Parvalbumin deficiency and GABAergic dysfunction in mice lacking PGC-1alpha

J Neurosci. 2010 May 26;30(21):7227-35. doi: 10.1523/JNEUROSCI.0698-10.2010.

Abstract

The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) is a master regulator of metabolism in peripheral tissues, and it has been proposed that PGC-1alpha plays a similar role in the brain. Recent evidence suggests that PGC-1alpha is concentrated in GABAergic interneurons, so we investigated whether male and female PGC-1alpha -/- mice exhibit abnormalities in interneuron gene expression and/or function. We found a striking reduction in the expression of the Ca(2+)-binding protein parvalbumin (PV), but not other GABAergic markers, throughout the cerebrum in PGC-1alpha +/- and -/- mice. Furthermore, PGC-1alpha overexpression in cell culture was sufficient to robustly induce PV expression. Consistent with a reduction in PV rather than a loss of PV-expressing interneurons, spontaneous synaptic inhibition was not altered in PGC-1alpha -/- mice. However, evoked synaptic responses displayed less paired-pulse depression and dramatic facilitation in response to repetitive stimulation at the gamma frequency. PV transcript expression was also significantly reduced in retina and heart of PGC-1alpha -/- animals, suggesting that PGC-1alpha is required for proper expression of PV in multiple tissues. Together these findings indicate that PGC-1alpha is a novel regulator of interneuron gene expression and function and a potential therapeutic target for neurological disorders associated with interneuron dysfunction.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Animals, Newborn
  • Biophysics
  • Cells, Cultured
  • DNA-Binding Proteins / metabolism
  • Electric Stimulation / methods
  • GTP Phosphohydrolases / metabolism
  • Gene Expression Regulation, Developmental / genetics*
  • Glutamate Decarboxylase / metabolism
  • Heart
  • High Mobility Group Proteins / metabolism
  • Hippocampus / cytology
  • Humans
  • Inhibitory Postsynaptic Potentials / drug effects
  • Inhibitory Postsynaptic Potentials / genetics
  • Interneurons / metabolism
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / genetics
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Myocardium / metabolism
  • Parvalbumins / deficiency*
  • Patch-Clamp Techniques / methods
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • RNA, Messenger / metabolism
  • Shaw Potassium Channels / metabolism
  • Trans-Activators / deficiency*
  • Trans-Activators / metabolism
  • Transcription Factors / metabolism
  • Transfection / methods
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • DNA-Binding Proteins
  • GLUT4 enhancer factor, mouse
  • High Mobility Group Proteins
  • Parvalbumins
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Ppargc1a protein, mouse
  • RNA, Messenger
  • Shaw Potassium Channels
  • Tfam protein, mouse
  • Trans-Activators
  • Transcription Factors
  • gamma-Aminobutyric Acid
  • GTP Phosphohydrolases
  • Mfn2 protein, mouse
  • Glutamate Decarboxylase
  • glutamate decarboxylase 1
  • glutamate decarboxylase 2