Stress and hippocampal neurogenesis

Gould, Elizabeth; Tanapat, Patima

doi:10.1016/s0006-3223(99)00247-4

Cited by 707 publications

(420 citation statements)

References 52 publications

Supporting

Mentioning

386

Contrasting

Unclassified

Order By: Relevance

“…Nous avons par la suite caractérisé le phénotype de ces nouveaux neurones et trouvé qu'ils exprimaient la GAD67 (glutamic acid decarboxylase 67), enzyme de synthèse du GABA. Les données recueillies en microscopie confocale ont mis en évidence une colocalisation des deux marqueurs BrdU et GAD67 ( Figure 3C) présentes en bordure du IV e ventricule ou encore de certains types d'astrocytes capables de se dédifférencier [26,27]. Une autre piste se dessine également : des progéniteurs pourraient migrer de la zone sous-ventriculaire jusqu'aux NV, en se déplaçant éventuellement le long de vaisseaux sanguins [28,29].…”

Section: Naissance Et Intégration De Nouveaux Neurones Dans Les Noyauunclassified

“…Dans une étude récente, nous avons également observé que les glucocorticoïdes, connus pour entraver la neurogenèse [27], étaient régulés négativement dans les NV après NVU [28]. Ces résultats sont à rapprocher de données de la littérature mentionnant le rôle de ces facteurs respectifs dans la modulation des différentes étapes de la neurogenèse, allant de la prolifération des cellules souches neurales jusqu'à leur différencia-tion et intégration dans des circuits neuronaux complexes [8,[29][30][31].…”

Section: Revuesunclassified

See 1 more Smart Citation

Une nouvelle zone de neurogenèse fonctionnelle

2011

View full text Add to dashboard Cite

> En dehors de deux structures précises : la zone sous-granulaire et la zone sous-ventriculaire, le cerveau du mammifère adulte est considéré comme non neurogène, c'est-à-dire incapable de produire de nouveaux neurones. Cependant, les influences environnementales qui s'opposent à cette activité peuvent être mises entre parenthèses dans certaines conditions. C'est ce qui se passe lorsque l'on réalise une neurectomie vestibulaire unilatérale chez le chat adulte. Nos travaux révèlent en effet l'existence d'une neurogenèse réactionnelle dans les noyaux vestibulaires désafférentés situés dans le tronc cérébral. Plus étonnant encore, nous avons montré que cette prolifération cellulaire postlésionnelle était fonctionnelle et participait aux processus de restauration des fonctions posturolocomotrices. < SNC du mammifère adulte. Toutefois, à ce jour, seulement deux structures bien précises, la zone sous-granulaire du gyrus dentelé de l'hippocampe et la zone sous-ventriculaire qui borde les ventricules latéraux, renouvellent continuellement leur stock de neurones (Figure 1). Ces zones sont dites de neurogenèse car elles génèrent de nouveaux neurones [39]. La grande majorité d'entre eux survit et s'intègre ensuite dans des circuits neuronaux qui contribuent à la transmission de l'information dans le cerveau : tâches d'apprentissage, de mémorisation, d'orientation spatiale, ou encore de reconnaissance olfactive [1]. Par contraste, tout le reste du SNC est considéré comme étant non neurogène car les progéniteurs neuraux potentiellement présents sont maintenus dans un état de quiescence. L'environnement ne permet pas la prolifération, la survie et la différenciation cellulaires. Ainsi, des progéniteurs neuraux de la zone sous-granulaire ou de la zone sousventriculaire transplantés dans des zones non neurogènes meurent ou s'y différencient uniquement en cellules gliales [2][3][4]. En revanche, lorsque des progéniteurs provenant de n'importe quelle région du SNC sont transplantés dans des zones de neurogenèse, ils s'y différencient selon le type neuronal requis par le tissu hôte, neurones granulaires dans la zone sous-granulaire et interneurones dans la zone sous-ventriculaire [3][4][5][6]. Il apparaît donc que le devenir des progéniteurs neuraux au sein de leur tissu hôte est avant tout commandité par l'environnement extracellulaire, au détriment des paramètres intrinsèques aux cellules [7,8]. De manière intéressante, les influences qui semblent s'opposer à la neurogenèse dans la quasi-totalité du SNC pourraient être ponctuellement mises entre parenthèses dans certaines conditions. En effet, de nombreux travaux chez le mammifère adulte ont révélé que des pathologies particulières (ischémie, scléroses multiples, Le renouvellement des neurones dans le cerveau adulteAu même titre que les cellules intestinales ou sanguines, de nouveaux neurones sont capables d'être générés tout au long de la vie au sein de leur tissu d'appartenance. Ainsi, contrairement au dogme érigé en 1928 par Ramon y Cajal 1 : « Une fois le développement term...

