title: Degeneration of cholinergic rat basal forebrain neurons after experimental subarachnoid hemorrhage.
abstract: OBJECTIVE
  The reasons for neuropsychological deficits after subarachnoid hemorrhage (SAH) are fairly unknown. Cholinergic basal forebrain (BFB) neurons are essential for attention, memory, and emotion. We investigated possible changes in the cholinergic BFB and its hippocampal and neocortical terminals after experimental SAH.
  
  
  METHODS
  SAH was induced in 19 male Wistar rats by stereotactic injection of 150 microL of autologous blood into the prechiasmatic cistern. Five control animals received 150 microL of saline. Continuous monitoring of brain tissue oxygen tension, intracranial pressure, and cerebral perfusion pressure was performed. After 4 and 14 days, the BFB was analyzed for cholinergic and gamma-aminobutyric acid-ergic cell counts. The number of cholinergic terminals in the hippocampus and neocortex was calculated by optical densitometry.
  
  
  RESULTS
  SAH resulted in a 20 to 30% decrease in cholinergic BFB neurons in the medial septum and diagonal band at 4 and 14 days. A similar decline in the density of hippocampal and neocortical cholinergic terminals was demonstrated. Animals treated with saline did not exhibit significant cholinergic cell loss, and gamma-aminobutyric acid-ergic neurons appeared unaffected by the SAH. Courses of intracranial pressure and cerebral perfusion pressure did not differ between animals injected with blood and saline, but brain tissue oxygen tension decreased considerably and continued to stay below baseline in SAH, although it returned to normal values after saline injection.
  
  
  CONCLUSIONS
  The present study provides evidence for a decrease of cholinergic BFB neurons after SAH. The direct effect of blood in the basal cisterns seemed to result in an enduring tissue hypoxia as a significant mechanism for cholinergic degeneration.
authors.affiliation: Department of General Neurosurgery, Center of Neurosurgery, University of Cologne, Cologne, Lindenthal, Germany. Mario.Loehr@uk-koeln.de
authors.forename: Mario
authors.initials: M
authors.lastname: Löhr
authors.forename: Georgios
authors.initials: G
authors.lastname: Tzouras
authors.forename: Marek
authors.initials: M
authors.lastname: Molcanyi
authors.forename: Ralf-Ingo
authors.initials: RI
authors.lastname: Ernestus
authors.forename: Jürgen A
authors.initials: JA
authors.lastname: Hampl
authors.forename: Jürgen H
authors.initials: JH
authors.lastname: Fischer
authors.forename: Kurtulus
authors.initials: K
authors.lastname: Sahin
authors.forename: Thomas
authors.initials: T
authors.lastname: Arendt
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Härtig
mesh_terms: D000818:Animals; D002799:Cholinergic Fibers / Q000473:pathology*; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D009474:Neurons / Q000473:pathology*; D016548:Prosencephalon / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000473:pathology* / Q000503:physiopathology