Wise Young
12-02-2006, 07:39 PM
I came across this fascinating study the other day.
http://www.sciam.com/article.cfm?chanID=sa003&articleID=2BA97749-E7F2-99DF-326B17915B7EC2AA
November 27, 2006
Stressed Rats Cast Doubt on Sleep's Ability to Produce New Neurons
New results challenge the view that a good night's sleep can leave behind a dense bloom of brain cells in the morning. Prior studies had found that sleep-deprived rodents grow fewer new neurons than well-rested animals, suggesting that sleep somehow promotes the birth of brain cells, called neurogenesis. But that might not be the case: researchers report instead that lack of sleep likely cuts into neurogenesis by triggering a harmful stress response.
Neurogenesis is a mysterious process that can be amplified by Prozac and other depression treatments, although its exact role in the brain is unclear. Neuroscientist Elizabeth Gould of Princeton University and other researchers have found that many types of stress inhibit neurogenesis in rodents and primates. "We were very curious to see whether the reported effect of sleep deprivation on neurogenesis was related to stress or whether this is something specific to sleep," she says.
<snip>
Neuroscientist Dennis McGinty of the University of California, Los Angeles, disagrees. Different methods of sleep deprivation induce varying amounts of stress or even no stress response, and "she's using the most stressful method of sleep deprivation," he says. The result does support the view that neurogenesis is unaffected by REM sleep, he acknowledges. "It's probably not the last word, but it's certainly strongly suggestive."
The key mechanism appears to be the increase of corticosteroids associated with sleep deprivation, or at least the stress associated with sleep deprivation.
http://www.medscape.com/viewarticle/548359
Sleep Deprivation Blocks Hippocampal Neurogenesis Through Steroid Effect
NEW YORK (Reuters Health) Nov 28 - Sleep deprivation causes a rise in glucocorticoid levels that works to inhibit neurogenesis in the hippocampus, results of an animal study suggest.
This finding may help explain the adverse cognitive effects associated with sleep deprivation, according to the report in the November 28th Early Edition of the Proceedings of the National Academy of Sciences.
In the new study, Dr. Elizabeth Gould and colleagues, from Princeton University in New Jersey, show that 72 hours of sleep deprivation in rats causes a drop in hippocampal neurogenesis, which coincides with an elevation in circulating levels of corticosterone.
When corticosteroid levels were maintained at a normal level, the sleep-deprived animals no longer showed a reduction in hippocampal neurogenesis, the report indicates.
<more>
Here is another recent study that seems to support the finding the sleep deprivation reduces neurogenesis in the hippocampus.
http://cat.inist.fr/?aModele=afficheN&cpsidt=17275178
Titre du document / Document title
Sleep restriction suppresses neurogenesis induced by hippocampus-dependent learning
Auteur(s) / Author(s)
HAIRSTON Ilana S. ; LITTLE Milton T. M. ; SCANLON Michael D. ; BARAKAT Monique T. ; PALMER Theo D. ; SAPOLSKY Robert M. ; HELLER H. Craig ;
Résumé / Abstract
Sleep deprivation impairs hippocampal-dependent learning, which, in turn, is associated with increased survival of newborn cells in the hippocampus. We tested whether the deleterious effects of sleep restriction on hippocampus-dependent memory were associated with reduced cell survival in the hippocampus. We show that sleep restriction impaired hippocampus-dependent learning and abolished learning-induced neurogenesis. Animals were trained in a water maze on either a spatial learning (hippocampus-dependent) task or a nonspatial (hippocampus-independent) task for 4 days. Sleep-restricted animals were kept awake for one-half of their rest phase on each of the training days. Consistent with previous reports, animals trained on the hippocampus-dependent task expressed increased survival of newborn cells in comparison with animals trained on the hippocampus-independent task. This increase was abolished by sleep restriction that caused overall reduced cell survival in all animals. Sleep restriction also selectively impaired spatial learning while performance in the nonspatial task was, surprisingly, improved. Further analysis showed that in both training groups fully rested animals applied a spatial strategy irrespective of task requirements; this strategy interfered with performance in the nonspatial task. Conversely, in sleep-restricted animals, this preferred spatial strategy was eliminated, favoring the use of nonspatial information, and hence improving performance in the nonspatial task. These findings suggest that sleep loss altered behavioral strategies to those that do not depend on the hippocampus. concomitantly reversing the neurogenic effects of hippocampus-dependent learning.
