PMID- 21865474
OWN - NLM
STAT- MEDLINE
DCOM- 20111107
LR  - 20211020
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 31
IP  - 34
DP  - 2011 Aug 24
TI  - Endogenous brain-derived neurotrophic factor in the nucleus tractus solitarius 
      tonically regulates synaptic and autonomic function.
PG  - 12318-29
LID - 10.1523/JNEUROSCI.0746-11.2011 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, are highly 
      expressed in the nucleus tractus solitarius (nTS), the principal target of 
      cardiovascular primary afferent input to the brainstem. However, little is known 
      about the role of BDNF signaling in nTS in cardiovascular homeostasis. We 
      examined whether BDNF in nTS modulates cardiovascular function in vivo and 
      regulates synaptic and/or neuronal activity in isolated brainstem slices. 
      Microinjection of BDNF into the rat medial nTS (mnTS), a region critical for 
      baroreflex control of sympathetic outflow, produced dose-dependent increases in 
      mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve 
      activity (LSNA) that were blocked by the tyrosine kinase inhibitor K252a. In 
      contrast, immunoneutralization of endogenous BDNF (anti-BDNF), or microinjection 
      of K252a alone, decreased MAP, HR, and LSNA. The effects of anti-BDNF were 
      abolished by blockade of ionotropic glutamate receptors, indicating a role for 
      glutamate signaling in the response to BDNF. In vitro, BDNF reduced the amplitude 
      of miniature EPSCs as well as solitary tract (TS) evoked EPSC amplitude and 
      action potential discharge (APD) in second-order nTS neurons. BDNF effects on 
      EPSCs were independent of GABAergic signaling and abolished by AMPA receptor 
      blockade. In contrast, K252a increased spontaneous EPSC frequency and TS evoked 
      EPSC amplitude. BDNF also attenuated APD evoked by injection of depolarizing 
      current into second-order neurons, indicating reduced intrinsic neuronal 
      excitability. Our data demonstrate that BDNF signaling in mnTS plays a tonic role 
      in regulating cardiovascular function, likely via modulation of primary afferent 
      glutamatergic excitatory transmission and neural activity.
FAU - Clark, Catharine G
AU  - Clark CG
AD  - Dalton Cardiovascular Research Center, Department of Biomedical Sciences, 
      University of Missouri, Columbia, Missouri 65211, USA.
FAU - Hasser, Eileen M
AU  - Hasser EM
FAU - Kunze, Diana L
AU  - Kunze DL
FAU - Katz, David M
AU  - Katz DM
FAU - Kline, David D
AU  - Kline DD
LA  - eng
GR  - R01 HL055306/HL/NHLBI NIH HHS/United States
GR  - R01 HL085108/HL/NHLBI NIH HHS/United States
GR  - HL-085108/HL/NHLBI NIH HHS/United States
GR  - R01 NS057398/NS/NINDS NIH HHS/United States
GR  - HL-55306/HL/NHLBI NIH HHS/United States
GR  - 5T32AR048523-05/AR/NIAMS NIH HHS/United States
GR  - T32 AR048523/AR/NIAMS NIH HHS/United States
GR  - NS-057398/NS/NINDS NIH HHS/United States
GR  - R56 NS057398/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
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)
SB  - IM
MH  - Action Potentials/physiology
MH  - Animals
MH  - Autonomic Pathways/*physiology
MH  - Brain-Derived Neurotrophic Factor/antagonists & inhibitors/*physiology
MH  - *Cardiovascular Physiological Phenomena
MH  - Male
MH  - Neurons/*physiology
MH  - Organ Culture Techniques
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Solitary Nucleus/*physiology
MH  - Synaptic Transmission/*physiology
PMC - PMC3408222
MID - NIHMS320271
EDAT- 2011/08/26 06:00
MHDA- 2011/11/08 06:00
PMCR- 2012/02/24
CRDT- 2011/08/26 06:00
PHST- 2011/08/26 06:00 [entrez]
PHST- 2011/08/26 06:00 [pubmed]
PHST- 2011/11/08 06:00 [medline]
PHST- 2012/02/24 00:00 [pmc-release]
AID - 31/34/12318 [pii]
AID - 3717780 [pii]
AID - 10.1523/JNEUROSCI.0746-11.2011 [doi]
PST - ppublish
SO  - J Neurosci. 2011 Aug 24;31(34):12318-29. doi: 10.1523/JNEUROSCI.0746-11.2011.