Satb2 ablation decreases PTZ-induced seizure susceptibility and pyramidal neuronal excitability

Brain Res. 2018 Sep 15:1695:102-107. doi: 10.1016/j.brainres.2018.05.006. Epub 2018 May 8.

Abstract

Special AT-rich sequence-binding protein 2 (Satb2) is a transcriptional regulator and people with SATB2 mutation or duplication could display epilepsy. However, whether Satb2 is related with epilepsy and its mechanisms are largely unexplored. Here we found that the expression of Satb2 was decreased following the neuronal hyperactivities. Ablation of Satb2 in mice would decrease incidence and stage of seizure induced by intraperitoneal injection of pentylenetetrazol (PTZ). At cellular levels, we found pyramidal neuronal excitability and excitatory synaptic inputs in CA1 were decreased in Satb2 mutant mice. Taking together, we proved that deletion of Satb2 in mice increased PTZ seizure threshold probably by modulating neuronal excitability.

Keywords: CaMKIIα; Epilepsy; Neuronal excitability; PTZ; Pyramidal neurons; Satb2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Epilepsy / metabolism
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Matrix Attachment Region Binding Proteins / drug effects*
  • Matrix Attachment Region Binding Proteins / metabolism
  • Mice, Transgenic
  • Pentylenetetrazole / pharmacology*
  • Pyramidal Cells / drug effects
  • Pyramidal Cells / metabolism*
  • Seizures / chemically induced
  • Seizures / metabolism*
  • Transcription Factors / drug effects*
  • Transcription Factors / metabolism

Substances

  • Matrix Attachment Region Binding Proteins
  • SATB2 protein, human
  • Transcription Factors
  • Pentylenetetrazole