PMID- 10215918
OWN - NLM
STAT- MEDLINE
DCOM- 19990526
LR  - 20190815
IS  - 0953-816X (Print)
IS  - 0953-816X (Linking)
VI  - 11
IP  - 5
DP  - 1999 May
TI  - BDNF and NT-4 differentiate two pathways in the modulation of neuropeptide 
      protein levels in postnatal hippocampal interneurons.
PG  - 1647-56
AB  - Neuropeptide protein levels in hippocampal interneurons exhibit a considerable 
      maturation in postnatal animals. This study characterizes the role of neuronal 
      activity in determining neuropeptide protein levels in postnatal hippocampal 
      interneurons, and the involvement of neurotrophins. In hippocampal slices from 
      7-day-old rats cultured for 2 weeks, treatment with the gamma-aminobutyric acidA 
      (GABAA) receptor antagonist bicuculline increased the staining intensity and the 
      number of neurons immunoreactive for neuropeptide Y (NPY). An opposite effect was 
      observed when non-N-methyl-d-aspartate (non-NMDA) excitatory transmission was 
      blocked. The effects of either treatment were reversed after return to control 
      medium. These findings were similar to those previously obtained on the effects 
      of activity on somatostatin immunostaining. Blockade of endogenous tyrosine 
      kinase neurotrophin receptors using K252a prevented the effects of bicuculline on 
      NPY- and somatostatin-immunoreactive neurons. Application of exogenous 
      neurotrophin-3 (NT-3) increased NPY and somatostatin protein levels in long-term 
      but not short-term cultures, while nerve growth factor (NGF) had no effect. In 
      contrast, brain-derived neurotrophic factor (BDNF) or neurotrophin-4 (NT-4) did 
      not affect equally NPY and somatostatin immunoreactivity: they mimicked the 
      effects of bicuculline treatment on NPY-immunoreactive neurons, but exerted no 
      conspicuous effect on somatostatin immunostaining. These results indicate that 
      although neuronal activity plays a major role in determining neuropeptide protein 
      levels in postnatal hippocampal interneurons, its effects on different 
      neuropeptides might be exerted through different mechanisms, with or without the 
      mediation of BDNF or NT-4.
FAU - Marty, S
AU  - Marty S
AD  - INSERM Unite 421, Faculte de Medecine, Creteil, France. marty@im3.inserm.fr
FAU - Onteniente, B
AU  - Onteniente B
LA  - eng
PT  - Journal Article
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Antibodies)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (GABA Antagonists)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuropeptide Y)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Quinoxalines)
RN  - 0 (Receptor, Ciliary Neurotrophic Factor)
RN  - 0 (Receptors, GABA-A)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 51110-01-1 (Somatostatin)
RN  - 62T278S1MX (FG 9041)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - P658DCA9XD (neurotrophin 4)
RN  - Y37615DVKC (Bicuculline)
SB  - IM
MH  - Animals
MH  - Antibodies
MH  - Bicuculline/pharmacology
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - GABA Antagonists/pharmacology
MH  - Hippocampus/*cytology/metabolism
MH  - Interneurons/chemistry/*metabolism
MH  - Nerve Growth Factors/*pharmacology
MH  - Neuropeptide Y/analysis/immunology/*metabolism
MH  - Neuroprotective Agents/metabolism
MH  - Neurotrophin 3
MH  - Organ Culture Techniques
MH  - Quinoxalines/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor Protein-Tyrosine Kinases/physiology
MH  - Receptor, Ciliary Neurotrophic Factor
MH  - Receptors, GABA-A/physiology
MH  - Receptors, N-Methyl-D-Aspartate/physiology
MH  - Receptors, Nerve Growth Factor/physiology
MH  - Somatostatin/analysis/immunology/pharmacology
EDAT- 1999/04/24 00:00
MHDA- 1999/04/24 00:01
CRDT- 1999/04/24 00:00
PHST- 1999/04/24 00:00 [pubmed]
PHST- 1999/04/24 00:01 [medline]
PHST- 1999/04/24 00:00 [entrez]
AID - 10.1046/j.1460-9568.1999.00582.x [doi]
PST - ppublish
SO  - Eur J Neurosci. 1999 May;11(5):1647-56. doi: 10.1046/j.1460-9568.1999.00582.x.