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Anaplastic lymphoma kinase and leukocyte tyrosine kinase: functions and genetic interactions in learning, memory and adult neurogenesis
- Source :
- Pharmacology, biochemistry, and behavior. 100(3)
- Publication Year :
- 2011
-
Abstract
- Anaplastic Lymphoma Kinase (Alk) is a receptor tyrosine kinase expressed throughout the adult mammalian hippocampus. Recent studies in Drosophila and prior studies in Caenorhabditis elegans have implicated Alk signaling in learning and neurogenesis. We have studied the roles of Alk and the closely related receptor Leukocyte Tyrosine Kinase (Ltk) in learning, behavior and neurogenesis. In the hippocampus, both receptors are expressed throughout the dentate gyrus, CA1 and CA3. To assess the functional roles of Alk and Ltk in the mammalian brain, we analyzed phenotypes in Alk mutant, Ltk mutant and Alk/Ltk double-mutant mice compared to wild-type littermates. Similar to Drosophila, we found enhanced performance in spatial memory in Alk mutant mice. Also similar to Drosophila, we observed reduced neurogenesis associated with loss of Alk function. We also report genetic interactions between Alk and Ltk with respect to neurogenesis and behavioral measures such as activity, anxiety levels, and retention of spatial memory.
- Subjects :
- Male
Neurogenesis
Clinical Biochemistry
Receptor Protein-Tyrosine Kinases
Hippocampus
Spatial Behavior
Nerve Tissue Proteins
Anxiety
Motor Activity
Toxicology
Biochemistry
Receptor tyrosine kinase
Gene Expression Regulation, Enzymologic
Behavioral Neuroscience
Mice
Memory
hemic and lymphatic diseases
Anaplastic lymphoma kinase
Animals
Learning
Anaplastic Lymphoma Kinase
RNA, Messenger
Receptor
Biological Psychiatry
Pharmacology
Mice, Knockout
Neurons
biology
Behavior, Animal
Kinase
Dentate gyrus
Mice, Mutant Strains
Cell biology
Organ Specificity
Mutation
biology.protein
Neuroscience
Subjects
Details
- ISSN :
- 18735177
- Volume :
- 100
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- Pharmacology, biochemistry, and behavior
- Accession number :
- edsair.doi.dedup.....6c0cfe72770e861458dda97ef0215d37