Revue / Journal Title
Journal of neurophysiology (J. neurophysiol.) ISSN 0022-3077 CODEN JONEA4
One study suggests that a single night of sleep deprivation increases neurogenesis:
http://www.biopsychiatry.com/neurogenesis-sleepdep.htm
'One night' sleep deprivation stimulates hippocampal neurogenesis
by
Grassi Zucconi G, Cipriani S, Balgkouranidou I, Scattoni R.
Department of Cellular and Environmental Biology,
University of Perugia, Perugia, Italy.
Brain Res Bull. 2006 Apr 28;69(4):375-81.
ABSTRACT
Neurogenesis in the adult hippocampus can be up- or downregulated in response to a variety of physiological and pathological conditions. Among these, dysregulation of hippocampal neurogenesis has been recently implicated in the pathogenesis of depression. In addition, in animal models of depression, a variety of antidepressant treatments reverse that condition by increasing neurogenesis. As one night sleep deprivation is known to improve mood in depressed patients for at least 1 day, we investigated whether a comparable treatment may affect hippocampal neurogenesis in adult rats. Accordingly, rats were sleep-deprived by gentle handling for 12h during their physiological period of rest, and were injected with bromodeoxyuridine 4h and 2h before the end of sleep deprivation. They were then perfused immediately thereafter, or after 15 days and 30 days. We found that 12h sleep deprivation significantly increased cell proliferation and the total number of surviving cells in the hippocampal dentate gyrus soon after sleep deprivation, as well as 15 days and 30 days later, in comparison to control rats allowed to sleep. No changes were instead found in the subventricular zone of the lateral ventricles, indicating that 12h sleep deprivation selectively triggers neurogenic signals to the hippocampus. The present data include acute sleep deprivation among the conditions which upregulate hippocampal neurogenesis and raise the possibility that such response could be implicated in the beneficial effects elicited in depressed patients by one night sleep deprivation. Thus, the findings could contribute to the understanding of the intriguing relationship between depression and neurogenesis in the adult brain.
Finally, there is a strong linkage of depression to inhibition of neurogenesis in the brain Source (http://en.wikibooks.org/wiki/Demystifying_Depression:Speculation_on_the_Physiol ogy_of_Depression) and a large body of evidence suggesting that lithium's effect on depression may be related to its ability to stimulate neurotrophin expression and neurogenesis in the brain (Source (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10987856&dopt=Abstract)) Many studies have confirmed the initial studies that reported that lithium increases neurogenesis in 2000 (Source (http://www.sciencenews.org/articles/20001111/fob3ref.asp)) although some studies suggest that it increases long-term potentiation in the hippocampus (a mechanism of memory) without increasing neurogenesis, i.e.
http://cat.inist.fr/?aModele=afficheN&cpsidt=14749484
Titre du document / Document title
Chronic lithium enhances hippocampal long-term potentiation, but not neurogenesis, in the aged rat dentate gyrus
Auteur(s) / Author(s)
IN TAG YU ; JIN SEUK KIM ; LEE Sang-Hun ; LEE Yong-Sung ; SON Hyeon ;
Résumé / Abstract
We investigated the hippocampal long-term potentiation (LTP), neurogenesis, and the activation of signaling molecules in the 20-month-old aged rats following chronic lithium treatment. Chronic lithium treatment produced asignificant 79% increase in the numbers of BrdU(+) cells after treatment completion in the dentate gyrus (DG). Both LTP obtained from slices perfused with artificial cerebrospinal fluid (ACSF-LTP), and LTP recorded in the presence of bicuculline (bicuculline-LTP) were significantly greater in the lithium group than in the saline controls. Our results show that as with young rats, chronic lithium can substantially increase LTP and the number of BrdU(+) cells in the aged rats. However, neurogenesis, assessed by colocalization of NeuN and BrdU, was not detected in the aged rat DG subjected to chronic lithium treatment. Therefore, it is concluded that the increase in LTP and the number of BrdU(+) cells might not be associated with increases in neurogenesis in the granule cell layer of the DG. Lithium might has a beneficial effects through other signaling pathways in the aged brain.