show abstract

Section: Naissance Et Intégration De Nouveaux Neurones Dans Les Noyauunclassified

Section: Revuesunclassified

Une nouvelle zone de neurogenèse fonctionnelle

2011

View full text Add to dashboard Cite

show abstract

“…[141][142][143] Furthermore, chronic stress and glucocorticoids induce neural atrophy in limbic structures, mainly the hippocampus, and reduce cell proliferation and neurogenesis in the hippocampus. [144][145][146][147][148][149][150] These changes have been related to the development of depression, including the cognitive symptoms of this disorder. 151 Antidepressants can increase GR function and expression 140 and normalization of the HPA axis could be important for clinical improvement and prediction of relapse.…”

Section: Stressmentioning

confidence: 99%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

View full text Add to dashboard Cite

In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

show abstract

“…Alternatively, and considering that physical and psychological stress lead to a decrease in hippocampal cell proliferation and neurogenesis [51][52][53], rewarded running may pose a 'stressful' situation, in which running is no more performed on a strictly voluntary basis.…”

Section: Running For a Rewardmentioning

confidence: 99%

A reward increases running-wheel performance without changing cell proliferation, neuronal differentiation or cell death in the dentate gyrus of C57BL/6 mice

Klaus

Hauser

Slomianka

et al. 2009

Behavioural Brain Research

View full text Add to dashboard Cite

A reward increases running-wheel performance without changing cell proliferation, neuronal differentiation or cell death in the dentate gyrus of C57BL/6 mice Klaus, F; Hauser, T; Slomianka, L; Amrein, I; Lipp, H P Klaus, F; Hauser, T; Slomianka, L; Amrein, I; Lipp, H P (2009). A reward increases running-wheel performance without changing cell proliferation, neuronal differentiation or cell death in the dentate gyrus of C57BL/6 mice. A reward increases running-wheel performance without changing cell proliferation, neuronal differentiation or cell death in the dentate gyrus of C57BL/6 mice Abstract Exercise is one of the best-known stimulators of adult hippocampal neurogenesis, but it is not known if voluntary changes in the intensity of exercise are accompanied by changes in neurogenesis. In this study we investigated whether a reward influences the performance in a running wheel and the rate of cell proliferation, neuronal differentiation and cell death in C57BL/6 mice. Mice had free access to a running wheel during the first week of the experiment. In the second week, animals were rewarded for their performance and compared to normal voluntary running and control mice. A reward significantly increased the performance by 78% when compared to the non-rewarded performance of the first week.The performance of the non-rewarded runners remained relatively constant. Fourteen days of exercise significantly increased cell proliferation by 27% and the number of doublecortin immunoreactive cells by 46%. A reward and the associated increase of performance did not modulate proliferation, cell death or the number of cells entering the neuronal lineage. We suggest that, in C57BL/6 mice, either exercise increases adult hippocampal neurogenesis to a ceiling value, which is reached by a performance at or below the level achieved by voluntary wheel running, or that a possible positive effect of increased running-wheel activity is balanced by stress resulting from rewarded running, which is no longer performed on a strictly voluntary basis. We suggest that, in C57BL/6 mice, either exercise increases adult hippocampal neurogenesis to a ceiling value, which is reached by a performance at or below the level achieved by voluntary wheel running, or that a possible positive effect of increased is balanced by stress resulting from rewarded running, which is no longer performed on a strictly voluntary basis.

show abstract

Stress and hippocampal neurogenesis

Cited by 707 publications

References 52 publications

Une nouvelle zone de neurogenèse fonctionnelle

Une nouvelle zone de neurogenèse fonctionnelle

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

A reward increases running-wheel performance without changing cell proliferation, neuronal differentiation or cell death in the dentate gyrus of C57BL/6 mice

Contact Info

Product

Resources

About