The Experts below are selected from a list of 62874 Experts worldwide ranked by ideXlab platform
Diane C Lagace - One of the best experts on this subject based on the ideXlab platform.
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in vivo contribution of nestin and glast lineage cells to adult hippocampal Neurogenesis
Hippocampus, 2013Co-Authors: Nathan A Decarolis, David Petrik, Maxwell Mechanic, Adam Carlton, Jessica L Ables, Shveta Malhotra, Robert Bachoo, Magdalena Gotz, Diane C LagaceAbstract:Radial glia-like cells (RGCs) are the hypothesized source of adult hippocampal Neurogenesis. However, the current model of hippocampal Neurogenesis does not fully incorporate the in vivo heterogeneity of RGCs. In order to better understand the contribution of different RGC subtypes to adult hippocampal Neurogenesis, we employed widely used transgenic lines (Nestin-CreER(T2) and GLAST::CreER(T2) mice) to explore how RGCs contribute to Neurogenesis under basal conditions and after stimulation and depletion of neural progenitor cells. We first used these inducible fate-tracking transgenic lines to define the similarities and differences in the contribution of nestin- and GLAST-lineage cells to basal long-term hippocampal Neurogenesis. We then explored the ability of nestin- and GLAST-lineage RGCs to contribute to Neurogenesis after experimental manipulations that either ablate Neurogenesis (i.c.v. application of the anti-mitotic AraC, cytosine-β-D-arabinofuranoside) or stimulate Neurogenesis (wheel running). Interestingly, in both ablation and stimulation experiments, labeled RGCs in GLAST::CreER(T2) mice appear to contribute to Neurogenesis, whereas RGCs in Nestin-CreER(T2) mice do not. Finally, using NestinGFP reporter mice, we expanded on previous research by showing that not all RGCs in the adult dentate gyrus subgranular zone express nestin, and therefore RGCs are antigenically heterogeneous. These findings are important for the field, as they allow appropriately conservative interpretation of existing and future data that emerge from these inducible transgenic lines. These findings also raise important questions about the differences between transgenic driver lines, the heterogeneity of RGCs, and the potential differences in progenitor cell behavior between transgenic lines. As these findings highlight the possible differences in the contribution of cells to long-term Neurogenesis in vivo, they indicate that the current models of hippocampal Neurogenesis should be modified to include RGC lineage heterogeneity.
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in vivo contribution of nestin and glast lineage cells to adult hippocampal Neurogenesis
Hippocampus, 2013Co-Authors: Nathan A Decarolis, David Petrik, Maxwell Mechanic, Adam Carlton, Jessica L Ables, Shveta Malhotra, Robert Bachoo, Magdalena Gotz, Diane C LagaceAbstract:Radial glia-like cells (RGCs) are the hypothesized source of adult hippocampal Neurogenesis. However, the current model of hippocampal Neurogenesis does not fully incorporate the in vivo heterogeneity of RGCs. In order to better understand the contribution of different RGC subtypes to adult hippocampal Neurogenesis, we employed widely used transgenic lines (Nestin-CreERT2 and GLAST::CreERT2 mice) to explore how RGCs contribute to Neurogenesis under basal conditions and after stimulation and depletion of neural progenitor cells. We first used these inducible fate-tracking transgenic lines to define the similarities and differences in the contribution of nestin- and GLAST-lineage cells to basal long-term hippocampal Neurogenesis. We then explored the ability of nestin- and GLAST-lineage RGCs to contribute to Neurogenesis after experimental manipulations that either ablate Neurogenesis (i.c.v. application of the anti-mitotic AraC, cytosine-β-D-arabinofuranoside) or stimulate Neurogenesis (wheel running). Interestingly, in both ablation and stimulation experiments, labeled RGCs in GLAST::CreERT2 mice appear to contribute to Neurogenesis, whereas RGCs in Nestin-CreERT2 mice do not. Finally, using NestinGFP reporter mice, we expanded on previous research by showing that not all RGCs in the adult dentate gyrus subgranular zone express nestin, and therefore RGCs are antigenically heterogeneous. These findings are important for the field, as they allow appropriately conservative interpretation of existing and future data that emerge from these inducible transgenic lines. These findings also raise important questions about the differences between transgenic driver lines, the heterogeneity of RGCs, and the potential differences in progenitor cell behavior between transgenic lines. As these findings highlight the possible differences in the contribution of cells to long-term Neurogenesis in vivo, they indicate that the current models of hippocampal Neurogenesis should be modified to include RGC lineage heterogeneity. © 2013 Wiley Periodicals, Inc.