Revue / Journal Title
Biochemical and biophysical research communications (Biochem. biophys. res. commun.) ISSN 0006-291X CODEN BBRCA9
Source / Source
2003, vol. 303, no4, pp. 1193-1198 [6 page(s) (article)]
Lithium has been used for over 100 years to treat depression and is now being touted as a new "life-enhancement" drug (Source (http://www.life-enhancement.com/LE/article_template.asp?ID=1675)). It is also interesting that another mood stabilizing drug, the anti-epileptic drug Valproate also stimulates neurogenesis.
http://www.jneurosci.org/cgi/content/full/24/29/6590
Mood Stabilizer Valproate Promotes ERK Pathway-Dependent Cortical Neuronal Growth and Neurogenesis
Yanlei Hao,1 Thomas Creson,1 Lei Zhang,1 Pipeng Li,1 Fu Du,2 Peixiong Yuan,1 Todd D. Gould,1 Husseini K. Manji,1 and Guang Chen1
1Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892-4405, and 2FD NeuroTechnologies, Ellicott City, Maryland 21041
Manic-depressive illness has been conceptualized as a neurochemical illness. However, brain imaging and postmortem studies reveal gray-matter reductions, as well as neuronal and glial atrophy and loss in discrete brain regions of manic-depressive patients. The roles of such cerebral morphological deficits in the neuropathophysiology and therapeutic mechanisms of manic-depressive illness are unknown. Valproate (2-propylpentanoate) is a commonly used mood stabilizer. The ERK (extracellular signal-regulated kinase) pathway is used by neurotrophic factors to regulate neurogenesis, neurite outgrowth, and neuronal survival. We found that chronic treatment of rats with valproate increased levels of activated phospho-ERK44/42 in neurons of the anterior cingulate, a region in which we found valproate-induced increases in expression of an ERK pathway-regulated gene, bcl-2. Valproate time and concentration dependently increased activated phospho-ERK44/42 and phospho-RSK1 (ribosomal S6 kinase 1) levels in cultured cortical cells. These increases were attenuated by Raf and MEK (mitogen-activated protein kinase/ERK kinase) inhibitors. Although valproate affects the functions of GSK-3 (glycogen synthase kinase-3) and histone deacetylase (HDAC), its effects on the ERK pathway were not fully mimicked by selective inhibitors of GSK-3 or HDAC. Similar to neurotrophic factors, valproate enhanced ERK pathway-dependent cortical neuronal growth. Valproate also promoted neural stem cell proliferation-maturation (neurogenesis), demonstrated by bromodeoxyuridine (BrdU) incorporation and double staining of BrdU with nestin, Tuj1, or the neuronal nuclei marker NeuN (neuronal-specific nuclear protein). Chronic treatment with valproate enhanced neurogenesis in the dentate gyrus of the hippocampus. Together, these data demonstrate that valproate activates the ERK pathway and induces ERK pathway-mediated neurotrophic actions. This cascade of events provides a potential mechanism whereby mood stabilizers alleviate cerebral morphometric deficits associated with manic-depressive illness.
Key words: valproate; ERK; neurite outgrowth; neurogenesis; mania; mood disorders
It seems that Prozac (another anti-depressive drug) stimulates neurogenesis in the brain:
http://www.sciam.com/article.cfm?articleID=000E44B7-2B2F-1514-A59B83414B7F0133
September 25, 2006
Does Sprouting New Brain Cells Cure Depression?
By JR Minkel
Article Tools E-mail ArticleE-mail Print ViewPrint LinkLink RSSRSS del.icio.usdel.icio.us diggDigg
Science Image: depression
Image: © BROOKE FASANI/CORBIS
In recent years, researchers have discovered tantalizing evidence that antidepressants combat depression by promoting neurogenesis, the growth of new neurons in the brain. The evidence derives from several striking observations. One is that stressed monkeys grow fewer new cells in the hippocampus region of the brain than their healthy counterparts do. Secondly, most depression treatments, from drugs such as Prozac to a type of powerful magnetic stimulation, increase new neuron growth by up to 75 percent in rodents.
And in the most telling study to date, scientists from Columbia University and Yale University directed radiation at the hippocampi of mice to prevent neurogenesis. When given fluoxetine, also known as Prozac, the mice exhibited none of the behavioral changes normally associated with the drug. If neurogenesis is required to kick depression, as the result suggested, maybe its loss sends the mind into a tailspin. "It's a very appealing idea," comments Eric Nestler of the University of Texas Southwestern Medical Center at Dallas. "It provides a mechanism to explain why many cases of depression are chronic and progressive." It would also explain why Prozac takes a few weeks to exert its effects. The growth of neurons from stem cells takes a few weeks as well.
<more>
This is a fascinating field. I wonder if lithium will reverse the deleterious effects of sleep restriction on neurogenesis. Of course, my interest in this area is prompted by our proposal to use lithium to try to enhance regeneration in the spinal cord.
