It was once believed that human keep mantain the same number of neurons in the brain that we are born with and that we lose the capacity to produce new neurons. This once unshakable dogma of neurobiology has been shaken to the core. However, there has been a number of groundbreaking studies over the past ten years suggesting that new neurons can be produced throughout all stages of life and this phenomenon is called neurogenesis.
On the other hand, are these neurons required by the brain for any specific function? Are they just simply filler cells in the brain or do they really serve a purpose?
One particular scientific study may had solved this question. By using a highly specialized mouse model to study the role of new memory neurons in the adult mice, a group of scientists from the Department of Physiology at the University of Toronto published a study at the Journal of Neuroscience a few days ago. They showed that new neurons formed during adulthood are needed for the formation of new memories, specifically with memories associated with fear and spatial memory. Throughout our lifetime, new neurons are constantly being formed in the subgranular zone of the hippocampus and these new neurons migrate towards the edge of the hippocampus and the cortex to form novel synaptic connections.
To specifically determine the role of new hippocampal neurons formed in the young adult mouse, the hippocampal progenitor neurons artificially expressed a receptor for diphtheria toxin in order to target for destruction by treating adult mice with diphtheria toxin. This artificially generated mouse model gave the researchers the necessary tools to specifically determine the role of hippocampal progenitor neurons when targeted for destruction.
Overall, the researchers corroborated that progrenitor cells in neurogenic regions of the hippocampus expressed CRE and the dyptheria toxin receptor while other neuronal populations did not. More importantly, only these neurons and not other neuronal populations were specifically killed by diphtheria toxin while only produce a mild and temporary brain inflammation near the hippocampus were other neuronal populations are located.
Next, the scientists wanted to whether any effects on memory and cognitive skills are seen in mice that lacked hippocampal progenitor cells. Indeed, scientists found that mice that lacked hippocampal progenitor cells after training did not respond favorably to contextual fear memory compared to normal mice. Moreover, normal that were preshocked at their paws or feet froze considerably longer compared to diphtheria toxin treated mice suggesting that mice lacking hippocampal progenitor neurons as adults failed to learn and associate fear with a familiar context or scenario. The scientists did not found any significant effects on the general health of mice that lacked hippocampal progenitor cells compared to normal mice. Moreover, the physical strength and endurance of mice were the same regardless of whether hippocampal progenitor cells were destroyed or remained intact.
Interestingly, mice responded and froze similary regardless of whether neurons were destroyed prior to training suggesting that new neurons are required for long term but not short term learning of fear conditioning. More importantly, scientists found that adult hippocampal neurons are also required for consolidating spatial (space and time) memory. Mice whose hippocampal neurons were ablated after undergoing training in a water mouse had a much harder time finding the exit or other visual cues compared to normal mice strongly suggesting that new adult hippocampus neurons are needed for not only spatial memory but for visual discrimination.
Why do we care about this study?
Patients affected with Alzheimer's disease suffer from brain atropy (shrinkage) over time. The primary brain area affected by Alzheimer's disease is the hippocampus and the destruction of more than 90% of this important brain region leads to severe memory loss, inability to recognize objects and speech impairment. More importantly, patients may end up with dementia and a complete lack of independence.
The fact that adults do produce new neurons with the sole purpose of consolidating new memories as shown in this study suggests that promoting neurogenesis in the hippocampus may be beneficial for Alzheimer's patients. Indeed, tryciclic antidepressants and serotonin receptor reuptake inhibitors like Prozac may induce neurogenesis in normal and AD individuals. The role of antidepressants as potential AD therapy has been reviewed in another Examiner article.
Moreover, treating patients with different neuronal prosurvival factors may not only delay cell death of the neurons but may induce neurogenesis to replace the dead neurons. This study offers hope in the fact that the brain adults do "produce" new neurons. Hence, this dogma of biology that postmitotic cells (like neurons) cannot reproduce has been debunked at least for right now.
Interested in donating for a good cause while promoting science education? Help develop a neuroscience lab manual for middle school, high school and college students and get directly involved in the project.. To get started click on the following link from RocketHub (Crowdfunding website) below:
http://www.rockethub.com/projects/4264-cool-student-manual-of-neuroscience-projects
Continue reading on Examiner.com Prenatal stress changes genes in the brain and cause mood disorders in the adult - Pittsburgh Medical Technology | Examiner.com http://www.examiner.com/medical-technology-in-pittsburgh/prenatal-stress-changes-genes-the-brain-and-cause-mood-disorders-the-adult#ixzz1ex7gt1G1
References:
Arruda-Carvhalo et al., 2011, Postraining ablation of adult-generated neurons degrades previously acquired memories. The Journal of Neuroscience. 31(42): 15113-15127.
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