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PDE11A negatively regulates lithium responsivity.

G Pathak1, M J Agostino2, K Bishara1

  • 1Department of Pharmacology, Physiology & Neuroscience, University of South Carolina School of Medicine, Columbia, SC, USA.

Molecular Psychiatry
|September 21, 2016
PubMed
Summary
This summary is machine-generated.

Decreasing Phosphodiesterase 11A (PDE11A) expression enhances lithium responsivity in mice, suggesting a role in bipolar disorder treatment. Lower PDE11A levels correlate with better lithium response and may involve interleukin-6 pathways.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Lithium is a key treatment for bipolar disorder, but patient response varies.
  • Genetic factors, including Phosphodiesterase 11A (PDE11A), are linked to lithium responsivity.
  • PDE11A, an enzyme in the hippocampus, regulates cyclic AMP and cyclic GMP levels.

Purpose of the Study:

  • To investigate if reduced PDE11A expression is sufficient to improve lithium responsivity in mice.
  • To explore the functional relevance of PDE11A genetic variations in lithium response.

Main Methods:

  • Compared PDE11A4 protein expression and compartmentalization in hippocampus of lithium-responsive and unresponsive mouse strains.
  • Analyzed PDE11A4 expression in Pde11a knockout (KO) versus wild-type (WT) mice.
  • Assessed lithium responsivity in KO mice using antidepressant- and anti-manic predictive assays.

Main Results:

  • Lithium-responsive mice exhibited lower PDE11A4 protein expression and altered compartmentalization in the hippocampus.
  • A specific single-nucleotide polymorphism (SNP) in PDE11A4 affects homodimerization and membrane localization.
  • Pde11a KO mice showed significantly greater lithium responsivity compared to WT littermates.
  • Reduced PDE11A4 expression correlated with increased interleukin-6 (IL-6) expression, suggesting a pro-inflammatory link.

Conclusions:

  • Decreased PDE11A4 expression positively regulates lithium responsivity in mice.
  • PDE11A4 negatively impacts lithium response, and its genetic variations may be functionally relevant in bipolar disorder patients.
  • Targeting PDE11A could be a potential therapeutic strategy for bipolar disorder.