PMID- 23840662
OWN - NLM
STAT- MEDLINE
DCOM- 20171006
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 6
DP  - 2013
TI  - BDNF Depresses Excitability of Parvalbumin-Positive Interneurons through an 
      M-Like Current in Rat Dentate Gyrus.
PG  - e67318
LID - 10.1371/journal.pone.0067318 [doi]
LID - e67318
AB  - In addition to their classical roles in neuronal growth, survival and 
      differentiation, neurotrophins are also rapid regulators of excitability, 
      synaptic transmission and activity-dependent synaptic plasticity. We have 
      recently shown that mature BDNF (Brain Derived Neurotrophic Factor), but not 
      proBDNF, modulates the excitability of interneurons in dentate gyrus within 
      minutes. Here, we used brain slice patch-clamp recordings to study the mechanisms 
      through which BDNF modulates the firing of interneurons in rat dentate gyrus by 
      binding to TrkB receptors. Bath application of BDNF (15 ng/ml) under 
      current-clamp decreased the firing frequency (by 80%) and input resistance, 
      blocking the delayed firing observed at near-threshold voltage ranges, with no 
      changes in resting membrane potential or action potential waveform. Using TEA 
      (tetraethylammonium), or XE991(a Kv7/KCNQ channel antagonist), the effect of BDNF 
      was abolished, whereas application of retigabine (a Kv7/KCNQ channel opener) 
      mimicked the effect of BDNF, suggesting that the M-current could be implicated in 
      the modulation of the firing. In voltage-clamp experiments, BDNF increased the 
      M-like current amplitude with no change in holding current. This effect was again 
      blocked by XE991 and mimicked by retigabine, the latter accompanied with a change 
      in holding current. In agreement with the electrophysiology, parvalbumin-positive 
      interneurons co-expressed TrkB receptors and Kv7.2/KCNQ2 channels. In conclusion, 
      BDNF depresses the excitability of interneurons by activating an M-like current 
      and possibly blocking Kv1 channels, thereby controlling interneuron resting 
      membrane potential and excitability.
FAU - Nieto-Gonzalez, Jose Luis
AU  - Nieto-Gonzalez JL
AD  - Department of Biomedicine, Aarhus University, Aarhus C, Denmark.
FAU - Jensen, Kimmo
AU  - Jensen K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130619
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Parvalbumins)
RN  - 0 (Potassium Channel Blockers)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - EC 3.6.1.- (GTP-Binding Proteins)
SB  - IM
MH  - *Action Potentials
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*physiology
MH  - Dentate Gyrus/cytology/drug effects/*physiology
MH  - Female
MH  - GTP-Binding Proteins/physiology
MH  - In Vitro Techniques
MH  - Interneurons/drug effects/metabolism/*physiology
MH  - Male
MH  - Parvalbumins/metabolism
MH  - Patch-Clamp Techniques
MH  - Potassium Channel Blockers/pharmacology
MH  - Rats
MH  - Rats, Wistar
MH  - Type C Phospholipases/physiology
PMC - PMC3686736
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/07/11 06:00
MHDA- 2013/07/11 06:01
PMCR- 2013/06/19
CRDT- 2013/07/11 06:00
PHST- 2013/02/05 00:00 [received]
PHST- 2013/05/16 00:00 [accepted]
PHST- 2013/07/11 06:00 [entrez]
PHST- 2013/07/11 06:00 [pubmed]
PHST- 2013/07/11 06:01 [medline]
PHST- 2013/06/19 00:00 [pmc-release]
AID - PONE-D-13-05506 [pii]
AID - 10.1371/journal.pone.0067318 [doi]
PST - epublish
SO  - PLoS One. 2013 Jun 19;8(6):e67318. doi: 10.1371/journal.pone.0067318. Print 2013.