Behavioral alterations are associated with vitamin B12 deficiency in the transcobalamin receptor/CD320 KO mouse
| Autor: | Jeffrey M. Sequeira, Edward V. Quadros, Alejandro Ivan Hernandez, Juan Marcos Alarcon, Kaveri Arora |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Social Sciences lcsh:Medicine Hippocampus Mice chemistry.chemical_compound Learning and Memory Cognition 0302 clinical medicine Psychology lcsh:Science Mammals Cognitive Impairment Mice Knockout Neurons Multidisciplinary Animal Behavior Behavior Animal Cognitive Neurology Pyramidal Cells Anemia Megaloblastic anemia Long-term potentiation Animal Models Hematology Anxiety Disorders 3. Good health Nutritional deficiencies Vitamin B12 deficiency Experimental Organism Systems Neurology Vertebrates Knockout mouse Research Article medicine.medical_specialty Cognitive Neuroscience Mouse Models Receptors Cell Surface Biology Research and Analysis Methods Rodents Cobalamin vitamin D deficiency 03 medical and health sciences Model Organisms Transcobalamin Memory Internal medicine Avoidance Learning medicine Animals Learning Receptors AMPA Vitamin B12 Nutrition Medicine and health sciences Behavior Vitamin D deficiency lcsh:R Organisms Cognitive Psychology Biology and Life Sciences Vitamin B 12 Deficiency medicine.disease Mice Inbred C57BL 030104 developmental biology Endocrinology chemistry Amniotes Cognitive Science lcsh:Q Zoology 030217 neurology & neurosurgery Neuroscience |
| Zdroj: | PLoS ONE, Vol 12, Iss 5, p e0177156 (2017) PLoS ONE |
| ISSN: | 1932-6203 |
| DOI: | 10.1371/journal.pone.0177156 |
| Popis: | Vitamin B12 (cobalamin) deficiency is prevalent worldwide and causes megaloblastic anemia and neurologic deficits. While the anemia can be treated, the neurologic deficits can become refractive to treatment as the disease progresses. Therefore, timely intervention is critical for a favorable outcome. Moreover, the metabolic basis for the neuro-pathologic changes and the role of cobalamin deficiency in the pathology still remains unexplained. Using a transcobalamin receptor / CD320 knockout mouse that lacks the receptor for cellular uptake of transcobalamin bound cobalamin, we aimed to determine whether cobalamin deficiency in the central nervous system produced functional neurologic deficits in the mouse that would parallel those observed in humans. Our behavioral analyses indicate elevated anxiety and deficits in learning, memory and set-shifting of a spatial memory task in the KO mouse. Consistent with the behavioral deficits, the knockout mouse shows impaired expression of the early phase of hippocampal long-term potentiation along with reduced expression of GluR1, decreased brain mass and a significant reduction in the size of nuclei of the hippocampal pyramidal neurons. Our study suggests that the CD320 knockout mouse develops behavioral deficits associated with cobalamin deficiency and therefore could provide a model to understand the metabolic and genetic basis of neuro-pathologic changes due to cobalamin deficiency. |
| Databáze: | OpenAIRE |
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