|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5557966||1403192||2018||5 صفحه PDF||سفارش دهید||دانلود کنید|
- Cyclin D2 knock out (KO) mice are profoundly impaired in adult brain neurogenesis.
- Cyclin D2 KO mice do not show major deficits in hippocampal learning and memory.
- Antidepressant response and epileptogenesis are not disrupted in cyclin D2 KO mice.
- They show minor changes e.g. in species-typical behaviors and alcohol consumption.
- These can be due to reduced hippocampal size and other developmental impairments.
The discovery of new neurons being produced in the brains of adult mammals (adult brain neurogenesis) began a quest to determine the function(s) of these cells. Major hypotheses in the field have assumed that these neurons play pivotal role, in particular, in learning and memory phenomena, mood control, and epileptogenesis. In our studies summarized herein, we used cyclin D2 knockout (KO) mice, as we have shown that cyclin D2 is the key factor in adult brain neurogenesis and thus its lack produces profound impairment of the process. On the other hand, developmental neurogenesis responsible for the brain formation depends only slightly on cyclin D2, as the mutants display minor structural abnormalities, such as smaller hippocampus and more severe disturbances in the structure of the olfactory bulbs. Surprisingly, the studies have revealed that cyclin D2 KO mice did not show major deficits in several behavioral paradigms assessing hippocampal learning and memory. Furthermore, missing adult brain neurogenesis affected neither action of antidepressants, nor epileptogenesis. On the other hand, minor deficits observed in cyclin D2 KO mice in fine tuning of cognitive functions, species-typical behaviors and alcohol consumption might be explained by a reduced hippocampal size and/or other developmentally driven brain impairments observed in these mutant mice. In aggregate, surprisingly, missing almost entirely adult brain neurogenesis produces only very limited behavioral phenotype that could be attributed to the consequences of the development-dependent minor brain abnormalities.
Journal: Progress in Neuro-Psychopharmacology and Biological Psychiatry - Volume 80, Part A, 3 January 2018, Pages 63-67