Wise.
http://www.sciam.com/article.cfm?chanID=sa003&articleID=2BA97749-E7F2-99DF-326B17915B7EC2AA
November 27, 2006
Stressed Rats Cast Doubt on Sleep's Ability to Produce New Neurons
New results challenge the view that a good night's sleep can leave behind a dense bloom of brain cells in the morning. Prior studies had found that sleep-deprived rodents grow fewer new neurons than well-rested animals, suggesting that sleep somehow promotes the birth of brain cells, called neurogenesis. But that might not be the case: researchers report instead that lack of sleep likely cuts into neurogenesis by triggering a harmful stress response.
Neurogenesis is a mysterious process that can be amplified by Prozac and other depression treatments, although its exact role in the brain is unclear. Neuroscientist Elizabeth Gould of Princeton University and other researchers have found that many types of stress inhibit neurogenesis in rodents and primates. "We were very curious to see whether the reported effect of sleep deprivation on neurogenesis was related to stress or whether this is something specific to sleep," she says.
<snip>
Neuroscientist Dennis McGinty of the University of California, Los Angeles, disagrees. Different methods of sleep deprivation induce varying amounts of stress or even no stress response, and "she's using the most stressful method of sleep deprivation," he says. The result does support the view that neurogenesis is unaffected by REM sleep, he acknowledges. "It's probably not the last word, but it's certainly strongly suggestive."
The key mechanism appears to be the increase of corticosteroids associated with sleep deprivation, or at least the stress associated with sleep deprivation.
http://www.medscape.com/viewarticle/548359
Sleep Deprivation Blocks Hippocampal Neurogenesis Through Steroid Effect
NEW YORK (Reuters Health) Nov 28 - Sleep deprivation causes a rise in glucocorticoid levels that works to inhibit neurogenesis in the hippocampus, results of an animal study suggest.
This finding may help explain the adverse cognitive effects associated with sleep deprivation, according to the report in the November 28th Early Edition of the Proceedings of the National Academy of Sciences.
In the new study, Dr. Elizabeth Gould and colleagues, from Princeton University in New Jersey, show that 72 hours of sleep deprivation in rats causes a drop in hippocampal neurogenesis, which coincides with an elevation in circulating levels of corticosterone.
When corticosteroid levels were maintained at a normal level, the sleep-deprived animals no longer showed a reduction in hippocampal neurogenesis, the report indicates.
<more>
Here is another recent study that seems to support the finding the sleep deprivation reduces neurogenesis in the hippocampus.
http://cat.inist.fr/?aModele=afficheN&cpsidt=17275178
Titre du document / Document title
Sleep restriction suppresses neurogenesis induced by hippocampus-dependent learning
Auteur(s) / Author(s)
HAIRSTON Ilana S. ; LITTLE Milton T. M. ; SCANLON Michael D. ; BARAKAT Monique T. ; PALMER Theo D. ; SAPOLSKY Robert M. ; HELLER H. Craig ;
Résumé / Abstract
Sleep deprivation impairs hippocampal-dependent learning, which, in turn, is associated with increased survival of newborn cells in the hippocampus. We tested whether the deleterious effects of sleep restriction on hippocampus-dependent memory were associated with reduced cell survival in the hippocampus. We show that sleep restriction impaired hippocampus-dependent learning and abolished learning-induced neurogenesis. Animals were trained in a water maze on either a spatial learning (hippocampus-dependent) task or a nonspatial (hippocampus-independent) task for 4 days. Sleep-restricted animals were kept awake for one-half of their rest phase on each of the training days. Consistent with previous reports, animals trained on the hippocampus-dependent task expressed increased survival of newborn cells in comparison with animals trained on the hippocampus-independent task. This increase was abolished by sleep restriction that caused overall reduced cell survival in all animals. Sleep restriction also selectively impaired spatial learning while performance in the nonspatial task was, surprisingly, improved. Further analysis showed that in both training groups fully rested animals applied a spatial strategy irrespective of task requirements; this strategy interfered with performance in the nonspatial task. Conversely, in sleep-restricted animals, this preferred spatial strategy was eliminated, favoring the use of nonspatial information, and hence improving performance in the nonspatial task. These findings suggest that sleep loss altered behavioral strategies to those that do not depend on the hippocampus. concomitantly reversing the neurogenic effects of hippocampus-dependent learning.
