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Adult neurogenesis - Scholarpedia


adult neurogenesis

2/1/ · A milestone is marked in our understanding of the brain with the recent acceptance, contrary to early dogma, that the adult nervous system can generate new rosnconsnis.ml by: Learn what research says about how adult humans grow new brain cells in a process called neurogenesis. 5/26/ · Adult neurogenesis, a process of generating functional neurons from adult neural precursors, occurs throughout life in restricted brain regions in rosnconsnis.ml by:

Adult neurogenesis - Wikipedia

Adult neurogenesis is the process by which neurons are generated from neural stem cells in the adult. This process is different from the embryonic development of neurogenesis. In most mammals, new neurons are continually born throughout adulthood in two regions of the brain: [3].

More attention has been given to neurogenesis in the dentate gyrus than in the striatum. In rodentsmany of the newborn dentate gyrus neurons die shortly after they are born, [4] but a number of them become functionally integrated into the surrounding brain tissue, adult neurogenesis.

Adult neurogenesis is reported to play a adult neurogenesis in learning and memory, emotion, stress, depression, response to injury, and other conditions. Neural stem cells NSCs are the self-renewing, multipotent cells that generate the main phenotypes of the nervous system. Emerging evidence suggests that neural microvascular pericytes, under instruction from resident glial cells, are adult neurogenesis into interneurons and enrich local neuronal microcircuits.

Planarian are one of the earliest model organisms used to study regeneration with Pallas as the forefather of planarian studies. Planarian are a classical invertebrate model that in recent decades have been used to examine neurogenesis, adult neurogenesis. The central nervous system of a planarian is simple, adult neurogenesis, though fully formed with two lobes located in the head and two ventral nerve cords. This model reproduces asexually producing a complete and fully functioning nervous system after division allowing for consistent examination of neurogenesis.

The axolotl is less commonly used than other vertebrates, adult neurogenesis, but is still a classical model for examining adult neurogenesis and neurogenesis. Though the axolotl has made its place in biomedical research in terms of limb regeneration, [16] [17] the model organism has displayed a robust ability to generate new neurons following damage.

Zebrafish have long been a classical developmental model due to their transparency during organogenesis and have been utilized heavily in early development neurogenesis.

The zebrafish displays a strong neurogenerative capacity capable of regenerating a variety of tissues and complete neuronal diversity with the exception of astrocytesas they have yet to be identified within the zebrafish brain with continued neurogenesis through the life span.

In recent decades the model has solidified its role in adult regeneration and neurogenesis following damage. The zebrafish is a rapidly developing organism that is relatively inexpensive to maintain, while providing the field ease of genetic manipulation and a complex nervous system, adult neurogenesis.

Though avians have been used primarily to study adult neurogenesis embryonic development, in recent decades the adult neurogenesis chick has played a critical role in the examination of neurogenesis and regeneration as the young adult neurogenesis is capable of neuronal-turnover at a young age, but loses the neurogenerative capacity into adulthood, adult neurogenesis.

Rodents, mice and rats, have been the most prominent model organism since the discovery of modern neurons by Santiago Ramon y Cajal. Rodents have a very similar architecture and a complex nervous system with very little regenerative capacity similar to that found in humans.

For that reason, rodents have been heavily used in pre-clinical testing. Rodents adult neurogenesis a wide range of neural circuits responsible for complex behaviors making them ideal for studies of dendritic pruning and axonal shearing. The creation of new functional brain cells can be measured in several ways, [28] summarized in the following sections. Labelled DNA can trace dividing cell's lineage, and determine the location of its daughter cells.

A nucleic acid analog is inserted into the genome of a neuron-generating cell such as a glial cell or neural stem cell. DNA labeling can be used in conjunction with neuronal lineage markers to determine the fate of new functional brain cells.

First, adult neurogenesis, incorporated labeled nucleotides are used to detect the populations of newly divided daughter cells. Adult neurogenesis cell types are then determined with unique differences in their expression of proteinswhich can be used as antigens in an immunoassay.

Ki67 is the most commonly used antigen to detect cell proliferation. Some antigens can be used to measure specific stem cell stages. For example, adult neurogenesis, stem cells requires the sox2 gene to maintain pluripotency and is used to detect enduring concentrations of stem cells in CNS tissue. The protein nestin is an intermediate filamentwhich is essential for the radial growth of axonsand is therefore used to detect the formation of new synapses, adult neurogenesis.