L R Clark - One of the best experts on this subject based on the ideXlab platform.
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mild traumatic brain injury induces transient sequential increases in proliferation neuroblasts immature neurons and cell survival a time course study in the male mouse dentate gyrus
Frontiers in Neuroscience, 2021Co-Authors: L R Clark, Sanghee Yun, N K Acquah, Priya Kumar, Hannah E Metheny, Rikley C C PaixaoAbstract:Mild traumatic brain injuries (mTBIs) are prevalent worldwide. mTBIs can impair hippocampal-based functions such as memory and cause network hyperexcitability of the dentate gyrus (DG), a key entry point to hippocampal circuitry. One candidate for mediating mTBI-induced hippocampal cognitive and physiological dysfunction is injury-induced changes in the process of DG Neurogenesis. There are conflicting results on how TBI impacts the process of DG Neurogenesis; this is not surprising given that both the Neurogenesis process and the post-injury period are dynamic, and that the quantification of Neurogenesis varies widely in the literature. Even within the minority of TBI studies focusing specifically on mild injuries, there is disagreement about if and how mTBI changes the process of DG Neurogenesis. Here we utilized a clinically relevant rodent model of mTBI (lateral fluid percussion injury, LFPI), gold-standard markers and quantification of the Neurogenesis process, and three time points post-injury to generate a comprehensive picture of how mTBI affects adult hippocampal DG Neurogenesis. Male C57BL/6J mice (6-8 weeks old) received either sham surgery or mTBI via LFPI. Proliferating cells, neuroblasts/immature neurons, and surviving cells were quantified via stereology in DG subregions (subgranular zone [SGZ], outer granule cell layer [oGCL], molecular layer, and hilus) at short-term (3 days post-injury, dpi), intermediate (7 dpi), and long-term (31 dpi) time points. The data show this model of mTBI induces transient, sequential increases in ipsilateral SGZ/GCL proliferating cells, neuroblasts/immature neurons, and surviving cells which is suggestive of mTBI-induced Neurogenesis. In contrast to these ipsilateral hemisphere findings, measures in the contralateral hemisphere were not increased in key neurogenic DG subregions after LFPI. Our work in this mTBI model is in line with most literature on other and more severe models of TBI in showing TBI stimulates the process of DG Neurogenesis. However, as our DG data in mTBI provide temporal, subregional, and Neurogenesis-stage resolution, these data are important to consider in regard to the functional importance of TBI-induction of the Neurogenesis process and future work assessing the potential of replacing and/or repairing DG neurons in the brain after TBI.
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mild traumatic brain injury induces transient sequential increases in proliferation neuroblasts immature neurons and cell survival a time course study in the male mouse dentate gyrus
bioRxiv, 2020Co-Authors: L R Clark, Sanghee Yun, N K Acquah, Priya Kumar, Hannah E Metheny, Rikley C C PaixaoAbstract:Mild traumatic brain injuries (mTBIs) are prevalent worldwide. mTBIs can impair hippocampal-based functions such as memory and cause network hyperexcitability of the dentate gyrus (DG), a key entry point to hippocampal circuitry. One candidate for mediating mTBI-induced hippocampal cognitive and physiological dysfunction is injury-induced changes in the process of DG Neurogenesis. There are conflicting results on how TBI impacts the process of DG Neurogenesis; this is not surprising given that both the Neurogenesis process and the post-injury period are dynamic, and that the quantification of Neurogenesis varies widely in the literature. Even within the minority of TBI studies focusing specifically on mild injuries, there is disagreement about if and how mTBI changes the process of DG Neurogenesis. Here we utilized a clinically-relevant rodent model of mTBI (lateral fluid percussion injury, LFPI), gold-standard markers and quantification of the Neurogenesis process, and three time points post-injury to generate a comprehensive picture of how mTBI affects adult hippocampal DG Neurogenesis. Male C57BL/6J mice (6-8 weeks old) received either sham surgery or mTBI via LFPI. Proliferating cells, neuroblasts/immature neurons, and surviving cells were quantified via stereology in DG subregions (subgranular zone [SGZ], outer granule cell layer [oGCL], molecular layer, and hilus) at short-term (3 days post-injury, dpi), intermediate (7 dpi), and long-term (31 dpi) time points. The data suggest this model of mTBI induces transient, sequential increases in ipsilateral SGZ/GCL proliferating cells, neuroblasts/immature neurons, and surviving cells which are suggestive of mTBI-induced Neurogenesis. In contrast to these ipsilateral hemisphere findings, measures in the contralateral hemisphere were not increased in key neurogenic DG subregions after LFPI. Our work in this mTBI model is in line with most literature on other and more severe models of TBI in showing TBI stimulates the process of DG Neurogenesis. However, as our DG data in mTBI provide temporal, subregional, and Neurogenesis-stage resolution, these data are important to consider in regard to the functional importance of TBI-induction of the Neurogenesis process and future work assessing the potential of replacing and/or repairing DG neurons in the brain after TBI.
