title: Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia in the rat.
abstract: Perinatal asphyxia (PA) is considered to lead to a variety of brain disorders including spasticity, epilepsy, mental retardation, and minimal brain disorder syndromes and may form the basis for psychiatric and neurodegenerative diseases later in life. We examined markers for neuronal transmission involved in the pathomechanisms of PA and candidates as mediators for long-term sequelae. We tested tyrosine hydroxylase (TH) and the vesicular monoamine transporter (VMAT) representing the monoaminergic system, the vesicular acetylcholine transporter (VAChT), and the excitatory amino acid carrier 1 (EAAC1), a neuronal subtype of the glutamate transporter, using immunohistochemistry on brain sections of rats subjected to graded PA. Three months following the asphyxiant insult immunoreactive (IR)-TH was decreased in striatum, hippocampus, thalamus, frontal cortex, and cerebellum; IR-VMAT was increased, and IR-VAChT was decreased in striatum. IR-EAAC1 glutamate transporter was increased in frontal cortex. The cholinergic, monoaminergic, and glutamatergic changes, still observed 3 months after the asphyxiant insult, may reflect their involvement in the pathomechanisms of PA and indicate mechanisms leading to long-term complications of PA. The variable consequences on the individual markers in several brain regions may be explained by specific susceptibility of cholinergic, monoaminergic, and glutamatergic neurons to the asphyxiant insult.
authors.affiliation: Department of Pediatrics, University of Vienna, Austria.
authors.forename: C
authors.initials: C
authors.lastname: Kohlhauser
authors.forename: W
authors.initials: W
authors.lastname: Mosgoeller
authors.forename: H
authors.initials: H
authors.lastname: Hoeger
authors.forename: G
authors.initials: G
authors.lastname: Lubec
authors.forename: B
authors.initials: B
authors.lastname: Lubec
mesh_terms: D000367:Age Factors; D027322:Amino Acid Transport System X-AG; D000818:Animals; D001238:Asphyxia Neonatorum / Q000150:complications / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism; D001927:Brain Diseases / Q000209:etiology / Q000378:metabolism; D002352:Carrier Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D050580:Excitatory Amino Acid Transporter 3; D050491:Glutamate Plasma Membrane Transport Proteins; D006801:Humans; D007150:Immunohistochemistry; D007231:Infant, Newborn; D008562:Membrane Glycoproteins / Q000378:metabolism; D026901:Membrane Transport Proteins; D009479:Neuropeptides; D018377:Neurotransmitter Agents / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D027981:Symporters; D014018:Tissue Distribution; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D050494:Vesicular Acetylcholine Transport Proteins; D050492:Vesicular Biogenic Amine Transport Proteins; D050493:Vesicular Monoamine Transport Proteins; D033921:Vesicular Transport Proteins
chemical_list: D027322:Amino Acid Transport System X-AG; D002352:Carrier Proteins; D050580:Excitatory Amino Acid Transporter 3; D050491:Glutamate Plasma Membrane Transport Proteins; D008562:Membrane Glycoproteins; D026901:Membrane Transport Proteins; D009479:Neuropeptides; D018377:Neurotransmitter Agents; C493459:SLC18A3 protein, human; C493400:SLC1A1 protein, human; C493461:Slc18a3 protein, rat; C493398:Slc1a1 protein, rat; D027981:Symporters; D050494:Vesicular Acetylcholine Transport Proteins; D050492:Vesicular Biogenic Amine Transport Proteins; D050493:Vesicular Monoamine Transport Proteins; D033921:Vesicular Transport Proteins; D014446:Tyrosine 3-Monooxygenase