Some genetic tracing studies utilize cre-lox recombination to bind a promoter to a reporter genesuch as lacZ or GFP gene, adult neurogenesis. It has adult neurogenesis become more common adult neurogenesis use recombinant viruses to insert the genetic information encoding specific markers usually protein adult neurogenesis such as GFP that are only expressed in cells of a certain kind.

The marker gene is inserted downstream of a promoter adult neurogenesis, leading to transcription adult neurogenesis that marker only in cells containing the transcription factor s that bind to that promoter. For example, a recombinant plasmid may contain the promoter for doublecortina protein expressed predominantly by neuronsadult neurogenesis, upstream of a sequence adult neurogenesis for GFPthereby making infected cells fluoresce green upon exposure to light in the blue to ultraviolet range [33] while adult neurogenesis non doublecortin expressing cells unaffected, even if they contain the plasmid, adult neurogenesis.

Many cells will contain multiple copies of the plasmid and the fluorphore itself, allowing the fluorescent properties to be transferred along an infected cell's lineage. By labeling a cell that gives rise to neurons, such as a neural stem cells or neural precursor cells, one can track the creation, proliferation, and even migration of newly created neurons. The insertion of genetic material via a viral vector tends to be sporadic and infrequent relative to the total number of cells in a given region of tissuemaking quantification of cell division inaccurate.

However, the above method can provide highly accurate data with respect to when a cell was born as well as full cellular morphologies. Many studies analyzing the role of adult neurogenesis utilize a method of inhibiting cell proliferation in specific brain regions, mimicking an inhibition of neurogenesis, to observe the effects on behavior. Pharmacological inhibition is widely used in various studies, as it provides many benefits. It is generally inexpensive as compared to other methods, such as irradiation, can be used on various species, and does not require any invasive procedures or surgeries for the subjects.

However, it does pose certain challenges, adult neurogenesis, as these inhibitors can't be used to inhibit proliferation in specific regions, thus leading to nonspecific effects adult neurogenesis other systems being affected. To avoid these effects, adult neurogenesis, more work must be done to determine optimal doses in order to minimize the effects on systems unrelated to neurogenesis.

A common pharmacological inhibitor for adult neurogenesis is methylazoxymethanol acetate MAMadult neurogenesis, a chemotherapeutic agent. Other cell division inhibitors adult neurogenesis used in studies are cytarabine and temozolomide. Another method used to study the effects of adult neurogenesis is using pharmacogenetic models. These models provide different benefits from the pharmacological route, as it allows for more specificity by targeting specific precursors to neurogenesis and specific stem cell promoters.

It also allows for temporal specificity with the interaction of certain drugs. This is beneficial in looking specifically at neurogenesis in adulthood, after normal development of other regions in the brain. The herpes simplex virus thymidine kinase HSV-TK has been used in studies in conjunction with antiviral drugs to inhibit adult neurogenesis, adult neurogenesis. It works by targeting stem cells using glial fibrillary acidic proteins and nestin expression.

These targeted stem cells undergo cell death instead of cell proliferation when exposed to antiviral drugs, adult neurogenesis. Cre protein is also commonly used in targeting stem adult neurogenesis that will undergo gene changes upon treatment with tamoxifen. Irradiation is a method that allows for very specific inhibition of adult neurogenesis, adult neurogenesis.

It can be targeted to the brain to avoid affecting other systems and having nonspecific effects. It can even be used to target specific brain regions, adult neurogenesis, which is important in determining how adult neurogenesis in different areas of the brain affects behavior. However, irradiation is more expensive than the other methods and also requires large equipment with trained individuals. Many studies have observed how inhibiting adult neurogenesis in other mammals, such as rats and mice, adult neurogenesis, affect their behavior.

Impaired fear conditioning has been seen in studies involving rats with a lack of adult neurogenesis in the hippocampus. The changes in adult neurogenesis and memory seen in the adult neurogenesis mentioned previously are thought to be related to the role of adult neurogenesis in regulating pattern separation.

This impairment in pattern separation could explain the impairments seen in other learning and memory tasks, adult neurogenesis. A decreased ability in reducing interference could lead to greater difficulty in forming and retaining new memories. Studies show that rats adult neurogenesis inhibited adult neurogenesis demonstrate difficulty in differentiating and learning contextualized fear conditioning. Behavioral inhibition is important in rats and other animals in halting whatever they are currently doing in order to reassess a situation in response to a threat or anything else that may require their attention.

