PMID- 22306205
OWN - NLM
STAT- MEDLINE
DCOM- 20121127
LR  - 20211021
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Print)
IS  - 0306-4522 (Linking)
VI  - 207
DP  - 2012 Apr 5
TI  - Glia determine the course of brain-derived neurotrophic factor-mediated 
      dendritogenesis and provide a soluble inhibitory cue to dendritic growth in the 
      brainstem.
PG  - 333-46
LID - 10.1016/j.neuroscience.2012.01.013 [doi]
AB  - Cardiorespiratory control neurons in the brainstem nucleus tractus solitarius 
      (NTS) undergo dramatic expansion of dendritic arbors during the early postnatal 
      period, when functional remodeling takes place within the NTS circuitry. However, 
      the underlying molecular mechanisms of morphological maturation of NTS neurons 
      are largely unknown. Our previous studies point to the neurotrophin brain-derived 
      neurotrophic factor (BDNF), which is abundantly expressed by NTS-projecting 
      primary sensory neurons, as a candidate mediator of NTS dendritogenesis. In the 
      current study, we used neonatal rat NTS neurons in vitro to examine the role of 
      BDNF in the dendritic development of neurochemically identified subpopulations of 
      NTS neurons. In the presence of abundant glia, BDNF promoted NTS dendritic 
      outgrowth and complexity, with the magnitude of the BDNF effect dependent on 
      neuronal phenotype. Surprisingly, BDNF switched from promoting to inhibiting NTS 
      dendritogenesis upon glia depletion. Moreover, glia depletion alone led to a 
      significant increase in NTS dendritic outgrowth. Consistent with this result, 
      astrocyte-conditioned medium (ACM), which promoted hippocampal dendritogenesis, 
      inhibited dendritic growth of NTS neurons. The latter effect was abolished by 
      heat-inactivation of ACM, pointing to a diffusible astrocyte-derived negative 
      regulator of NTS dendritic growth. Together, these data demonstrate a role for 
      BDNF in the postnatal development of NTS neurons, and reveal novel effects of 
      glia on this process. Moreover, previously documented dramatic increases in NTS 
      glial proliferation in victims of sudden infant death syndrome (SIDS) underscore 
      the importance of our findings and the need to better understand the role of glia 
      and their interactions with BDNF during NTS circuit maturation. Furthermore, 
      while it has previously been demonstrated that the specific effects of BDNF on 
      dendritic growth are context-dependent, the role of glia in this process is 
      unknown. Thus, our data carry important implications for mechanisms of 
      dendritogenesis likely beyond the NTS.
CI  - Copyright (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Martin, J L
AU  - Martin JL
AD  - Department of Integrative Biosciences, Oregon Health and Science University 
      School of Dentistry, Portland, OR 97239, USA.
FAU - Brown, A L
AU  - Brown AL
FAU - Balkowiec, A
AU  - Balkowiec A
LA  - eng
GR  - R01 HL076113-01A1/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113-05S1/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113-03/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113-04/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113-05/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113-02/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120118
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Growth Inhibitors)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Brain Stem/cytology/growth & development
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Cell Differentiation/physiology
MH  - Cues
MH  - Dendrites/metabolism/*physiology
MH  - Growth Inhibitors/*metabolism
MH  - Neurogenesis/*physiology
MH  - Neuroglia/*metabolism/physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Solitary Nucleus/cytology/*growth & development
PMC - PMC3307896
MID - NIHMS349465
COIS- The authors declare no conflict of interest.
EDAT- 2012/02/07 06:00
MHDA- 2012/12/10 06:00
PMCR- 2012/04/05
CRDT- 2012/02/07 06:00
PHST- 2011/09/02 00:00 [received]
PHST- 2011/11/21 00:00 [revised]
PHST- 2012/01/11 00:00 [accepted]
PHST- 2012/02/07 06:00 [entrez]
PHST- 2012/02/07 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
PHST- 2012/04/05 00:00 [pmc-release]
AID - S0306-4522(12)00035-8 [pii]
AID - 10.1016/j.neuroscience.2012.01.013 [doi]
PST - ppublish
SO  - Neuroscience. 2012 Apr 5;207:333-46. doi: 10.1016/j.neuroscience.2012.01.013. 
      Epub 2012 Jan 18.