PMID- 10627605
OWN - NLM
STAT- MEDLINE
DCOM- 20000127
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 20
IP  - 1
DP  - 2000 Jan 1
TI  - Evidence that brain-derived neurotrophic factor from presynaptic nerve terminals 
      regulates the phenotype of calbindin-containing neurons in the lateral septum.
PG  - 274-82
AB  - Brain-derived neurotrophic factor (BDNF) is transported anterogradely in neurons 
      of the CNS and can be released by activity-dependent mechanisms to regulate 
      synaptic plasticity. However, few neural networks have been identified in which 
      the production, transport, and effects of BDNF on postsynaptic neurons can be 
      analyzed in detail. In this study, we have identified such a network. BDNF has 
      been colocalized by immunocytochemistry with tyrosine hydroxylase (TH) in nerve 
      fibers and nerve terminals within the lateral septum of rats. BDNF-containing 
      nerve fibers terminate on a population of calbindin-containing neurons in lateral 
      septum that contain TrkB, the high-affinity receptor for BDNF. Overexpression of 
      BDNF in noradrenergic neurons increased levels of calbindin in septum, as well as 
      in whole-brain lysates. Septal levels of calbindin and BDNF partially decreased 
      after unilateral lesions of the medial forebrain bundle (MFB), induced with 
      6-hydroxydopamine, a treatment that abolished TH staining. These data suggest 
      that BDNF is anterogradely transported within the MFB in catecholaminergic 
      neurons arising from brainstem nuclei. To determine whether BDNF affects the 
      production of calbindin in lateral septal neurons directly, we tested the effects 
      of BDNF on cultures of septal neurons from embryonic day 16-17 rats. BDNF 
      promoted the expression of calbindin, as well as the arborization of 
      calbindin-containing neurons, but BDNF had no effect on cell division or 
      survival. Together, these results suggest that BDNF, anterogradely transported in 
      catecholaminergic neurons, regulates calbindin expression within the lateral 
      septum.
FAU - Fawcett, J P
AU  - Fawcett JP
AD  - Center for Neuronal Survival and Division of Neurosurgery, and Montreal 
      Neurological Institute and the Department of Neurology and Neurosurgery, McGill 
      University, Montreal, Quebec, Canada H3A 2B4.
FAU - Alonso-Vanegas, M A
AU  - Alonso-Vanegas MA
FAU - Morris, S J
AU  - Morris SJ
FAU - Miller, F D
AU  - Miller FD
FAU - Sadikot, A F
AU  - Sadikot AF
FAU - Murphy, R A
AU  - Murphy RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Calbindins)
RN  - 0 (S100 Calcium Binding Protein G)
RN  - 0 (Sympatholytics)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - EC 1.14.17.1 (Dopamine beta-Hydroxylase)
RN  - X4W3ENH1CV (Norepinephrine)
SB  - IM
MH  - Age Factors
MH  - Animals
MH  - Axonal Transport/physiology
MH  - Brain-Derived Neurotrophic Factor/analysis/*genetics/metabolism
MH  - Calbindins
MH  - Cells, Cultured
MH  - Dopamine beta-Hydroxylase/genetics
MH  - Female
MH  - Gene Expression Regulation, Enzymologic
MH  - Mice
MH  - Mice, Transgenic
MH  - Nerve Fibers/chemistry/enzymology
MH  - Neurons/*chemistry/enzymology/ultrastructure
MH  - Norepinephrine/physiology
MH  - Oxidopamine
MH  - Phenotype
MH  - Pregnancy
MH  - Presynaptic Terminals/*chemistry
MH  - Promoter Regions, Genetic/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - S100 Calcium Binding Protein G/*analysis
MH  - Septal Nuclei/*cytology
MH  - Sympatholytics
MH  - Tyrosine 3-Monooxygenase/analysis
PMC - PMC6774122
EDAT- 2000/01/11 00:00
MHDA- 2000/01/11 00:01
PMCR- 2000/07/01
CRDT- 2000/01/11 00:00
PHST- 2000/01/11 00:00 [pubmed]
PHST- 2000/01/11 00:01 [medline]
PHST- 2000/01/11 00:00 [entrez]
PHST- 2000/07/01 00:00 [pmc-release]
AID - 3801 [pii]
AID - 10.1523/JNEUROSCI.20-01-00274.2000 [doi]
PST - ppublish
SO  - J Neurosci. 2000 Jan 1;20(1):274-82. doi: 10.1523/JNEUROSCI.20-01-00274.2000.