Rats with lesioned hippocampi show less behavioral inhibition when exposed to threats, such as cat odor. This impairment in behavioral inhibition also ties into the process of learning and memory, as repressing wrong answers or behaviors requires the ability to inhibit that response.

The functional relevance of adult neurogenesis is uncertain, [47] but there is some evidence that hippocampal adult neurogenesis is important for learning and memory. Some studies suggest that decreased hippocampal neurogenesis can lead to development of Alzheimer's disease AD. Levels of adult neurogenesis in the brain decline in old age and Alzheimer's disease.

Studies suggest that people with schizophrenia adult neurogenesis a reduced hippocampus volume, which is believed to be caused by a reduction of adult neurogenesis. Correspondingly, this phenomenon might be the underlying cause of many of the symptoms of the disease. However, further research must be done in order to clearly demonstrate this relationship. Research indicates that adult hippocampal neurogenesis is inversely related to major depressive disorder MDD.

It has been theorized that decreased hippocampal neurogenesis in individuals with major depressive disorder may be related to the high levels of stress hormones called glucocorticoidswhich are also associated with the disorder.

The hippocampus instructs the hypothalamic-pituitary-adrenal axis to produce fewer glucocorticoids when glucocorticoid levels are high. A malfunctioning hippocampus, therefore, might explain the chronically high glucocorticoid levels in individuals with major depressive disorder, adult neurogenesis. However, some studies have indicated that hippocampal neurogenesis is not lower in individuals with major depressive disorder and that blood glucocorticoid levels do not change when hippocampal neurogenesis changes, so the associations are adult neurogenesis uncertain.

Many now believe stress to be the most significant factor for the onset of depressionaside from genetics. As discussed above, hippocampal cells are sensitive to stress which can lead to decreased neurogenesis.

This area is being considered more frequently when examining the causes and treatments of depression. Studies have shown that removing the adrenal gland in rats caused increased neurogenesis in the dentate gyrus. In a normal brain, an increase in serotonin causes suppression of the corticotropin-releasing hormone CRH through connection to the hippocampus.

It directly acts on the paraventricular nucleus to decrease CRH release and down regulate norepinephrine functioning in the locus coeruleus. This allows for the production of more brain cells, in particular at the 5-HT1a receptor in the dentate gyrus of the hippocampus which has been shown to improve symptoms of depression.

It normally takes neurons approximately three to six weeks to mature, [69] which is approximately the same amount of time it takes for SSRIs to take effect, adult neurogenesis. This correlation strengthens the hypothesis that SSRIs act through neurogenesis to decrease the symptoms adult neurogenesis depression.

Some neuroscientists have expressed skepticism that neurogenesis is functionally significant, given that a tiny number of nascent neurons are actually integrated into existing neural circuitry.

However, a recent study used the irradiation of nascent hippocampal neurons adult neurogenesis non-human primates NHP to demonstrate that neurogenesis is required for antidepressant efficacy.

Adult-born neurons appear to have a role in the regulation of stress. Under chronic stress conditions, the elevation of newborn neurons by antidepressants improves the hippocampal-dependent control on the stress response; without newborn neurons, antidepressants are unable to restore the regulation of the stress response and recovery becomes impossible.

Some studies have hypothesized adult neurogenesis learning and memory are linked to depression, and that neurogenesis may promote neuroplasticity. One study proposes that mood may be regulated, at a base level, by plasticity, and thus not chemistry.

Accordingly, the effects of antidepressant treatment would only be secondary to change in plasticity. One study has linked lack of sleep to a reduction in rodent hippocampal neurogenesis. The proposed mechanism for the observed decrease was increased levels of glucocorticoids.

It was shown that two weeks of sleep deprivation acted as a neurogenesis-inhibitor, which was reversed adult neurogenesis return of normal sleep and even shifted to a temporary increase in normal cell proliferation.


The Science Behind How New Brain Cells Are Generated


adult neurogenesis


Learn what research says about how adult humans grow new brain cells in a process called neurogenesis. 5/26/ · Adult neurogenesis, a process of generating functional neurons from adult neural precursors, occurs throughout life in restricted brain regions in rosnconsnis.ml by: 2/1/ · A milestone is marked in our understanding of the brain with the recent acceptance, contrary to early dogma, that the adult nervous system can generate new rosnconsnis.ml by: