Adult neurogenesis
Adult neurogenesis is the process in which neurons are generated from neural stem cells in the adult. This process differs from prenatal neurogenesis.
In most mammals, new neurons are born throughout adulthood in two regions of the brain:[3]
- The subgranular zone (SGZ), part of the dentate gyrus of the hippocampus,[4][5] where neural stem cells give birth to granule cells (implicated in memory formation and learning).[6]
- The
More attention has been given to the neurogenesis in the dentate gyrus than in the striatum. In rodents, many 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.[10][11][12] Adult neurogenesis in rodents is reported to play a role in learning and memory, emotion, stress, depression, response to injury, and other conditions.[13]
The numbers of neurons born in the human adult hippocampus remains controversial; some studies have reported that in adult humans about 700 new neurons are added in the hippocampus every day,[14] while more recent studies show that adult hippocampal neurogenesis does not exist in humans, or, if it does, it is at undetectable levels.[15] Recent evidence shows that adult neurogenesis is basically extinct in humans.[16] The experiments advocating for the presence of adult neurogenesis have focused on how dual antigen retrieval finds that DCX antibodies are staining many cells within the adult human dentate gyrus. This finding is not as clear though as supporters of adult neurogenesis suggest; the dentate gyrus cells stained with DCX have been shown to have a mature morphology, contrasting the idea that novel neurons are being generated within the adult brain.[17] The role of new neurons in human adult brain function thus remains unclear.
Mechanism
Adult neural stem cells
Neural
Lineage reprogramming (trans-differentiation)
Emerging evidence suggests that neural microvascular pericytes, under instruction from resident glial cells, are reprogrammed into interneurons and enrich local neuronal microcircuits.[18] This response is amplified by concomitant angiogenesis.
Model organisms of neurogenesis
Planarian
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. The central nervous system of a planarian is simple, 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.
Axolotl
The axolotl is less commonly used than other vertebrates, but is still a classical model for examining regeneration and neurogenesis. Though the axolotl has made its place in biomedical research in terms of limb regeneration,[19][20] the model organism has displayed a robust ability to generate new neurons following damage .[21][22] Axolotls have contributed as a bridge organism between invertebrates and mammals, as the species has the regenerative capacity to undergo complete neurogenesis forming a wide range of neuronal populations not limited to a small niche,[23] yet the complexity and architecture is complex and analogous in many ways to human neural development.
Zebrafish
Chick
Though avians have been used primarily to study early embryonic development, in recent decades the developing chick has played a critical role in the examination of neurogenesis and regeneration as the young chick is capable of neuronal-turnover at a young age, but loses the neurogenerative capacity into adulthood.[30] The loss of neuroregenerative ability over maturation has allowed investigators to further examine genetic regulators of neurogenesis.
Rodents
To some extent, adult neurogenesis in rodents may be induced by selective disruption of
Adult neurogenesis in the subventricular zone and dentate gyrus of rodents generates oxidative stress and production of reactive oxygen species that can damage both DNA and lipids.[34] The oxidative stress caused by postnatal neurogenesis may significantly contribute to the reduced learning and memory that occurs with increasing age.[34]
Octopus
A cephalopod also known as the common octopus, this organism has an intricate nervous system that demonstrates the brains capacity to produce new cells. In this case and in other taxa when compared, these organisms adapt to unpredictable environments by using newly formed brain cells.[35] This is over a short life-span (female about one year) where wild common octopuses focus most of their energy on mating and offspring care.[36][37] Findings suggest that the octopus vulgaris like other short-lived species have a complex hippocampal proliferation,[38][39] needed for spatial/navigation, and short and long-term memory.[40][circular reference]
Chickadees
Over the 2 decades since the initial discovery,[41] the specific role of chickadee hippocampus in memory has gained wide attention. In an experimental setting, hippocampal lesions affect memory for locations,[43] validating previous notions for this specific role. Further, experimentally inhibiting neuronal proliferation decreases scores on spatial memory tasks,[44] supporting that new neurons hold the same role as pre-existing ones. The specific function of the hippocampus, coupled with seasonal changes in their volume, point towards their temporary advantages for spatial memory consolidation. Taken all together, adult neurogenesis in the hippocampus of black-capped chickadees suggest a selective mechanisms for neuronal survival in direct correlation with seasonal food caching behavior.
Developmentally, progenitor cells called radial glial cells are thought to mitigate newly born neurons to their destinations.[45] Radial glial cells extend processes from their soma in the avian ventricular zone to the parenchyma of the adult forebrain.[46] These New neurons have been observed as early as 3 days after thymidine administration in the HVC[47] and as early as 7 days before reaching the hippocampus.[42] Avian migration of new neurons are analogous to mammalian species,[46] providing a future direction in exploring neurogenesis in mammalian species and beyond. However, captivity has been shown to reduce hippocampal volumes when compared to wild counterparts.[48] Reduced neurogenesis in captive birds may be caused by stress, lack of exercise, diminished social interaction, and limited caching opportunities.[48]
Tracking neurogenesis
The creation of new functional neurons can be measured in several ways,[49] summarized in the following sections.
