisted with increased number of microglial cells and, especially after 12 months, with intense phagocytic activity within these cells. At the ultrastructural level, phagocyte microglial cells were hypertrophied with several broadened processes. Their cytoplasm contained rich lysosomal apparatus, numerous lipofuscin-like structures, lipid droplets and multilaminated bodies. The nuclei of these cells were characteristic oval or round and sometimes triangle in shape with dense and highly clumped heterochromatin, distinctly accumulated under nuclear envelope, and sparse euchromatin. Microglia/macrophages were frequently present in a close vicinity of changed neuronal somata and also close to the altered elements of the neuropil pyramidal layer of the cortex. Microglial response may, together with abnormalities in neurones, astroglia and blood-brain barrier, play a significant role in the development of experimental valproate encephalopathy.

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References
1.
Le W, Rowe D, Xie W, Ortiz I, He Y, Appel S . Microglial activation and dopaminergic cell injury: an in vitro model relevant to Parkinson's disease. J Neurosci. 2001; 21(21):8447-55. PMC: 6762816. View

2.
Chiang C, Powell H, GOLD L, Samimi A, Campbell I . Macrophage/microglial-mediated primary demyelination and motor disease induced by the central nervous system production of interleukin-3 in transgenic mice. J Clin Invest. 1996; 97(6):1512-24. PMC: 507212. DOI: 10.1172/JCI118574. View

3.
Sobaniec-Lotowska M, Sobaniec W, Augustynowicz A . Morphometric analysis of the cerebellar cortex capillaries in the course of experimental valproate encephalopathy and after chronic exposure to sodium valproate using transmission electron microscopy. Folia Neuropathol. 2002; 39(4):277-80. View

4.
Sobaniec-Lotowska M . Ultrastructure of synaptic junctions in the cerebellar cortex in experimental valproate encephalopathy and after terminating chronic application of the antiepileptic. Folia Neuropathol. 2002; 40(2):87-96. View

5.
Sobaniec-Lotowska M, Sobaniec W . Morphological features of encephalopathy after chronic administration of the antiepileptic drug valproate to rats. A transmission electron microscopic study of capillaries in the cerebellar cortex. Exp Toxicol Pathol. 1996; 48(1):65-75. DOI: 10.1016/S0940-2993(96)80094-7. View