PMID- 10518995
OWN - NLM
STAT- MEDLINE
DCOM- 19991026
LR  - 20061115
IS  - 1420-682X (Print)
IS  - 1420-682X (Linking)
VI  - 55
IP  - 11
DP  - 1999 Aug 30
TI  - Cholinergic, monoaminergic and glutamatergic changes following perinatal asphyxia 
      in the rat.
PG  - 1491-501
AB  - 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.
FAU - Kohlhauser, C
AU  - Kohlhauser C
AD  - Department of Pediatrics, University of Vienna, Austria.
FAU - Mosgoeller, W
AU  - Mosgoeller W
FAU - Hoeger, H
AU  - Hoeger H
FAU - Lubec, G
AU  - Lubec G
FAU - Lubec, B
AU  - Lubec B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Cell Mol Life Sci
JT  - Cellular and molecular life sciences : CMLS
JID - 9705402
RN  - 0 (Amino Acid Transport System X-AG)
RN  - 0 (Carrier Proteins)
RN  - 0 (Excitatory Amino Acid Transporter 3)
RN  - 0 (Glutamate Plasma Membrane Transport Proteins)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Membrane Transport Proteins)
RN  - 0 (Neuropeptides)
RN  - 0 (Neurotransmitter Agents)
RN  - 0 (SLC18A3 protein, human)
RN  - 0 (SLC1A1 protein, human)
RN  - 0 (Slc18a3 protein, rat)
RN  - 0 (Slc1a1 protein, rat)
RN  - 0 (Symporters)
RN  - 0 (Vesicular Acetylcholine Transport Proteins)
RN  - 0 (Vesicular Biogenic Amine Transport Proteins)
RN  - 0 (Vesicular Monoamine Transport Proteins)
RN  - 0 (Vesicular Transport Proteins)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
SB  - IM
MH  - Age Factors
MH  - *Amino Acid Transport System X-AG
MH  - Animals
MH  - Asphyxia Neonatorum/complications/*physiopathology
MH  - Brain/metabolism
MH  - Brain Diseases/etiology/metabolism
MH  - Carrier Proteins/metabolism
MH  - Disease Models, Animal
MH  - Excitatory Amino Acid Transporter 3
MH  - Glutamate Plasma Membrane Transport Proteins
MH  - Humans
MH  - Immunohistochemistry
MH  - Infant, Newborn
MH  - Membrane Glycoproteins/metabolism
MH  - *Membrane Transport Proteins
MH  - *Neuropeptides
MH  - Neurotransmitter Agents/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Symporters
MH  - Tissue Distribution
MH  - Tyrosine 3-Monooxygenase/metabolism
MH  - Vesicular Acetylcholine Transport Proteins
MH  - Vesicular Biogenic Amine Transport Proteins
MH  - Vesicular Monoamine Transport Proteins
MH  - *Vesicular Transport Proteins
EDAT- 1999/10/16 00:00
MHDA- 1999/10/16 00:01
CRDT- 1999/10/16 00:00
PHST- 1999/10/16 00:00 [pubmed]
PHST- 1999/10/16 00:01 [medline]
PHST- 1999/10/16 00:00 [entrez]
AID - 10.1007/s000180050388 [pii]
AID - 10.1007/s000180050388 [doi]
PST - ppublish
SO  - Cell Mol Life Sci. 1999 Aug 30;55(11):1491-501. doi: 10.1007/s000180050388.