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Publication : Inactivation of sodium channel Scn8A (Na-sub(v)1.6) in Purkinje neurons impairs learning in Morris water maze and delay but not trace eyeblink classical conditioning.

First Author  Woodruff-Pak DS Year  2006
Journal  Behav Neurosci Volume  120
Issue  2 Pages  229-40
PubMed ID  16719687 Mgi Jnum  J:264802
Mgi Id  MGI:6198877 Doi  10.1037/0735-7044.120.2.229
Citation  Woodruff-Pak DS, et al. (2006) Inactivation of sodium channel Scn8A (Na-sub(v)1.6) in Purkinje neurons impairs learning in Morris water maze and delay but not trace eyeblink classical conditioning. Behav Neurosci 120(2):229-40
abstractText  To examine the isolated effects of altered currents in cerebellar Purkinje neurons, the authors used Scn8a-super(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.
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