PMID- 23172808
OWN - NLM
STAT- MEDLINE
DCOM- 20130530
LR  - 20211021
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 91
IP  - 2
DP  - 2013 Feb
TI  - Upregulation of brain-derived neurotrophic factor expression in nodose ganglia 
      and the lower brainstem of hypertensive rats.
PG  - 220-9
LID - 10.1002/jnr.23158 [doi]
AB  - Hypertension leads to structural and functional changes at baroreceptor synapses 
      in the medial nucleus tractus solitarius (NTS), but the underlying molecular 
      mechanisms remain unknown. Our previous studies show that brain-derived 
      neurotrophic factor (BDNF) is abundantly expressed by rat nodose ganglion (NG) 
      neurons, including baroreceptor afferents and their central terminals in the 
      medial NTS. We hypothesized that hypertension leads to upregulation of BDNF 
      expression in NG neurons. To test this hypothesis, we used two mechanistically 
      distinct models of hypertension, the spontaneously hypertensive rat (SHR) and the 
      deoxycorticosterone acetate (DOCA)-salt rat. Young adult SHRs, whose blood 
      pressure was significantly elevated compared with age-matched Wistar-Kyoto (WKY) 
      control rats, exhibited dramatic upregulation of BDNF mRNA and protein in the NG. 
      BDNF transcripts from exon 4, known to be regulated by activity, and exon 9 
      (protein-coding region) showed the largest increases. Electrical stimulation of 
      dispersed NG neurons with patterns that mimic baroreceptor activity during blood 
      pressure elevations led to increases in BDNF mRNA that were also mediated through 
      promoter 4. The increase in BDNF content of the NG in vivo was associated with a 
      significant increase in the percentage of BDNF-immunoreactive NG neurons. 
      Moreover, upregulation of BDNF in cell bodies of NG neurons was accompanied by a 
      significant increase in BDNF in the NTS region, the primary central target of NG 
      afferents. A dramatic increase in BDNF in the NG was also detected in DOCA-salt 
      hypertensive rats. Together, our study identifies BDNF as a candidate molecular 
      mediator of activity-dependent changes at baroafferent synapses during 
      hypertension.
CI  - Copyright (c) 2012 Wiley Periodicals, Inc.
FAU - Vermehren-Schmaedick, Anke
AU  - Vermehren-Schmaedick A
AD  - Department of Integrative Biosciences, Oregon Health & Science University, 
      Portland, Oregon 97239, USA.
FAU - Jenkins, Victoria K
AU  - Jenkins VK
FAU - Hsieh, Hui-ya
AU  - Hsieh HY
FAU - Brown, Alexandra L
AU  - Brown AL
FAU - Page, Mollie P
AU  - Page MP
FAU - Brooks, Virginia L
AU  - Brooks VL
FAU - Balkowiec, Agnieszka
AU  - Balkowiec A
LA  - eng
GR  - R01 HL070962/HL/NHLBI NIH HHS/United States
GR  - HL076113/HL/NHLBI NIH HHS/United States
GR  - HL070962/HL/NHLBI NIH HHS/United States
GR  - HL088552/HL/NHLBI NIH HHS/United States
GR  - R01 HL076113/HL/NHLBI NIH HHS/United States
GR  - R01 HL088552/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 - 20121122
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Cell Cycle Proteins)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Mineralocorticoids)
RN  - 0 (RNA, Messenger)
RN  - 0 (brain-derived integrating factor-1, rat)
RN  - 40GP35YQ49 (Desoxycorticosterone)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Blood Pressure/drug effects
MH  - Brain Stem/growth & development/*metabolism
MH  - Cell Cycle Proteins
MH  - Cells, Cultured
MH  - Desoxycorticosterone/toxicity
MH  - Disease Models, Animal
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - Hypertension/chemically induced/*pathology/physiopathology
MH  - Intracellular Signaling Peptides and Proteins/genetics/*metabolism
MH  - Male
MH  - Mineralocorticoids/toxicity
MH  - Neurons/drug effects/metabolism
MH  - Nodose Ganglion/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Rats, Sprague-Dawley
MH  - Up-Regulation/*physiology
PMC - PMC3927140
MID - NIHMS553188
COIS- DISCLOSURES: No conflicts of interest, financial or otherwise, are declared by 
      the authors.
EDAT- 2012/11/23 06:00
MHDA- 2013/06/01 06:00
PMCR- 2014/02/18
CRDT- 2012/11/23 06:00
PHST- 2012/07/26 00:00 [received]
PHST- 2012/09/12 00:00 [revised]
PHST- 2012/09/20 00:00 [accepted]
PHST- 2012/11/23 06:00 [entrez]
PHST- 2012/11/23 06:00 [pubmed]
PHST- 2013/06/01 06:00 [medline]
PHST- 2014/02/18 00:00 [pmc-release]
AID - 10.1002/jnr.23158 [doi]
PST - ppublish
SO  - J Neurosci Res. 2013 Feb;91(2):220-9. doi: 10.1002/jnr.23158. Epub 2012 Nov 22.