PMID- 23642472
OWN - NLM
STAT- MEDLINE
DCOM- 20131022
LR  - 20211021
IS  - 1948-7193 (Electronic)
IS  - 1948-7193 (Print)
IS  - 1948-7193 (Linking)
VI  - 4
IP  - 5
DP  - 2013 May 15
TI  - Probing the ability of presynaptic tyrosine kinase receptors to regulate striatal 
      dopamine dynamics.
PG  - 895-904
LID - 10.1021/cn4000742 [doi]
AB  - Brain-derived neurotrophic factor (BDNF) modulates the synaptic transmission of 
      several monoaminergic neuronal systems. Molecular techniques using synapatosomes 
      in previous studies have suggested that BDNF's receptor, tyrosine kinases (Trk), 
      can quickly regulate dopamine release and transporter dynamics. Our main 
      objective in this study is to determine whether slice fast scan cyclic 
      voltammetry can be used to investigate the role of the TrkB receptor on dopamine 
      release and uptake processes in the caudate-putamen. Fast scan cyclic voltammetry 
      measured dopamine release and uptake rates in the presence of BDNF, or its 
      agonist 7,8-dihydroxyflavone, or a TrkB inhibitor K252a. Superfusion of BDNF led 
      to partial recovery of the electrically stimulated dopamine release response in 
      BDNF(+/-) mice which is blunted compared to wildtype mice, with no effect in 
      wildtype mice. Conversely, infusion of 7,8-dihydroxyflavone increased 
      electrically stimulated dopamine release in wildtype mice with no difference in 
      BDNF(+/-) mice. Overall, BDNF and 7,8-dihydroxyflavone had no effect on dopamine 
      uptake rates. Concentrations greater than 3 muM 7,8-dihydroxyflavone affected 
      dopamine uptake rates in BDNF(+/-) mice only. To demonstrate that BDNF and 
      7,8-dihydroxyflavone modulate dopamine release by activating the TrkB receptor, 
      both genotypes were pretreated with K252a. K252a was able to block BDNF and 
      7,8-DHF induced increases during stimulated dopamine release in BDNF(+/-) and 
      wildtype mice, respectively. Fast scan cyclic voltammetry demonstrates that acute 
      TrkB activation potentiates dopamine release in both genotypes.
FAU - Apawu, Aaron K
AU  - Apawu AK
AD  - Department of Chemistry, Wayne State University , Detroit, MI 48202, United 
      States.
FAU - Maina, Francis K
AU  - Maina FK
FAU - Taylor, James R
AU  - Taylor JR
FAU - Mathews, Tiffany A
AU  - Mathews TA
LA  - eng
GR  - AA-016967/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20130508
PL  - United States
TA  - ACS Chem Neurosci
JT  - ACS chemical neuroscience
JID - 101525337
RN  - 0 (6,7-dihydroxyflavone)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Carbazoles)
RN  - 0 (Flavones)
RN  - 0 (Indole Alkaloids)
RN  - 97161-97-2 (staurosporine aglycone)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/agonists/genetics/*physiology
MH  - Carbazoles/pharmacology
MH  - Caudate Nucleus/drug effects/physiology
MH  - Dopamine/*metabolism
MH  - Electrochemical Techniques
MH  - Flavones/pharmacology
MH  - Indole Alkaloids/pharmacology
MH  - Mice
MH  - Mice, Transgenic
MH  - Neostriatum/drug effects/*physiology
MH  - Presynaptic Terminals/drug effects/physiology
MH  - Putamen/drug effects/physiology
MH  - Receptor, trkB/antagonists & inhibitors/*physiology
PMC - PMC3656746
EDAT- 2013/05/07 06:00
MHDA- 2013/10/23 06:00
PMCR- 2014/05/15
CRDT- 2013/05/07 06:00
PHST- 2013/05/07 06:00 [entrez]
PHST- 2013/05/07 06:00 [pubmed]
PHST- 2013/10/23 06:00 [medline]
PHST- 2014/05/15 00:00 [pmc-release]
AID - 10.1021/cn4000742 [doi]
PST - ppublish
SO  - ACS Chem Neurosci. 2013 May 15;4(5):895-904. doi: 10.1021/cn4000742. Epub 2013 
      May 8.