title: Effects of lateral fluid percussion injury on cholinergic markers in the newborn piglet brain.
abstract: Traumatic brain injury is a leading cause of death and disability in children. Studies using adult animal models showed alterations of the central cholinergic neurotransmission as a result of trauma. However, there is a lack of knowledge about consequences of brain trauma on cholinergic function in the immature brain. It is hypothesized that trauma affects the relative acetylcholine esterase activity and causes a loss of cholinergic neurons in the immature brain. Severe fluid percussion trauma (FP-TBI, 3.8+/-0.3atm) was induced in 15 female newborn piglets, monitored for 6h and compared with 12 control animals. The hemispheres ipsilateral to FP-TBI obtained from seven piglets were used for acetylcholine esterase histochemistry on frozen sagittal slices, while regional cerebral blood flow and oxygen availability was determined in the remaining eight FP-TBI animals. Post-fixed slices were immunohistochemically labelled for choline acetyltransferase as well as for low-affinity neurotrophin receptor in order to characterize cholinergic neurons in the basal forebrain. Regional cerebral blood flow and brain oxygen availability were reduced during the first 2h after FP-TBI (P<0.05). In addition, acetylcholine esterase activity was significantly increased in the neocortex, basal forebrain, hypothalamus and medulla after trauma (P<0.05), whereas the number of choline acetyltransferase and low-affinity neurotrophin receptor positive cells in the basal forebrain were unaffected by the injury. Thus, traumatic brain injury evoked an increased relative activity of the acetylcholine esterase in the immature brain early after injury, without loss of cholinergic neurons in the basal forebrain. These changes may contribute to developmental impairments after immature traumatic brain injury.
authors.affiliation: Institute of Interdisciplinary Isotope Research, Leipzig, Germany. donat@iif-leipzig.de
authors.forename: Cornelius K
authors.initials: CK
authors.lastname: Donat
authors.forename: Bernd
authors.initials: B
authors.lastname: Walter
authors.forename: Tanja
authors.initials: T
authors.lastname: Kayser
authors.forename: Winnie
authors.initials: W
authors.lastname: Deuther-Conrad
authors.forename: Reinhard
authors.initials: R
authors.lastname: Schliebs
authors.forename: Karen
authors.initials: K
authors.lastname: Nieber
authors.forename: Reinhard
authors.initials: R
authors.lastname: Bauer
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Härtig
authors.forename: Peter
authors.initials: P
authors.lastname: Brust
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000098:blood supply / Q000201:enzymology / Q000503:physiopathology*; D001930:Brain Injuries / Q000201:enzymology / Q000503:physiopathology*; D002560:Cerebrovascular Circulation; D002795:Choline O-Acetyltransferase / Q000378:metabolism*; D005260:Female; D005455:Fluorescent Antibody Technique; D007150:Immunohistochemistry; D009474:Neurons / Q000378:metabolism*; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism; D020800:Receptor, Nerve Growth Factor / Q000378:metabolism*; D013552:Swine; D013997:Time Factors
chemical_list: D020800:Receptor, Nerve Growth Factor; D002795:Choline O-Acetyltransferase; D000110:Acetylcholinesterase; D010100:Oxygen