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
| Autor: | John T. Green, Diana S. Woodruff-Pak, Stephen I. Levin, Miriam H. Meisler |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Male
Eyelid Conditioning Cerebellum Purkinje cell Morris water navigation task Hippocampus Nerve Tissue Proteins Biology Sodium Channels Behavioral Neuroscience Mice Purkinje Cells medicine Reaction Time Animals Maze Learning Swimming Mice Knockout Analysis of Variance Behavior Animal Learning Disabilities Classical conditioning Conditioning Eyelid medicine.anatomical_structure Eyeblink conditioning NAV1.6 Voltage-Gated Sodium Channel Cerebellar cortex Neuroscience |
| Zdroj: | Behavioral neuroscience. 120(2) |
| ISSN: | 0735-7044 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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