2006
DOI: 10.1016/j.expneurol.2006.02.113
|View full text |Cite
|
Sign up to set email alerts
|

Brain damage in neonatal rats following kaolin induction of hydrocephalus

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

3
82
0
10

Year Published

2007
2007
2021
2021

Publication Types

Select...
8
2

Relationship

1
9

Authors

Journals

citations
Cited by 125 publications
(95 citation statements)
references
References 51 publications
3
82
0
10
Order By: Relevance
“…Immunohistochemical evidence of gliosis, as expected following cell damage, was not detected in the region of the ventral respiratory group. Neuronal damage secondary to various mechanisms induces a 3-to 16-fold increase in GFAP label in neonatal animals (Khan et al, 2006;Svedin et al, 2007). Our results therefore indicate that neuronal damage is not a major mechanism in the pathogenic pathway linking nicotine to central respiratory dysfunction.…”
Section: Discussionmentioning
confidence: 54%
“…Immunohistochemical evidence of gliosis, as expected following cell damage, was not detected in the region of the ventral respiratory group. Neuronal damage secondary to various mechanisms induces a 3-to 16-fold increase in GFAP label in neonatal animals (Khan et al, 2006;Svedin et al, 2007). Our results therefore indicate that neuronal damage is not a major mechanism in the pathogenic pathway linking nicotine to central respiratory dysfunction.…”
Section: Discussionmentioning
confidence: 54%
“…[22][23][24][25]27,57,79,80,136 Metabolic disturbances contribute to reversible dysfunction, but the clinical syndrome of hydrocephalic brain dysfunction may be due predominantly to a subcortical disconnection syndrome. Possible causes of ventricular dilation include obstructed CSF flow with associated increased CSF pulsatility.…”
Section: Pathophysiological Modificationsmentioning
confidence: 99%
“…11,28 Uncontrolled hydrocephalus in children is associated with disruptions of myelination processes during development. 26 Research in animal models indicates that an arrested hydrocephalus produces an ongoing insult to the periventricular WM by gradually degenerating axons and by increasing myelin turnover, the extent of which correlates with larger ventricular volumes. 13 Repeated shunt failure produces multiple episodes of ventricular enlargement and recurrent effects on cerebral WM.…”
mentioning
confidence: 99%