Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1998-1-21
pubmed:abstractText
Structural and/or functional injury of the basal ganglia can lead to motor functional disabilities, abnormal gait and posture, and intellectual/emotional impairment, disorders also frequently seen in hydrocephalus. Previous reports have documented changes in dopamine levels in the neostriatum in experimental hydrocephalus. The present study was designed to investigate possible functional injury of cholinergic, GABAergic and dopaminergic systems in the basal ganglia immunohistochemically in a model of kaolin-induced hydrocephalus. Hydrocephalus was induced in 12 Wistar rats by intracisternal injection of 0.05 ml volume of 25% kaolin solution under microscopic guidance. Four controls received an equal volume of sterile saline. The animals were killed at 2, 4 and 8 weeks after injection. The numbers of choline acetyltransferase (ChAT)- and glutamic acid decarboxylase (GAD)-immunoreactive (IR) neostriatal neurons and tyrosine hydroxylase (TH)-IR nigral neurons, were counted in 60-micron thick representative sections and the IR cellular densities (counted cell number/neostriatal area) were calculated in the neostriatum. The number of total neostriatal neurons was also counted in 15-micron thick sections stained by cresyl violet (Nissl staining) to calculate the cellular density. The number and cellular density of neostriatal ChAT-IR neurons were significantly reduced at 2, 4, and 8 weeks after injection (P < 0.05), while those of GAD-IR neurons decreased at 4 and 8 weeks (P < 0.05). There was a linear correlation between degree of ventricular enlargement, and reduction in number of ChAT- and GAD-IR neurons (P < 0.001) as well as in the cellular density (P < 0.001). However, Nissl staining revealed no reduction in the cellular density of total neostriatal neurons (P < 0.001). TH immunoreactivity was reduced in neostriatal axons and in nigral compacta neurons, particularly in the medial portion of the dopaminergic nigrostriatal pathway. These findings suggest that progressive hydrocephalus results in functional injuries of cholinergic and GABAergic neurons in the neostriatum and dopaminergic neurons in the substantia nigra compacta by mechanical distortion. The disturbance in balance of these neurotransmitter systems in the basal ganglia may explain some of motor functional disabilities in hydrocephalus.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
770
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
45-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9372201-Acetylcholine, pubmed-meshheading:9372201-Age Factors, pubmed-meshheading:9372201-Animals, pubmed-meshheading:9372201-Cell Count, pubmed-meshheading:9372201-Choline O-Acetyltransferase, pubmed-meshheading:9372201-Cholinergic Fibers, pubmed-meshheading:9372201-Dopamine, pubmed-meshheading:9372201-Glutamate Decarboxylase, pubmed-meshheading:9372201-Hydrocephalus, pubmed-meshheading:9372201-Immunohistochemistry, pubmed-meshheading:9372201-Kaolin, pubmed-meshheading:9372201-Male, pubmed-meshheading:9372201-Mesencephalon, pubmed-meshheading:9372201-Movement Disorders, pubmed-meshheading:9372201-Neostriatum, pubmed-meshheading:9372201-Neurons, pubmed-meshheading:9372201-Nissl Bodies, pubmed-meshheading:9372201-Pharmaceutic Aids, pubmed-meshheading:9372201-Rats, pubmed-meshheading:9372201-Rats, Wistar, pubmed-meshheading:9372201-Staining and Labeling, pubmed-meshheading:9372201-Stress, Mechanical, pubmed-meshheading:9372201-Tyrosine 3-Monooxygenase, pubmed-meshheading:9372201-gamma-Aminobutyric Acid
pubmed:year
1997
pubmed:articleTitle
Functional injury of cholinergic, GABAergic and dopaminergic systems in the basal ganglia of adult rat with kaolin-induced hydrocephalus.
pubmed:affiliation
Division of Neurosurgery, Hospital for Sick Children, Faculty of Medicine, University of Toronto, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't