PMID- 26594153
OWN - NLM
STAT- MEDLINE
DCOM- 20160621
LR  - 20181113
IS  - 1662-5110 (Electronic)
IS  - 1662-5110 (Linking)
VI  - 9
DP  - 2015
TI  - High-Speed imaging reveals opposing effects of chronic stress and antidepressants 
      on neuronal activity propagation through the hippocampal trisynaptic circuit.
PG  - 70
LID - 10.3389/fncir.2015.00070 [doi]
LID - 70
AB  - Antidepressants (ADs) are used as first-line treatment for most stress-related 
      psychiatric disorders. The alterations in brain circuit dynamics that can arise 
      from stress exposure and underlie therapeutic actions of ADs remain, however, 
      poorly understood. Here, enabled by a recently developed voltage-sensitive dye 
      imaging (VSDI) assay in mouse brain slices, we examined the impact of chronic 
      stress and concentration-dependent effects of eight clinically used ADs 
      (belonging to different chemical/functional classes) on evoked neuronal activity 
      propagations through the hippocampal trisynaptic circuitry (HTC: perforant path --> 
      dentate gyrus (DG) --> area CA3 --> area CA1). Exposure of mice to chronic social 
      defeat stress led to markedly weakened activity propagations ("HTC-Waves"). In 
      contrast, at concentrations in the low micromolar range, all ADs, which were bath 
      applied to slices, caused an amplification of HTC-Waves in CA regions (invariably 
      in area CA1). The fast-acting "antidepressant" ketamine, the mood stabilizer 
      lithium, and brain-derived neurotrophic factor (BDNF) exerted comparable 
      enhancing effects, whereas the antipsychotic haloperidol and the anxiolytic 
      diazepam attenuated HTC-Waves. Collectively, we provide direct experimental 
      evidence that chronic stress can depress neuronal signal flow through the HTC and 
      demonstrate shared opposing effects of ADs. Thus, our study points to a 
      circuit-level mechanism of ADs to counteract stress-induced impairment of 
      hippocampal network function. However, the observed effects of ADs are impossible 
      to depend on enhanced neurogenesis.
FAU - Stepan, Jens
AU  - Stepan J
AD  - Max Planck Institute of Psychiatry Munich, Germany ; Department Stress 
      Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry Munich, 
      Germany ; Scientific Core Unit "Electrophysiology and Neuronal Network Dynamics", 
      Max Planck Institute of Psychiatry Munich, Germany ; Clinical Department, Max 
      Planck Institute of Psychiatry Munich, Germany.
FAU - Hladky, Florian
AU  - Hladky F
AD  - Max Planck Institute of Psychiatry Munich, Germany ; Department Stress 
      Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry Munich, 
      Germany ; Scientific Core Unit "Electrophysiology and Neuronal Network Dynamics", 
      Max Planck Institute of Psychiatry Munich, Germany.
FAU - Uribe, Andres
AU  - Uribe A
AD  - Max Planck Institute of Psychiatry Munich, Germany ; Department Stress 
      Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry Munich, 
      Germany ; Research Group "Stress Resilience", Max Planck Institute of Psychiatry 
      Munich, Germany.
FAU - Holsboer, Florian
AU  - Holsboer F
AD  - Max Planck Institute of Psychiatry Munich, Germany ; HMNC GmbH Munich, Germany.
FAU - Schmidt, Mathias V
AU  - Schmidt MV
AD  - Max Planck Institute of Psychiatry Munich, Germany ; Department Stress 
      Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry Munich, 
      Germany ; Research Group "Stress Resilience", Max Planck Institute of Psychiatry 
      Munich, Germany.
FAU - Eder, Matthias
AU  - Eder M
AD  - Max Planck Institute of Psychiatry Munich, Germany ; Department Stress 
      Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry Munich, 
      Germany ; Scientific Core Unit "Electrophysiology and Neuronal Network Dynamics", 
      Max Planck Institute of Psychiatry Munich, Germany.
LA  - eng
PT  - Journal Article
DEP - 20151106
PL  - Switzerland
TA  - Front Neural Circuits
JT  - Frontiers in neural circuits
JID - 101477940
RN  - 0 (ANA 12 compound)
RN  - 0 (Antidepressive Agents)
RN  - 0 (Azepines)
RN  - 0 (Benzamides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Central Nervous System Agents)
RN  - 0 (Lithium Compounds)
RN  - 01K63SUP8D (Fluoxetine)
RN  - 690G0D6V8H (Ketamine)
RN  - J6292F8L3D (Haloperidol)
RN  - Q3JTX2Q7TU (Diazepam)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents/*pharmacology
MH  - Azepines/pharmacology
MH  - Benzamides/pharmacology
MH  - Brain-Derived Neurotrophic Factor/pharmacology
MH  - Central Nervous System Agents/pharmacology
MH  - Chronic Disease
MH  - Diazepam/pharmacology
MH  - Disease Models, Animal
MH  - Dominance-Subordination
MH  - Fluoxetine/pharmacology
MH  - Haloperidol/pharmacology
MH  - Hippocampus/*drug effects/*physiopathology
MH  - Ketamine/pharmacology
MH  - Lithium Compounds/pharmacology
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Neural Pathways/drug effects/physiopathology
MH  - Stress, Psychological/*drug therapy/*physiopathology
MH  - Tissue Culture Techniques
MH  - Voltage-Sensitive Dye Imaging
PMC - PMC4635222
OTO - NOTNLM
OT  - activity propagation
OT  - antidepressants
OT  - hippocampus
OT  - imaging
OT  - ketamine
OT  - stress
OT  - trisynaptic circuit
OT  - voltage-sensitive dye
EDAT- 2015/11/26 06:00
MHDA- 2016/06/22 06:00
PMCR- 2015/01/01
CRDT- 2015/11/24 06:00
PHST- 2015/08/22 00:00 [received]
PHST- 2015/10/22 00:00 [accepted]
PHST- 2015/11/24 06:00 [entrez]
PHST- 2015/11/26 06:00 [pubmed]
PHST- 2016/06/22 06:00 [medline]
PHST- 2015/01/01 00:00 [pmc-release]
AID - 10.3389/fncir.2015.00070 [doi]
PST - epublish
SO  - Front Neural Circuits. 2015 Nov 6;9:70. doi: 10.3389/fncir.2015.00070. 
      eCollection 2015.