PMID- 10103122
OWN - NLM
STAT- MEDLINE
DCOM- 19990520
LR  - 20190815
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 11
IP  - 4
DP  - 1999 Apr
TI  - Absence of the dopamine D2 receptor leads to a decreased expression of GDNF and 
      NT-4 mRNAs in restricted brain areas.
PG  - 1275-84
AB  - Neurotrophic factors (NTFs) control the metabolic and electrophysiological 
      properties of dopaminergic neurons in the brain. At the level of the substantia 
      nigra, NTFs have been proposed to control dopamine release by regulating the 
      firing rate of dopaminergic cells. This function is normally controlled by 
      presynaptic dopaminergic autoreceptors. Dopamine has also been proposed to 
      regulate the expression of NTFs and their receptors in the nigrostriatal pathway. 
      Thus, an interaction between the signalling cascades activated by NTFs and 
      dopamine receptors might possibly influence the physiology of dopaminergic 
      neurons. Among dopamine receptors, D2 receptors (D2R) are the most abundant on 
      dopaminergic neurons, where they exert autoreceptor functions. To test for an 
      interaction between the NTF and dopaminergic pathways we have analysed the 
      expression of NTFs and their receptors in D2R-deficient (D2R -/-) mice. Our study 
      shows that the mRNA levels of brain-derived neurotrophic factor (BDNF), 
      neurotrophin-3 and their corresponding receptors are not modified in the 
      dopaminergic system of D2R -/- adult mice compared with wild-type littermates. 
      However, a marked reduction of glial cell line-derived neurotrophic factor (GDNF) 
      and neurotrophin-4 (NT-4) mRNAs is observed in the striatum and parietal cortex 
      of D2R -/- mice, respectively. These results implicate dopamine, acting through 
      D2 receptors, in the local control of specific NTF expression. The 
      down-regulation of GDNF and NT-4 expression might also contribute to the 
      locomotor phenotype of D2R -/- mice.
FAU - Bozzi, Y
AU  - Bozzi Y
AD  - Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/ULP, 
      Illkirch, C.U. de Strasbourg, France.
FAU - Borrelli, E
AU  - Borrelli E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Gdnf protein, mouse)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Dopamine D2)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Animals
MH  - Brain/*metabolism
MH  - *Brain Mapping
MH  - Glial Cell Line-Derived Neurotrophic Factor
MH  - Mice
MH  - Mice, Knockout
MH  - Neocortex/metabolism
MH  - Nerve Growth Factors/*genetics
MH  - Nerve Tissue Proteins/*genetics
MH  - RNA, Messenger/*biosynthesis
MH  - Receptors, Dopamine D2/*analysis
EDAT- 1999/04/02 00:00
MHDA- 1999/04/02 00:01
CRDT- 1999/04/02 00:00
PHST- 1999/04/02 00:00 [pubmed]
PHST- 1999/04/02 00:01 [medline]
PHST- 1999/04/02 00:00 [entrez]
AID - 10.1046/j.1460-9568.1999.00541.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 1999 Apr;11(4):1275-84. doi: 10.1046/j.1460-9568.1999.00541.x.