Fred H. Gage - One of the best experts on this subject based on the ideXlab platform.
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Adult hippocampal Neurogenesis and its role in Alzheimer's disease
Molecular Neurodegeneration, 2011Co-Authors: Fred H. GageAbstract:The hippocampus, a brain area critical for learning and memory, is especially vulnerable to damage at early stages of Alzheimer's disease (AD). Emerging evidence has indicated that altered Neurogenesis in the adult hippocampus represents an early critical event in the course of AD. Although causal links have not been established, a variety of key molecules involved in AD pathogenesis have been shown to impact new neuron generation, either positively or negatively. From a functional point of view, hippocampal Neurogenesis plays an important role in structural plasticity and network maintenance. Therefore, dysfunctional Neurogenesis resulting from early subtle disease manifestations may in turn exacerbate neuronal vulnerability to AD and contribute to memory impairment, whereas enhanced Neurogenesis may be a compensatory response and represent an endogenous brain repair mechanism. Here we review recent findings on alterations of Neurogenesis associated with pathogenesis of AD, and we discuss the potential of Neurogenesis-based diagnostics and therapeutic strategies for AD.
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an in vivo correlate of exercise induced Neurogenesis in the adult dentate gyrus
Proceedings of the National Academy of Sciences of the United States of America, 2007Co-Authors: Ana C Pereira, René Hen, Fred H. Gage, Daniel E Huddleston, Adam M Brickman, Alexander A Sosunov, Guy M Mckhann, Richard P Sloan, Truman R Brown, Scott A SmallAbstract:With continued debate over the functional significance of adult Neurogenesis, identifying an in vivo correlate of Neurogenesis has become an important goal. Here we rely on the coupling between Neurogenesis and angiogenesis and test whether MRI measurements of cerebral blood volume (CBV) provide an imaging correlate of Neurogenesis. First, we used an MRI approach to generate CBV maps over time in the hippocampal formation of exercising mice. Among all hippocampal subregions, exercise was found to have a primary effect on dentate gyrus CBV, the only subregion that supports adult Neurogenesis. Moreover, exercise-induced increases in dentate gyrus CBV were found to correlate with postmortem measurements of Neurogenesis. Second, using similar MRI technologies, we generated CBV maps over time in the hippocampal formation of exercising humans. As in mice, exercise was found to have a primary effect on dentate gyrus CBV, and the CBV changes were found to selectively correlate with cardiopulmonary and cognitive function. Taken together, these findings show that dentate gyrus CBV provides an imaging correlate of exercise-induced Neurogenesis and that exercise differentially targets the dentate gyrus, a hippocampal subregion important for memory and implicated in cognitive aging.
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natural variation and genetic covariance in adult hippocampal Neurogenesis
Proceedings of the National Academy of Sciences of the United States of America, 2006Co-Authors: Gerd Kempermann, Elissa J Chesler, Robert W Williams, Fred H. GageAbstract:Adult hippocampal Neurogenesis is highly variable and heritable among laboratory strains of mice. Adult Neurogenesis is also remarkably plastic and can be modulated by environment and activity. Here, we provide a systematic quantitative analysis of adult hippocampal Neurogenesis in two large genetic reference panels of recombinant inbred strains (BXD and AXB/BXA, n = 52 strains). We combined data on variation in Neurogenesis with a new transcriptome database to extract a set of 190 genes with expression patterns that are also highly variable and that covary with rates of (i) cell proliferation, (ii) cell survival, or the numbers of surviving (iii) new neurons, and (iv) astrocytes. Expression of a subset of these Neurogenesis-associated transcripts was controlled in cis across the BXD set. These self-modulating genes are particularly interesting candidates to control Neurogenesis. Among these were musashi (Msi1h) and prominin1/CD133 (Prom1), both of which are linked to stem-cell maintenance and division. Twelve Neurogenesis-associated transcripts had significant cis-acting quantitative trait loci, and, of these, six had plausible biological association with adult Neurogenesis (Prom1, Ssbp2, Kcnq2, Ndufs2, Camk4, and Kcnj9). Only one cis-acting candidate was linked to both Neurogenesis and gliogenesis, Rapgef6, a downstream target of ras signaling. The use of genetic reference panels coupled with phenotyping and global transcriptome profiling thus allowed insight into the complexity of the genetic control of adult Neurogenesis.
