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Effects of epidural compression on stellate neurons and thalamocortical afferent fibers in the rat primary somatosensory cortex.

Abstract A number of neurological disorders such as epidural hematoma can cause compression of cerebral cortex. We here tested the hypothesis that sustained compression of primary somatosensory cortex may affect stellate neurons and thalamocortical afferent (TCA) fibers. A rat model with barrel cortex subjected to bead epidural compression was used. Golgi-Cox staining analyses showed the shrinkage of dendritic arbors and the stripping of dendritic spines of stellate neurons for at least 3 months post-lesion. Anterograde tracing analyses exhibited a progressive decline of TCA fiber density in barrel field for 6 months post-lesion. Due to the abrupt decrease of TCA fiber density at 3 days after compression, we further used electron microscopy to investigate the ultrastructure of TCA fibers at this time. Some TCA fiber terminal profiles with dissolved or darkened mitochondria and fewer synaptic vesicles were distorted and broken. Furthermore, the disruption of mitochondria and myelin sheath was observed in some myelinated TCA fibers. In addition, expressions of oxidative markers 3-nitrotyrosine and 4-hydroxynonenal were elevated in barrel field post-lesion. Treatment of antioxidant ascorbic acid or apocynin was able to reverse the increase of oxidative stress and the decline of TCA fiber density, rather than the shrinkage of dendrites and the stripping of dendritic spines of stellate neurons post-lesion. Together, these results indicate that sustained epidural compression of primary somatosensory cortex affects the TCA fibers and the dendrites of stellate neurons for a prolonged period. In addition, oxidative stress is responsible for the reduction of TCA fiber density in barrels rather than the shrinkage of dendrites and the stripping of dendritic spines of stellate neurons.
PMID
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Authors

Mayor MeshTerms

Epidural Space

Keywords
Journal Title acta neurobiologiae experimentalis
Publication Year Start




PMID- 28379212
OWN - NLM
STAT- MEDLINE
DA  - 20170405
DCOM- 20170414
LR  - 20170414
IS  - 1689-0035 (Electronic)
IS  - 0065-1400 (Linking)
VI  - 77
IP  - 1
DP  - 2017
TI  - Effects of epidural compression on stellate neurons and thalamocortical afferent 
      fibers in the rat primary somatosensory cortex.
PG  - 1-17
AB  - A number of neurological disorders such as epidural hematoma can cause
      compression of cerebral cortex. We here tested the hypothesis that sustained
      compression of primary somatosensory cortex may affect stellate neurons and
      thalamocortical afferent (TCA) fibers. A rat model with barrel cortex subjected
      to bead epidural compression was used. Golgi-Cox staining analyses showed the
      shrinkage of dendritic arbors and the stripping of dendritic spines of stellate
      neurons for at least 3 months post-lesion. Anterograde tracing analyses exhibited
      a progressive decline of TCA fiber density in barrel field for 6 months
      post-lesion. Due to the abrupt decrease of TCA fiber density at 3 days after
      compression, we further used electron microscopy to investigate the
      ultrastructure of TCA fibers at this time. Some TCA fiber terminal profiles with 
      dissolved or darkened mitochondria and fewer synaptic vesicles were distorted and
      broken. Furthermore, the disruption of mitochondria and myelin sheath was
      observed in some myelinated TCA fibers. In addition, expressions of oxidative
      markers 3-nitrotyrosine and 4-hydroxynonenal were elevated in barrel field
      post-lesion. Treatment of antioxidant ascorbic acid or apocynin was able to
      reverse the increase of oxidative stress and the decline of TCA fiber density,
      rather than the shrinkage of dendrites and the stripping of dendritic spines of
      stellate neurons post-lesion. Together, these results indicate that sustained
      epidural compression of primary somatosensory cortex affects the TCA fibers and
      the dendrites of stellate neurons for a prolonged period. In addition, oxidative 
      stress is responsible for the reduction of TCA fiber density in barrels rather
      than the shrinkage of dendrites and the stripping of dendritic spines of stellate
      neurons.
FAU - Yeh, Tzu-Yin
AU  - Yeh TY
AD  - Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan.
FAU - Tseng, Guo-Fang
AU  - Tseng GF
AD  - Department of Anatomy, Tzu Chi University, Hualien, Taiwan, Institute of
      Physiological and Anatomical Medicine, Tzu Chi University, Hualien, Taiwan.
FAU - Tseng, Chi-Yu
AU  - Tseng CY
AD  - Department of Neurology, Taichung Tzu Chi Hospital, Taichung, Taiwan.
FAU - Huang, Yung-Hsin
AU  - Huang YH
AD  - Institute of Physiological and Anatomical Medicine, Tzu Chi University, Hualien, 
      Taiwan.
FAU - Liu, Pei-Hsin
AU  - Liu PH
AD  - Institute of Medical Sciences, Tzu Chi University, Hualien, Taiwan, Department of
      Anatomy, Tzu Chi University, Hualien, Taiwan, Institute of Physiological and
      Anatomical Medicine, Tzu Chi University, Hualien, Taiwan,
      [email protected]
LA  - eng
PT  - Journal Article
PL  - Poland
TA  - Acta Neurobiol Exp (Wars)
JT  - Acta neurobiologiae experimentalis
JID - 1246675
RN  - 0 (Acetophenones)
RN  - 0 (Aldehydes)
RN  - 0 (Antioxidants)
RN  - 0 (Dextrans)
RN  - 0 (biotinylated dextran amine)
RN  - 3604-79-3 (3-nitrotyrosine)
RN  - 42HK56048U (Tyrosine)
RN  - 6SO6U10H04 (Biotin)
RN  - B6J7B9UDTR (acetovanillone)
RN  - EC 1.9.3.1 (Electron Transport Complex IV)
RN  - K1CVM13F96 (4-hydroxy-2-nonenal)
RN  - PQ6CK8PD0R (Ascorbic Acid)
SB  - IM
MH  - Acetophenones/therapeutic use
MH  - Afferent Pathways/*pathology
MH  - Aldehydes/metabolism
MH  - Animals
MH  - Antioxidants/therapeutic use
MH  - Ascorbic Acid/therapeutic use
MH  - Biotin/analogs & derivatives/pharmacokinetics
MH  - Brain Injuries/drug therapy/*pathology
MH  - Dendrites/pathology/ultrastructure
MH  - Dextrans/pharmacokinetics
MH  - Disease Models, Animal
MH  - Electron Transport Complex IV/metabolism
MH  - *Epidural Space/physiology
MH  - Functional Laterality
MH  - Male
MH  - Neurons/*pathology/ultrastructure
MH  - Oxidative Stress/physiology
MH  - Rats
MH  - Somatosensory Cortex/injuries/*pathology
MH  - Thalamus/*pathology/ultrastructure
MH  - Time Factors
MH  - Tyrosine/analogs & derivatives/metabolism
EDAT- 2017/04/06 06:00
MHDA- 2017/04/15 06:00
CRDT- 2017/04/06 06:00
AID - 7701 [pii]
PST - ppublish
SO  - Acta Neurobiol Exp (Wars). 2017;77(1):1-17.

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