Inactivation of sodium channel Scn8A (NA v1.6) in Purkinje neurons impairs learning in morris water maze and delay but not trace eyeblink classical conditioning

Diana S. Woodruff-Pak*, John T. Green, Stephen I. Levin, Miriam H. Meisler

*Corresponding author for this work

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

To examine the isolated effects of altered currents in cerebellar Purkinje neurons, the authors used Scn8a flox/flox, Purkinje cell protein-CRE (Pcp-CRE) mice in which Exon 1 of Scn8a is deleted only in Purkinje neurons. Twenty male Purkinje Scn8a knockout (PKJ Scn8a KO) mice and 20 male littermates were tested on the Morris water maze (MWM). Subsequently, half were tested in 500-ms delay and half were tested in 500-ms trace eyeblink conditioning. PKJ Scn8a KO mice were impaired in delay conditioning and MWM but not in trace conditioning. These results provide additional support for the necessary participation of cerebellar cortex in normal acquisition of delay eyeblink conditioning and MWM and raise questions about the role, if any, of cerebellar cortex in trace eyeblink conditioning.

Original languageEnglish (US)
Pages (from-to)229-240
Number of pages12
JournalBehavioral Neuroscience
Volume120
Issue number2
DOIs
StatePublished - Apr 2006

Keywords

  • Cerebellar cortex
  • Cerebellum-dependent learning
  • Hippocampus-dependent learning
  • Interpositus nucleus
  • Place learning

ASJC Scopus subject areas

  • Behavioral Neuroscience

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