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adult brain Neurogenesis and psychiatry a novel theory of depression
Molecular Psychiatry, 2000Co-Authors: Barry L Jacobs, H Van Praag, Fred H. GageAbstract:Neurogenesis (the birth of new neurons) continues postnatally and into adulthood in the brains of many animal species, including humans. This is particularly prominent in the dentate gyrus of the hippocampal formation. One of the factors that potently suppresses adult Neurogenesis is stress, probably due to increased glucocorticoid release. Complementing this, we have recently found that increasing brain levels of serotonin enhance the basal rate of dentate gyrus Neurogenesis. These and other data have led us to propose the following theory regarding clinical depression. Stress-induced decreases in dentate gyrus Neurogenesis are an important causal factor in precipitating episodes of depression. Reciprocally, therapeutic interventions for depression that increase serotonergic neurotransmission act at least in part by augmenting dentate gyrus Neurogenesis and thereby promoting recovery from depression. Thus, we hypothesize that the waning and waxing of Neurogenesis in the hippocampal formation are important causal factors, respectively, in the precipitation of, and recovery from, episodes of clinical depression.
Rikley C C Paixao - One of the best experts on this subject based on the ideXlab platform.
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mild traumatic brain injury induces transient sequential increases in proliferation neuroblasts immature neurons and cell survival a time course study in the male mouse dentate gyrus
Frontiers in Neuroscience, 2021Co-Authors: L R Clark, Sanghee Yun, N K Acquah, Priya Kumar, Hannah E Metheny, Rikley C C PaixaoAbstract:Mild traumatic brain injuries (mTBIs) are prevalent worldwide. mTBIs can impair hippocampal-based functions such as memory and cause network hyperexcitability of the dentate gyrus (DG), a key entry point to hippocampal circuitry. One candidate for mediating mTBI-induced hippocampal cognitive and physiological dysfunction is injury-induced changes in the process of DG Neurogenesis. There are conflicting results on how TBI impacts the process of DG Neurogenesis; this is not surprising given that both the Neurogenesis process and the post-injury period are dynamic, and that the quantification of Neurogenesis varies widely in the literature. Even within the minority of TBI studies focusing specifically on mild injuries, there is disagreement about if and how mTBI changes the process of DG Neurogenesis. Here we utilized a clinically relevant rodent model of mTBI (lateral fluid percussion injury, LFPI), gold-standard markers and quantification of the Neurogenesis process, and three time points post-injury to generate a comprehensive picture of how mTBI affects adult hippocampal DG Neurogenesis. Male C57BL/6J mice (6-8 weeks old) received either sham surgery or mTBI via LFPI. Proliferating cells, neuroblasts/immature neurons, and surviving cells were quantified via stereology in DG subregions (subgranular zone [SGZ], outer granule cell layer [oGCL], molecular layer, and hilus) at short-term (3 days post-injury, dpi), intermediate (7 dpi), and long-term (31 dpi) time points. The data show this model of mTBI induces transient, sequential increases in ipsilateral SGZ/GCL proliferating cells, neuroblasts/immature neurons, and surviving cells which is suggestive of mTBI-induced Neurogenesis. In contrast to these ipsilateral hemisphere findings, measures in the contralateral hemisphere were not increased in key neurogenic DG subregions after LFPI. Our work in this mTBI model is in line with most literature on other and more severe models of TBI in showing TBI stimulates the process of DG Neurogenesis. However, as our DG data in mTBI provide temporal, subregional, and Neurogenesis-stage resolution, these data are important to consider in regard to the functional importance of TBI-induction of the Neurogenesis process and future work assessing the potential of replacing and/or repairing DG neurons in the brain after TBI.