DNA labelling
Labelled
Fate determination via neuronal lineage markers
. SomeCre-Lox recombination
Some genetic tracing studies utilize cre-lox recombination to bind a promoter to a reporter gene, such as lacZ or GFP gene.[50][53] This method can be used for long term quantification of cell division and labeling, whereas the previously mentioned procedures are only useful for short-term quantification.
Viral vectors
It has recently become more common to use recombinant viruses to insert the genetic information encoding specific markers (usually protein fluorophores such as GFP) that are only expressed in cells of a certain kind. The marker gene is inserted downstream of a promoter, leading to transcription of 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 doublecortin, a protein expressed predominantly by neurons, upstream of a sequence coding for GFP, thereby making infected cells fluoresce green upon exposure to light in the blue to ultraviolet range[54] while leaving non doublecortin expressing cells unaffected, even if they contain the plasmid. 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.[55] It is important to note, however, that while the plasmid is stable for long periods of time, its protein products may have highly variable half lives and their fluorescence may decrease as well as become too diluted to be seen depending on the number of round of replication they have undergone, making this method more useful for tracking self-similar neural precursor or neural stem cells rather than neurons themselves. 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 tissue, making 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.[56]
Methods for inhibiting neurogenesis
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.[13]
Pharmacological inhibition
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, as these inhibitors can't be used to inhibit proliferation in specific regions, thus leading to nonspecific effects from other systems being affected. To avoid these effects, 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 (MAM), a chemotherapeutic agent. Other cell division inhibitors commonly used in studies are cytarabine and temozolomide.
Pharmacogenetics
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. 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.
Cre protein is also commonly used in targeting stem cells that will undergo gene changes upon treatment with tamoxifen.
Irradiation
Irradiation, the process of exposing parts of something or someone to radiation, is a method that allows for very specific inhibition of 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, which is important in determining how adult neurogenesis in different areas of the brain affects behavior.
Irradiation has previously been tested in adult rats, with no significant changes in cognition having been reported. However, neurogenesis in this study was stopped from progressing when the irradiation was specifically directed towards the hippocampus.[57]
However, irradiation is more expensive than the other methods and also requires large equipment with trained individuals.
Inhibition of adult neurogenesis in the hippocampus
Many studies have observed how inhibiting adult neurogenesis in other mammals, such as rats and mice, affects their behavior.[13] Inhibition of adult neurogenesis in the hippocampus has been shown to have various effects on learning and memory, conditioning, and investigative behaviors.
Impaired fear conditioning has been seen in studies involving rats with a lack of adult neurogenesis in the hippocampus.[58] Inhibition of adult neurogenesis in the hippocampus has also been linked to changes in behavior in tasks involving investigation.[59] Rats also show decreased contextualized freezing behaviors in response to contextualized fear and impairment in learning spatial locations when lacking adult neurogenesis.[60][61]
Effects on pattern separation
The changes in learning and memory seen in the studies mentioned previously are thought to be related to the role of adult neurogenesis in regulating pattern separation.[13] Pattern separation is defined as "a process to remove redundancy from similar inputs so that events can be separated from each other and interference can be reduced, and in addition can produce a more orthogonal, sparse, and categorized set of outputs."[62]
This impairment in pattern separation could explain the impairments seen in other learning and memory tasks. A decreased ability in reducing interference could lead to greater difficulty in forming and retaining new memories,[13] although it's hard to discriminate between effects of neurogenesis in learning and pattern separation due to limitations in the interpretation of behavioral results.[63]
Studies show that rats with inhibited adult neurogenesis demonstrate difficulty in differentiating and learning contextualized fear conditioning.[13] Rats with blocked adult neurogenesis also show impaired differential freezing when they are required to differentiate between similar contexts.[64] This also affects their spatial recognition in radial arm maze tests when the arms are closer together rather than when they are further apart.[65] A meta-analysis of behavioral studies evaluating the effect of neurogenesis in different pattern separation tests has shown a consistent effect of neurogenesis ablation on performance, although there are exceptions in the literature.[66]
Effects on behavioral inhibition
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.[13]
Rats with lesioned hippocampi show less behavioral inhibition when exposed to threats, such as cat odor.[67] The disruption of normal cell proliferation and development of the dentate gyrus in developing rats also impairs their freezing response, which is an example of behavior inhibition, when exposed to an unfamiliar adult male rat.[68]
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.[13]
Implications
Role in learning
The functional relevance of adult neurogenesis is uncertain,
Alzheimer's disease
Some studies suggest that decreased hippocampal neurogenesis can lead to development of
Role in schizophrenia
Studies suggest that people with schizophrenia have 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. Furthermore, several research papers referred to four genes, dystrobrevin binding protein 1 (DTNBP1), neuregulin 1 (NRG1), disrupted in schizophrenia 1 (DISC1), and neuregulin 1 receptor (ERBB4), as being possibly responsible for this deficit in the normal regeneration of neurons.[85][86] Similarities between depression and schizophrenia suggest a possible biological link between the two diseases. However, further research must be done in order to clearly demonstrate this relationship.[87]
Adult neurogenesis and major depressive disorder
Research indicates that adult hippocampal neurogenesis is inversely related to major depressive disorder (MDD).
