PMID- 11175319
OWN - NLM
STAT- MEDLINE
DCOM- 20010517
LR  - 20191104
IS  - 1355-0284 (Print)
IS  - 1355-0284 (Linking)
VI  - 6
IP  - 6
DP  - 2000 Dec
TI  - Alterations in neurotrophin and neurotrophin receptor gene expression patterns in 
      the rat central nervous system following perinatal Borna disease virus infection.
PG  - 462-77
AB  - Infection of newborn rats with Borna disease virus (BDV) leads to persistence in 
      the absence of overt signs of inflammation. BDV persistence, however, causes 
      cerebellar hypoplasia and hippocampal dentate gyrus neuronal cell loss, which are 
      accompanied by diverse neurobehavioral abnormalities. Neurotrophins and their 
      receptors play important roles in the differentiation and survival of hippocampal 
      and cerebellar neurons. We have examined whether BDV can cause alterations in the 
      neurotrophin network, thus promoting neuronal damage. We have used RNase 
      protection assay to measure mRNA levels of the neurotrophins nerve growth factor 
      (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3), and 
      their trkC and trkB receptors, as well as the growth factors insulin-like growth 
      factor I (IGF-1) and basic fibroblast growth factor (bFGF), in the cerebellum and 
      hippocampus of BDV-infected and control rats at different time points p.i. 
      Reduced mRNA expression levels of NT-3, BDNF and NGF were found after day 14 p.i. 
      in the hippocampus, but not in the cerebellum, of newborn infected rats. Three 
      weeks after infection, trkC mRNA expression levels were reduced in both 
      hippocampus and cerebellum of infected rats, whereas decreased trkB mRNA levels 
      were only observed in the cerebellum. Reduced trkC mRNA expression was confined 
      to the dentate gyrus of the hippocampus, as assessed by in situ hybridization. 
      TUNEL assay revealed massive apoptotic cell death in the dentate gyrus of 
      infected rats at days 27 and 33 p.i. Increased numbers of apoptotic cells were 
      also detected in the cerebellar granular layer of infected rats after 8 days p.i. 
      Moreover, a dramatic loss of cerebellar Purkinje cells was seen after day 27 p.i. 
      Our results support the hypothesis, that BDV-induced alterations in neurotrophin 
      systems might contribute to selective neuronal cell death.
FAU - Zocher, M
AU  - Zocher M
AD  - Department of Virology, Institute for Medical Microbiology and Hygiene, 
      University of Freiburg, Hermann-Herder-Str. 11, 79104 Freiburg, Germany.
FAU - Czub, S
AU  - Czub S
FAU - Schulte-Monting, J
AU  - Schulte-Monting J
FAU - de La Torre, J C
AU  - de La Torre JC
FAU - Sauder, C
AU  - Sauder C
LA  - eng
GR  - MH57063/MH/NIMH NIH HHS/United States
GR  - NS12428/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurovirol
JT  - Journal of neurovirology
JID - 9508123
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - EC 2.7.10.1 (Receptor, trkC)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis
MH  - Borna Disease/*genetics/metabolism
MH  - Borna disease virus/*pathogenicity
MH  - Brain/*metabolism/virology
MH  - Brain-Derived Neurotrophic Factor/biosynthesis/deficiency/genetics
MH  - Cerebellum/metabolism/pathology
MH  - Female
MH  - Fibroblast Growth Factor 2/biosynthesis/genetics
MH  - *Gene Expression Regulation, Developmental
MH  - Hippocampus/metabolism/pathology
MH  - In Situ Hybridization
MH  - In Situ Nick-End Labeling
MH  - Insulin-Like Growth Factor I/biosynthesis/genetics
MH  - Male
MH  - Models, Neurological
MH  - Nerve Growth Factor/biosynthesis/deficiency/genetics
MH  - Nerve Growth Factors/*biosynthesis/genetics
MH  - Nerve Tissue Proteins/*biosynthesis/genetics
MH  - Neurons/metabolism/pathology
MH  - Neurotrophin 3/biosynthesis/deficiency/genetics
MH  - Protein Isoforms/biosynthesis/genetics
MH  - Purkinje Cells/pathology
MH  - RNA, Messenger/biosynthesis/genetics
MH  - Rats
MH  - Rats, Inbred Lew
MH  - Receptor, trkB/biosynthesis/genetics
MH  - Receptor, trkC/biosynthesis/genetics
MH  - Receptors, Nerve Growth Factor/*biosynthesis/genetics
EDAT- 2001/02/15 11:00
MHDA- 2001/05/18 10:01
CRDT- 2001/02/15 11:00
PHST- 2001/02/15 11:00 [pubmed]
PHST- 2001/05/18 10:01 [medline]
PHST- 2001/02/15 11:00 [entrez]
AID - 10.3109/13550280009091947 [doi]
PST - ppublish
SO  - J Neurovirol. 2000 Dec;6(6):462-77. doi: 10.3109/13550280009091947.