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BrdU (rojo), un marcador de replicación de ADN, resalta la neurogenesis en la zona subgranular del giro dentado del hipocampo. Fragmento de una ilustración de Faiz et al., 2005.[1]​


La neurogénesis (nacimiento de nuevas neuronas) es el proceso por medio el cual se generan nuevas neuronas a partir de células madre neurales y células progenitoras.[2]​ La neurogénesis está más activa durante el desarrollo prenatal, y es responsable por poblar con neuronas el cerebro en crecimiento. Recientemente, se ha demostrado que la neurogénesis continúa en dos partes del cerebro adulto de mamíferos: el hipocampo y la zona subventricular. Algunos estudios han mostrado que la testosterona en vertebrados, y la prohormona ecdisona en insectos, influyen en la velocidad de neurogénesis.

Presencia en adultos

Expresión de la proteína doblecortina en el giro dentado del cerebro de la rata, día 21 postnatal. Oomen et al., 2009.[3]​


Durante la adultez hay un constante nacimiento de nuevas neuronas mayormente en dos regiones del cerebro:

Muchas de las células recién nacidas mueren poco después de haber nacido,[6]​ aunque una cierta algunas de ellas se vuelven funcionales dentro del tejido cerebral circundante.[7]​[8]​[9]​

La neurogénesis en adultos es un ejemplo de una teoría científica ampliamente aceptada siendo estudiada a mayor detalle. Los primeros neuroanatomisas, incluyendo a Santiago Ramón y Cajal, consideraban que el sistema nervioso no sufría cambios y era incapaz de regenerarse. La primera evidencia de neurogénesis en mamíferos adultos en la corteza cerebral fue presentada por Joseph Altman en 1962,[10]​ seguido por el descubrimiento de neurogénesis en adultos en el giro dentado del hipocampo en 1963.[11]​ En 1969, Joseph Altman descubrió e identificó al sistema migratorio rostral como la fuente de las células granulosas generadas en adultos en el bulbo olfatorio.[12]​ Hasta la década de 1980, la comunidad científica ignoró estos descubrimientos a pesar de haberse demostrado de manera directa en estudios previos, esto es, por medio de la técnica autoradiografía con timidina tritiada. Para entonces, Shirley Bayer[13]​[14]​ (junto con Michael Kaplan) demostraron nuevamente que existe neurogénesis en mamíferos adultos (ratas), y Nottebohm demostró este fenómeno en aves[15]​ generan mayor interés en el tema. Estudios en la década de 1990[16]​[17]​ finalmente puso a la investigación en neurogénesis en adultos en la mira de la comunidad científica. A principios de la misma década se demostró la neurogénesis en el hipocampo de primates no humanos así como en humanos.[18]​[19]​ Recientemente, también ha sido caracterizada la neurogénesis en el cerebelo de conejos adultos.[20]​ Más adelante, algunos autores (particularme Elizabeth Gould) sugirieron que la neurogénesis en adultos podría también tener lugar en regiones del cerebro que generalmente no se asociaban con neurogénesis incluyendo el neocórtex.[21]​[22]​[23]​ Sin embargo, otros[24]​ han cuestionado la evidencia científica y los métodos de estos descubrimientos, argumentando que las células nuevas podrían ser de origen glial. Investigaciones recientes han dilucidado el efecto regulador de GABA en las células madre neurales. Los efectos inhibidores de GABA en el cerebro también afectan a las vías de señalización de las células madre para que estas entren en estado quiescente. Se ha encontrado que el Diazepam o Valium tiene efectos similares.[25]​

Su papel en el aprendizaje

La relevancia funcional de la neurogénesis en adultos es incierta,[26]​ aunque existe evidencia de que la neurogénesis en mamíferos adultos es importante para el proceso de aprendizaje y formación de memoria.[27]​ Múltiples mecanismos que relacionan un incremento en la neurogénesis con una mejora en los procesos cognitivos han sido propuestos, incluyendo modelos computacionales que demuestran que un incremento en el número de neuronas aumenta la capacidad de memoria,[28]​ disminuye la interferencia entre memorias,[29]​ o agrega información temporal a las memorias.[30]​ Los experimentos diseñados para probar que no existe neurogénesis en adultos ha sido inconclusa, pero algunos estudios han propuesto algunos tipos de aprendizaje dependientes de neurogénesis,[31]​ y otros en los que no se observa relación.[32]​ Ciertos estudios han mostrado que el acto de aprender por sí mismo está asociado a un aumento en la supervivencia de neuronas.[33]​ Sin embargo, en general, los descubrimientos que apuntan a que la neurogénesis es importante para cualquier tipo de aprendizaje son ambigüos.

