PMID- 12122142
OWN - NLM
STAT- MEDLINE
DCOM- 20030210
LR  - 20190513
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 542
IP  - Pt 2
DP  - 2002 Jul 15
TI  - Neurotrophin modulation of voltage-gated potassium channels in rat through TrkB 
      receptors is time and sensory experience dependent.
PG  - 413-29
AB  - The whole-cell configuration of the patch-clamp technique, immunoprecipitation 
      experiments and unilateral naris occlusions were used to investigate whether the 
      voltage-gated potassium channel Kv1.3 was a substrate for neurotrophin-induced 
      tyrosine phosphorylation and subsequent functional modulation of current 
      properties in cultured rat olfactory bulb (OB) neurons. Membrane proteins of the 
      OB included all three Trk receptor kinases, but the truncated form of the 
      receptor, lacking an intact kinase domain, was the predominant form of the 
      protein for TrkA and TrkC, while TrkB was predominantly found as the full-length 
      receptor. Acute (15 min) stimulation of OB neurons with bath application of 50 ng 
      ml(-1) brain-derived neurotrophic factor (BDNF), which is a selective ligand for 
      TrkB, caused suppression of the whole-cell outward current and no changes in the 
      kinetics of inactivation or deactivation. Acute stimulation with either nerve 
      growth factor or neurotrophin-3 failed to evoke any changes in Kv1.3 function in 
      the OB neurons. Chronic exposure to BDNF (days) caused an increase in the 
      magnitude of Kv1.3 current and speeding of the inactivation and deactivation of 
      the channel. Acute BDNF-induced activation of TrkB receptors significantly 
      increased tyrosine phosphorylation of Kv1.3 in the OB, as shown using a combined 
      immunoprecipitation and Western blot analysis. With unilateral naris occlusion, 
      the acute BDNF-induced tyrosine phosphorylation of Kv1.3 was increased in neurons 
      lacking odour sensory experience. In summary, the duration of neurotrophin 
      exposure and the sensory-dependent state of a neuron can influence the degree of 
      phosphorylation of a voltage-gated ion channel and its concomitant functional 
      modulation by neurotrophins.
FAU - Tucker, K
AU  - Tucker K
AD  - Florida State University, Department of Biological Science, Program in 
      Neuroscience and Molecular Biophysics, Biomedical Research Facility, Tallahassee, 
      FL 32306, USA.
FAU - Fadool, D A
AU  - Fadool DA
LA  - eng
GR  - R29 DC003387/DC/NIDCD NIH HHS/United States
GR  - R29 DC003387-06/DC/NIDCD NIH HHS/United States
GR  - R29 DC03387/DC/NIDCD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Immune Sera)
RN  - 0 (KCNA3 protein, human)
RN  - 0 (Kcna3 protein, rat)
RN  - 0 (Kv1.3 Potassium Channel)
RN  - 0 (Potassium Channels)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 0 (Recombinant Proteins)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Animals, Newborn
MH  - Brain-Derived Neurotrophic Factor/*pharmacology
MH  - Cell Membrane/physiology
MH  - Cells, Cultured
MH  - Electric Stimulation
MH  - Humans
MH  - Immune Sera
MH  - In Vitro Techniques
MH  - Kv1.3 Potassium Channel
MH  - Membrane Potentials/drug effects/physiology
MH  - Molecular Sequence Data
MH  - Neurons/drug effects/*physiology
MH  - Olfaction Disorders/physiopathology
MH  - Olfactory Bulb/physiology
MH  - Olfactory Pathways/*physiology
MH  - Potassium Channels/drug effects/*physiology
MH  - *Potassium Channels, Voltage-Gated
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, trkB/drug effects/*physiology
MH  - Receptors, Nerve Growth Factor/drug effects/physiology
MH  - Recombinant Proteins/pharmacology
MH  - Smell
MH  - Time Factors
PMC - PMC2290412
EDAT- 2002/07/18 10:00
MHDA- 2003/02/11 04:00
PMCR- 2003/07/15
CRDT- 2002/07/18 10:00
PHST- 2002/07/18 10:00 [pubmed]
PHST- 2003/02/11 04:00 [medline]
PHST- 2002/07/18 10:00 [entrez]
PHST- 2003/07/15 00:00 [pmc-release]
AID - PHY_17376 [pii]
AID - 10.1113/jphysiol.2002.017376 [doi]
PST - ppublish
SO  - J Physiol. 2002 Jul 15;542(Pt 2):413-29. doi: 10.1113/jphysiol.2002.017376.