Revue / Journal Title
Journal of neurophysiology (J. neurophysiol.) ISSN 0022-3077 CODEN JONEA4
One study suggests that a single night of sleep deprivation increases neurogenesis:
http://www.biopsychiatry.com/neurogenesis-sleepdep.htm
'One night' sleep deprivation stimulates hippocampal neurogenesis
by
Grassi Zucconi G, Cipriani S, Balgkouranidou I, Scattoni R.
Department of Cellular and Environmental Biology,
University of Perugia, Perugia, Italy.
Brain Res Bull. 2006 Apr 28;69(4):375-81.
ABSTRACT
Neurogenesis in the adult hippocampus can be up- or downregulated in response to a variety of physiological and pathological conditions. Among these, dysregulation of hippocampal neurogenesis has been recently implicated in the pathogenesis of depression. In addition, in animal models of depression, a variety of antidepressant treatments reverse that condition by increasing neurogenesis. As one night sleep deprivation is known to improve mood in depressed patients for at least 1 day, we investigated whether a comparable treatment may affect hippocampal neurogenesis in adult rats. Accordingly, rats were sleep-deprived by gentle handling for 12h during their physiological period of rest, and were injected with bromodeoxyuridine 4h and 2h before the end of sleep deprivation. They were then perfused immediately thereafter, or after 15 days and 30 days. We found that 12h sleep deprivation significantly increased cell proliferation and the total number of surviving cells in the hippocampal dentate gyrus soon after sleep deprivation, as well as 15 days and 30 days later, in comparison to control rats allowed to sleep. No changes were instead found in the subventricular zone of the lateral ventricles, indicating that 12h sleep deprivation selectively triggers neurogenic signals to the hippocampus. The present data include acute sleep deprivation among the conditions which upregulate hippocampal neurogenesis and raise the possibility that such response could be implicated in the beneficial effects elicited in depressed patients by one night sleep deprivation. Thus, the findings could contribute to the understanding of the intriguing relationship between depression and neurogenesis in the adult brain.
Finally, there is a strong linkage of depression to inhibition of neurogenesis in the brain Source (http://en.wikibooks.org/wiki/Demystifying_Depression:Speculation_on_the_Physiol ogy_of_Depression) and a large body of evidence suggesting that lithium's effect on depression may be related to its ability to stimulate neurotrophin expression and neurogenesis in the brain (Source (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10987856&dopt=Abstract)) Many studies have confirmed the initial studies that reported that lithium increases neurogenesis in 2000 (Source (http://www.sciencenews.org/articles/20001111/fob3ref.asp)) although some studies suggest that it increases long-term potentiation in the hippocampus (a mechanism of memory) without increasing neurogenesis, i.e.
http://cat.inist.fr/?aModele=afficheN&cpsidt=14749484
Titre du document / Document title
Chronic lithium enhances hippocampal long-term potentiation, but not neurogenesis, in the aged rat dentate gyrus
Auteur(s) / Author(s)
IN TAG YU ; JIN SEUK KIM ; LEE Sang-Hun ; LEE Yong-Sung ; SON Hyeon ;
Résumé / Abstract
We investigated the hippocampal long-term potentiation (LTP), neurogenesis, and the activation of signaling molecules in the 20-month-old aged rats following chronic lithium treatment. Chronic lithium treatment produced asignificant 79% increase in the numbers of BrdU(+) cells after treatment completion in the dentate gyrus (DG). Both LTP obtained from slices perfused with artificial cerebrospinal fluid (ACSF-LTP), and LTP recorded in the presence of bicuculline (bicuculline-LTP) were significantly greater in the lithium group than in the saline controls. Our results show that as with young rats, chronic lithium can substantially increase LTP and the number of BrdU(+) cells in the aged rats. However, neurogenesis, assessed by colocalization of NeuN and BrdU, was not detected in the aged rat DG subjected to chronic lithium treatment. Therefore, it is concluded that the increase in LTP and the number of BrdU(+) cells might not be associated with increases in neurogenesis in the granule cell layer of the DG. Lithium might has a beneficial effects through other signaling pathways in the aged brain.