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mild traumatic brain injury induces transient sequential increases in proliferation neuroblasts immature neurons and cell survival a time course study in the male mouse dentate gyrus
bioRxiv, 2020Co-Authors: L R Clark, Sanghee Yun, N K Acquah, Priya Kumar, Hannah E Metheny, Rikley C C PaixaoAbstract:Mild traumatic brain injuries (mTBIs) are prevalent worldwide. mTBIs can impair hippocampal-based functions such as memory and cause network hyperexcitability of the dentate gyrus (DG), a key entry point to hippocampal circuitry. One candidate for mediating mTBI-induced hippocampal cognitive and physiological dysfunction is injury-induced changes in the process of DG Neurogenesis. There are conflicting results on how TBI impacts the process of DG Neurogenesis; this is not surprising given that both the Neurogenesis process and the post-injury period are dynamic, and that the quantification of Neurogenesis varies widely in the literature. Even within the minority of TBI studies focusing specifically on mild injuries, there is disagreement about if and how mTBI changes the process of DG Neurogenesis. Here we utilized a clinically-relevant rodent model of mTBI (lateral fluid percussion injury, LFPI), gold-standard markers and quantification of the Neurogenesis process, and three time points post-injury to generate a comprehensive picture of how mTBI affects adult hippocampal DG Neurogenesis. Male C57BL/6J mice (6-8 weeks old) received either sham surgery or mTBI via LFPI. Proliferating cells, neuroblasts/immature neurons, and surviving cells were quantified via stereology in DG subregions (subgranular zone [SGZ], outer granule cell layer [oGCL], molecular layer, and hilus) at short-term (3 days post-injury, dpi), intermediate (7 dpi), and long-term (31 dpi) time points. The data suggest this model of mTBI induces transient, sequential increases in ipsilateral SGZ/GCL proliferating cells, neuroblasts/immature neurons, and surviving cells which are suggestive of mTBI-induced Neurogenesis. In contrast to these ipsilateral hemisphere findings, measures in the contralateral hemisphere were not increased in key neurogenic DG subregions after LFPI. Our work in this mTBI model is in line with most literature on other and more severe models of TBI in showing TBI stimulates the process of DG Neurogenesis. However, as our DG data in mTBI provide temporal, subregional, and Neurogenesis-stage resolution, these data are important to consider in regard to the functional importance of TBI-induction of the Neurogenesis process and future work assessing the potential of replacing and/or repairing DG neurons in the brain after TBI.
René Hen - One of the best experts on this subject based on the ideXlab platform.
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the current state of the neurogenic theory of depression and anxiety
Current Opinion in Neurobiology, 2015Co-Authors: Bradley R Miller, René HenAbstract:Newborn neurons are continuously added to the adult hippocampus. Early studies found that adult Neurogenesis is impaired in models of depression and anxiety and accelerated by antidepressant treatment. This led to the theory that depression results from impaired adult Neurogenesis and restoration of adult Neurogenesis leads to recovery. Follow up studies yielded a complex body of often inconsistent results, and the veracity of this theory is uncertain. We propose five criteria for acceptance of this theory, we review the recent evidence for each criterion, and we draw the following conclusions: Diverse animal models of depression and anxiety have impaired Neurogenesis. Neurogenesis is consistently boosted by antidepressants in animal models only when animals are stressed. Ablation of Neurogenesis in animal models impairs cognitive functions relevant to depression, but only a minority of studies find that ablation causes depression or anxiety. Recent human neuroimaging and postmortem studies are consistent with the neurogenic theory, but they are indirect. Finally, a novel drug developed based on the neurogenic theory is promising in animal models.
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implications of the functional integration of adult born hippocampal neurons in anxiety depression disorders
The Neuroscientist, 2010Co-Authors: Denis J David, Jingwen Wang, Benjamin Adam Samuels, Quentin Rainer, Indira David, Alain M Gardier, René HenAbstract:Adult Neurogenesis in the dentate gyrus of the hippocampus has gained considerable attention as a cellular substrate for both the pathophysiology and treatment of depression. Overall, the studies of adult hippocampal Neurogenesis are still in their infancy because most of them explore only one stage of this process. Importantly, given the built-in homeostatic mechanisms that act at each stage during the progression from stem cells to mature neurons (proliferation, differentiation, maturation, survival), it is very difficult to extrapolate the efficiency of a drug on adult Neurogenesis from analysis of one stage alone. Here, we review the most significant data on hippocampal Neurogenesis, focusing on the importance of studying each stage of adult hippocampal Neurogenesis and also on the importance of choosing the appropriate mouse strain to perform the experiment. Specifically, strains with a high number of basal proliferating cells in the dentate gyrus of the hippocampus should be used only under stressed conditions to detect the effects of antidepressants on adult Neurogenesis. We also discuss how adult hippocampal Neurogenesis could be involved in affective state disorders such as depression and anxiety. Finally, we reveal that the behavioral effects of fluoxetine are mediated through both Neurogenesis-dependent and -independent actions.