Stress and depression
Many now believe stress to be the most significant factor for the onset of
Adult-born neurons appear to have a role in the regulation of
Some studies have hypothesized that 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.[100] However another study has demonstrated an interaction between antidepressants and plasticity; the antidepressant fluoxetine has been shown to restore plasticity in the adult rat brain.[101] The results of this study imply that instead of being secondary to changes in plasticity, antidepressant therapy could promote it.
Effects of sleep reduction
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
Possible use in treating Parkinson's disease
Traumatic brain injury
Factors affecting
Changes in old age
Neurogenesis is substantially reduced in the hippocampus of aged animals, raising the possibility that it may be linked to age-related declines in hippocampal function. For example, the rate of neurogenesis in aged animals is predictive of memory.[115] However, new born cells in aged animals are functionally integrated.[116] Given that neurogenesis occurs throughout life, it might be expected that the hippocampus would steadily increase in size during adulthood, and that therefore the number of granule cells would be increased in aged animals. However, this is not the case, indicating that proliferation is balanced by cell death. Thus, it is not the addition of new neurons into the hippocampus that seems to be linked to hippocampal functions, but rather the rate of turnover of granule cells.[117]
Effects of exercise
Scientists have shown that physical activity in the form of voluntary exercise results in an increase in the number of newborn neurons in the hippocampus of mice and rats.[118][119] These and other studies have shown that learning in both species can be enhanced by physical exercise.[120] Recent research has shown that brain-derived neurotrophic factor and insulin-like growth factor 1 are key mediators of exercise-induced neurogenesis.[119][121] Exercise increases the production of BDNF, as well as the NR2B subunit of the NMDA receptor.[119] Exercise increases the uptake of IGF-1 from the bloodstream into various brain regions, including the hippocampus. In addition, IGF-1 alters c-fos expression in the hippocampus. When IGF-1 is blocked, exercise no longer induces neurogenesis.[121] Other research demonstrated that exercising mice that did not produce beta-endorphin, a mood-elevating hormone, had no change in neurogenesis. Yet, mice that did produce this hormone, along with exercise, exhibited an increase in newborn cells and their rate of survival.[122] While the association between exercise-mediated neurogenesis and enhancement of learning remains unclear, this study could have strong implications in the fields of aging and/or Alzheimer's disease.
Effects of cannabinoids
This section needs more primary sources. (November 2016) |
Some studies have shown that the stimulation of the
A few studies have reported a positive association between THC and hippocampal neurogenesis.[130][131] Some of them hypotethize a biphasic effect,[130] some of them express that part of the negative effects could be attributable to neuroadaptation due to exposure at a specific period of life, and that it could be reversed.[132]
Regulation
Many factors may affect the rate of hippocampal neurogenesis.
Circulating factors within the blood may reduce neurogenesis. In healthy aging humans, the plasma and cerebrospinal fluid levels of certain chemokines are elevated. In a mouse model, plasma levels of these chemokines correlate with reduced neurogenesis, suggesting that neurogenesis may be modulated by certain global age-dependent systemic changes. These chemokines include CCL11, CCL2 and CCL12, which are highly localized on mouse and human chromosomes, implicating a genetic locus in aging.[70] Another study implicated the cytokine, IL-1beta, which is produced by glia. That study found that blocking IL-1 could partially prevent the severe impairment of neurogenesis caused by a viral infection.[144]ephrin-A2 and ephrin-A3 have been showed to negatively regulate adult neurogenesis.[146]
History
Early neuroanatomists, including
See also
- Artificial neural membrane
- Neural development
- Neuroplasticity
- Neurotrophin
- Neurulation
- Gliogenesis
- Adult neurogenesis in songbirds
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External links
- Concise introduction to neurogenesis from Wellesley College
- Comprehensive website on neurogenesis from Lafayette College
- Early literature on adult neurogenesis
- Neurogenesis in adult brain - Fred H. Gage and Henriette van Praag
- "Neurogenesis and Parkinson´s disease"
- Scholarpedia Article on Adult Neurogenesis
- "Trends in Neurosciences, 10 October 2001 (Michael S. Kaplan MD, PhD)
- New York Times: Studies Find Brains Grow New Cells
- Michael Specter: Rethinking the Brain Archived 2019-06-30 at the Wayback Machine - How the songs of canaries upset a fundamental principle of science
- The Neurogenesis Experiment - Article series on adult human neurogenesis
- Seed magazine: The Reinvention of the Self - A historical background on the field of neurogenesis and implications of this research
- BBC Radio 4: The Memory Experience - Use it or Lose it
- PBS: Changing Your Mind Archived 2015-09-24 at the Wayback Machine - Grow Your Own Brain
- Lobes of Steel: Aerobic exercise appears to promote neurogenesis, New York Times, 19 August 2007.
- Media related to neurogenesis at Wikimedia Commons