Revue / Journal Title
Biochemical and biophysical research communications (Biochem. biophys. res. commun.) ISSN 0006-291X CODEN BBRCA9
Source / Source
2003, vol. 303, no4, pp. 1193-1198 [6 page(s) (article)]
Lithium has been used for over 100 years to treat depression and is now being touted as a new "life-enhancement" drug (Source (http://www.life-enhancement.com/LE/article_template.asp?ID=1675)). It is also interesting that another mood stabilizing drug, the anti-epileptic drug Valproate also stimulates neurogenesis.
http://www.jneurosci.org/cgi/content/full/24/29/6590
Mood Stabilizer Valproate Promotes ERK Pathway-Dependent Cortical Neuronal Growth and Neurogenesis
Yanlei Hao,1 Thomas Creson,1 Lei Zhang,1 Pipeng Li,1 Fu Du,2 Peixiong Yuan,1 Todd D. Gould,1 Husseini K. Manji,1 and Guang Chen1
1Laboratory of Molecular Pathophysiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892-4405, and 2FD NeuroTechnologies, Ellicott City, Maryland 21041
Manic-depressive illness has been conceptualized as a neurochemical illness. However, brain imaging and postmortem studies reveal gray-matter reductions, as well as neuronal and glial atrophy and loss in discrete brain regions of manic-depressive patients. The roles of such cerebral morphological deficits in the neuropathophysiology and therapeutic mechanisms of manic-depressive illness are unknown. Valproate (2-propylpentanoate) is a commonly used mood stabilizer. The ERK (extracellular signal-regulated kinase) pathway is used by neurotrophic factors to regulate neurogenesis, neurite outgrowth, and neuronal survival. We found that chronic treatment of rats with valproate increased levels of activated phospho-ERK44/42 in neurons of the anterior cingulate, a region in which we found valproate-induced increases in expression of an ERK pathway-regulated gene, bcl-2. Valproate time and concentration dependently increased activated phospho-ERK44/42 and phospho-RSK1 (ribosomal S6 kinase 1) levels in cultured cortical cells. These increases were attenuated by Raf and MEK (mitogen-activated protein kinase/ERK kinase) inhibitors. Although valproate affects the functions of GSK-3 (glycogen synthase kinase-3) and histone deacetylase (HDAC), its effects on the ERK pathway were not fully mimicked by selective inhibitors of GSK-3 or HDAC. Similar to neurotrophic factors, valproate enhanced ERK pathway-dependent cortical neuronal growth. Valproate also promoted neural stem cell proliferation-maturation (neurogenesis), demonstrated by bromodeoxyuridine (BrdU) incorporation and double staining of BrdU with nestin, Tuj1, or the neuronal nuclei marker NeuN (neuronal-specific nuclear protein). Chronic treatment with valproate enhanced neurogenesis in the dentate gyrus of the hippocampus. Together, these data demonstrate that valproate activates the ERK pathway and induces ERK pathway-mediated neurotrophic actions. This cascade of events provides a potential mechanism whereby mood stabilizers alleviate cerebral morphometric deficits associated with manic-depressive illness.
Key words: valproate; ERK; neurite outgrowth; neurogenesis; mania; mood disorders
It seems that Prozac (another anti-depressive drug) stimulates neurogenesis in the brain:
http://www.sciam.com/article.cfm?articleID=000E44B7-2B2F-1514-A59B83414B7F0133
September 25, 2006
Does Sprouting New Brain Cells Cure Depression?
By JR Minkel
Article Tools E-mail ArticleE-mail Print ViewPrint LinkLink RSSRSS del.icio.usdel.icio.us diggDigg
Science Image: depression
Image: © BROOKE FASANI/CORBIS
In recent years, researchers have discovered tantalizing evidence that antidepressants combat depression by promoting neurogenesis, the growth of new neurons in the brain. The evidence derives from several striking observations. One is that stressed monkeys grow fewer new cells in the hippocampus region of the brain than their healthy counterparts do. Secondly, most depression treatments, from drugs such as Prozac to a type of powerful magnetic stimulation, increase new neuron growth by up to 75 percent in rodents.
And in the most telling study to date, scientists from Columbia University and Yale University directed radiation at the hippocampi of mice to prevent neurogenesis. When given fluoxetine, also known as Prozac, the mice exhibited none of the behavioral changes normally associated with the drug. If neurogenesis is required to kick depression, as the result suggested, maybe its loss sends the mind into a tailspin. "It's a very appealing idea," comments Eric Nestler of the University of Texas Southwestern Medical Center at Dallas. "It provides a mechanism to explain why many cases of depression are chronic and progressive." It would also explain why Prozac takes a few weeks to exert its effects. The growth of neurons from stem cells takes a few weeks as well.
<more>
This is a fascinating field. I wonder if lithium will reverse the deleterious effects of sleep restriction on neurogenesis. Of course, my interest in this area is prompted by our proposal to use lithium to try to enhance regeneration in the spinal cord.
Wise.