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adult hippocampal Neurogenesis as target for the treatment of depression
Cns & Neurological Disorders-drug Targets, 2007Co-Authors: Michael R Drew, René HenAbstract:The dentate gyrus (DG) is one of only two brain structures known to retain the ability to produce new neurons in adulthood. The functional significance of adult Neurogenesis in the DG is not yet well understood, but recent evidence has implicated adult Neurogenesis in the etiology and treatment of depression. Elevated stress hormone levels, which are present in some depressed patients and can precipitate the onset of depression, reduce Neurogenesis in animal models. Conversely, virtually all antidepressant treatments studied to date, including drugs of various classes, electroconvulsive therapy, and behavioral treatments, increase Neurogenesis in the DG. We critically review this literature linking DG neu- rogenesis with depression, looking to both animal and human studies. We conclude that a reduction in Neurogenesis by it- self is not likely to produce depression. However, at least some therapeutic effects of antidepressant treatments appear to be Neurogenesis-dependent. We review the cellular pathways through which antidepressant drugs boost Neurogenesis and present several hypotheses about how DG Neurogenesis may be instrumental in the therapeutic effects of these drugs.
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an in vivo correlate of exercise induced Neurogenesis in the adult dentate gyrus
Proceedings of the National Academy of Sciences of the United States of America, 2007Co-Authors: Ana C Pereira, René Hen, Fred H. Gage, Daniel E Huddleston, Adam M Brickman, Alexander A Sosunov, Guy M Mckhann, Richard P Sloan, Truman R Brown, Scott A SmallAbstract:With continued debate over the functional significance of adult Neurogenesis, identifying an in vivo correlate of Neurogenesis has become an important goal. Here we rely on the coupling between Neurogenesis and angiogenesis and test whether MRI measurements of cerebral blood volume (CBV) provide an imaging correlate of Neurogenesis. First, we used an MRI approach to generate CBV maps over time in the hippocampal formation of exercising mice. Among all hippocampal subregions, exercise was found to have a primary effect on dentate gyrus CBV, the only subregion that supports adult Neurogenesis. Moreover, exercise-induced increases in dentate gyrus CBV were found to correlate with postmortem measurements of Neurogenesis. Second, using similar MRI technologies, we generated CBV maps over time in the hippocampal formation of exercising humans. As in mice, exercise was found to have a primary effect on dentate gyrus CBV, and the CBV changes were found to selectively correlate with cardiopulmonary and cognitive function. Taken together, these findings show that dentate gyrus CBV provides an imaging correlate of exercise-induced Neurogenesis and that exercise differentially targets the dentate gyrus, a hippocampal subregion important for memory and implicated in cognitive aging.
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hippocampal Neurogenesis regulation by stress and antidepressants
Biological Psychiatry, 2006Co-Authors: Alex Dranovsky, René HenAbstract:Accumulating evidence implicates hippocampal Neurogenesis in the pathophysiology of depression. Psychosocial stress reduces Neurogenesis in rodents, whereas chronic treatment with antidepressants increases Neurogenesis and blocks the effects of stress. The effects of stress and antidepressant treatment on hippocampal Neurogenesis parallel behavioral changes in animal models. Moreover, ablating hippocampal Neurogenesis renders antidepressants inactive in behavioral paradigms used to model antidepressant response and anxiety-like behavior in mice. In humans, monoamine-modulating antidepressants demonstrate clinical efficacy in treating depression and anxiety, which are often precipitated by psychosocial stress. This review examines the mounting evidence that stress and antidepressant treatment regulate Neurogenesis in animals. Special attention is paid to the cellular and molecular mechanisms by which this regulation takes place. An analysis of current animal models used to study response to stress and antidepressants indicates the importance of modeling chronic treatment, which reflects both changes in Neurogenesis and clinical response. Exploring responses of hippocampal Neurogenesis to experimental challenges in appropriate animal models should delineate the role of adult-born neurons in hippocampal physiology. Focusing on neurogenic response to experimental paradigms of stress and antidepressant treatment is particularly interesting for understanding the pathophysiology of major depressive disorder.