title: Acute and subacute hydrocephalus in a rat neonatal model: correlation with functional injury of neurotransmitter systems.
abstract: OBJECTIVE
  The evolution and severity of hydrocephalus in animal models varies in the species and mode of induction. This makes comparisons of the physiological system under investigation difficult between models. We noted that injection of kaolin into neonatal rats results in a dichotomous outcome into either an acute or subacute form. We investigated the clinical and functional transmitter system changes to compare these two types of hydrocephalus evolution.
  
  
  METHODS
  Hydrocephalus was induced in Wistar neonatal rats (within a week after their birth) by intracisternal injection of 0.02 ml volume of 25% kaolin solution under microscopic guidance. The same volume of sterile saline was injected into 12 neonatal rats as control group. The animals were assigned to either the acute or subacute group according to their head size, and sacrificed at 2, 4 and 8 weeks after injection. Biparietal diameter, ventricular size, cholinergic interneurons in the neostriatum and dopaminergic projection neurons in the substantia nigra were analyzed at each stage.
  
  
  RESULTS
  Animals affected with the acute type of hydrocephalus had obvious head enlargement, rapid ventricular enlargement, and all died at about 4 weeks. Animals with subacute type had slowly progressive ventricular enlargement, and all survived until 8 weeks. There appeared to be more kaolin ventral to the brainstem in the acute type. The number of cholinergic neostriatal neurons was significantly reduced at 2 and 4 weeks in the acute type, but only at 8 weeks in the subacute type. The number of dopaminergic nigral neurons was decreased at 4 weeks in the acute type, but unaffected in the subacute type.
  
  
  CONCLUSIONS
  The severity of onset of hydrocephalus in this animal model also correlates with the clinical outcome and changes in functional transmitter systems.
authors.affiliation: Department of Neurosurgery, Kyoto University, Graduate School of Medicine, Kyoto, Japan.
authors.forename: R
authors.initials: R
authors.lastname: Ishizaki
authors.forename: Y
authors.initials: Y
authors.lastname: Tashiro
authors.forename: T
authors.initials: T
authors.lastname: Inomoto
authors.forename: N
authors.initials: N
authors.lastname: Hashimoto
mesh_terms: D000109:Acetylcholine / Q000378:metabolism / Q000502:physiology*; D000208:Acute Disease; D000818:Animals; D001479:Basal Ganglia / Q000166:cytology / Q000503:physiopathology; D004396:Coloring Agents; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism / Q000502:physiology*; D006849:Hydrocephalus / Q000145:classification / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D007150:Immunohistochemistry; D007395:Interneurons / Q000378:metabolism; D017072:Neostriatum / Q000166:cytology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000166:cytology
chemical_list: D004396:Coloring Agents; D000109:Acetylcholine; D004298:Dopamine