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Lithium reverses behavioral and axonal transport-related changes associated with ANK3 bipolar disorder gene disruption

Overview of attention for article published in European Neuropsychopharmacology, January 2017
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Title
Lithium reverses behavioral and axonal transport-related changes associated with ANK3 bipolar disorder gene disruption
Published in
European Neuropsychopharmacology, January 2017
DOI 10.1016/j.euroneuro.2017.01.001
Pubmed ID
Authors

Michael G. Gottschalk, Melanie P. Leussis, Tillmann Ruland, Klaudio Gjeluci, Tracey L. Petryshen, Sabine Bahn

Abstract

Ankyrin 3 (ANK3) has been implicated as a genetic risk factor for bipolar disorder (BD), however the resulting pathophysiological and treatment implications remain elusive. In a preclinical systems biological approach, we aimed to characterize the behavioral and proteomic effects of Ank3 haploinsufficiency and chronic mood-stabilizer treatment in mice. Psychiatric-related behavior was evaluated with the novelty-suppressed feeding (NSF) paradigm, elevated plus maze (EPM) and a passive avoidance task (PAT). Tandem mass spectrometry (MS(E)) was employed for hippocampal proteome profiling. A functional enrichment approach based on protein-protein interactions (PPIs) was performed to outline which biological processes in the hippocampus were affected by Ank3 haploinsufficiency and lithium treatment. Proteomic abundance changes as detected by MS(E) or highlighted by PPI network modelling were followed up by targeted selected reaction monitoring (SRM). Increased psychiatric-related behavior in Ank3+/- mice was ameliorated by lithium in all assessments (NSF, EPM, PAT). MS(E) followed by modular PPI clustering and functional annotation enrichment pointed towards kinesin-related axonal transport and glutamate signaling as mediators of Ank3+/- pathophysiology and lithium treatment. SRM validated this hypothesis and further confirmed abundance changes of ANK3 interaction partners. We propose that psychiatric-related behavior in Ank3+/- mice is connected to a disturbance of the kinesin cargo system, resulting in a dysfunction of neuronal ion channel and glutamate receptor transport. Lithium reverses this molecular signature, suggesting the promotion of anterograde kinesin transport as part of its mechanism of action in ameliorating Ank3-related psychiatric-related behavior.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 33 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 33 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 33%
Researcher 5 15%
Student > Bachelor 4 12%
Student > Master 4 12%
Professor 1 3%
Other 2 6%
Unknown 6 18%
Readers by discipline Count As %
Medicine and Dentistry 8 24%
Psychology 5 15%
Neuroscience 3 9%
Agricultural and Biological Sciences 3 9%
Biochemistry, Genetics and Molecular Biology 2 6%
Other 3 9%
Unknown 9 27%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 24 January 2017.
All research outputs
#22,759,452
of 25,374,647 outputs
Outputs from European Neuropsychopharmacology
#1,927
of 2,571 outputs
Outputs of similar age
#362,458
of 421,363 outputs
Outputs of similar age from European Neuropsychopharmacology
#37
of 43 outputs
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