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Plasticity Response in the Contralesional Hemisphere after Subtle Neurotrauma: Gene Expression Profiling after Partial Deafferentation of the Hippocampus

Artikel i vetenskaplig tidskrift
Författare Daniel Andersson
Ulrika Wilhelmsson
Michael Nilsson
M. Kubista
Anders Ståhlberg
Marcela Pekna
Milos Pekny
Publicerad i Plos One
Volym 8
Nummer/häfte 7
Sidor s. e70699
ISSN 1932-6203
Publiceringsår 2013
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för biomedicin, avdelningen för patologi
Sidor s. e70699
Språk en
Länkar dx.doi.org/10.1371/journal.pone.007...
Ämnesord FIBRILLARY ACIDIC PROTEIN, CENTRAL-NERVOUS-SYSTEM, SYNAPSE FORMATION, MICE DEFICIENT, VIMENTIN, THROMBOSPONDIN-4, ASTROCYTES, STROKE, RAT, TRANSCRIPTOME
Ämneskategorier Klinisk medicin

Sammanfattning

Neurotrauma or focal brain ischemia are known to trigger molecular and structural responses in the uninjured hemisphere. These responses may have implications for tissue repair processes as well as for the recovery of function. To determine whether the plasticity response in the uninjured hemisphere occurs even after a subtle trauma, we subjected mice to a partial unilateral deafferentation of the hippocampus induced by stereotactically performed entorhinal cortex lesion (ECL). The expression of selected genes was assessed by quantitative real-time PCR in the hippocampal tissue at the injured side and the contralesional side at day 4 and 14 after injury. We observed that expression of genes coding for synaptotagmin 1, ezrin, thrombospondin 4, and C1q proteins, that have all been implicated in the synapse formation, re-arrangement and plasticity, were upregulated both in the injured and the contralesional hippocampus, implying a plasticity response in the uninjured hemisphere. Several of the genes, the expression of which was altered in response to ECL, are known to be expressed in astrocytes. To test whether astrocyte activation plays a role in the observed plasticity response to ECL, we took advantage of mice deficient in two intermediate filament (nanofilament) proteins glial fibrillary acidic protein (GFAP) and vimentin (GFAP(-/-) Vim(-/-)) and exhibiting attenuated astrocyte activation and reactive gliosis. The absence of GFAP and vimentin reduced the ECL-induced upregulation of thrombospondin 4, indicating that this response to ECL depends on astrocyte activation and reactive gliosis. We conclude that even a very limited focal neurotrauma triggers a distinct response at the contralesional side, which at least to some extent depends on astrocyte activation.

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