Enfermedad de Alzheimer

Algunos estudios han sugerido que la disminución de neurogénesis en el hipocampo puede llevar al desarrollo de la enfermedad de Alzheimer. A pesar de esto, otros han formulado hipótesis de que los pacientes de la enfermedad de Alzheimer presentan un aumento en la neurogénesis en la región CA1 (cornus ammonis o cuerno de Ammon) del hipocampo, la cual es la región del hipocampo más afectada en la enfermedad de alzheimer, para compensar la pérdida de neuronas.[34]​ Pese a que la verdadera naturaleza de la relación entre la neurogénesis y la enfermedad de Alzheimer es desconocida, la neurogénesis estimulada por el factor de crecimiento insulínico tipo 1 produce grandes cambios en la plasticidad hipocampal y parece estar involucrada en la patología del Alzheimer.[35]​ La alopregananolona, un neuroesteroide o esteroide neuroactivo, ayuda a la neurogénesis en el cerebro. Los niveles de alopregnanolona en el cerebro disminuyen durante la vejez y en la enfermedad de Alzheimer.[36]​ Se ha demostrado que el aumento de alopregnanolona revierte la disminución de neurogénesis para revertir el deterioro cognitivo en los modelos de Alzheimer en ratón.[37]​ Se ha demostrado que los receptores Eph o receptores de efrina y la señalización de efrinas regulan la neurogénesis en el hipocampo de adultos y se están estudiando como posibles blancos para taratar algunos síntomas de la enfermedad de alzheimer.[38]​ Se ha visto que las moléculas asociadas con el Alzheimer, incluyendo a la APOE, PS-1 y APP, Molecules associated with the pathology of AD, including ApoE, PS1 and APP, también impactan en la neurogénesis en el hipocampo de adultos.[39]​

Su papel en la esquizofrenia

Los estudios sugieren que las personas con esquizofrenia tienen un volumen hipocampal reducido, lo cual se cree que es causado por la reducción de neurogénesis adulta. De igual manera, este fenómeno podría ser la causa subyacente de muchos de los síntomas de la enfermedad. Además, varios artículos la deficiencia en la regeneración de neuronas se la atribuyen a cuatro genes, DTNBP1, NRG1, DISC1 y ERB4.[40]​ Es importante mencionar que, a diferencia de la enfermedad de Alzheimer, la esquizofrenia no se caracteriza por el detrimento de funciones neurales, sino por una tasa de neurogénesis y neuroplasticidad anormales. Por otra parte, los antipsicóticos han mostrado ser una forma prometedora de aumentar la tasa de neurogénesis.[41]​ Estos hallazgos le dan sentido a las similitudes que existen entre la depresión y la esquizofrenia puesto que estas dos enfermedades podrían estar biológicamente relacionadas. No obstante, se requiere que se lleven a cabo más investigaciones para dilucidar esta relación.[42]​

Implications for depression

Many now believe stress to be the most significant factor for the onset of depression, aside from genetics. As discussed above, hippocampal cells are sensitive to stress which can lead to decreased neurogenesis. This area is being considering more frequently when examining the causes and treatments of depression. Studies have shown that removing the adrenal gland in rats caused increased neurogenesis in the dentate gyrus.[43]​ The adrenal gland is responsible for producing cortisol in response to a stressor, a substance that when produced in chronic amounts causes the down regulation of serotonin receptors and suppresses the birth of neurons.[44]​ It was shown in the same study that administration of corticosterone to normal animals suppressed neurogenesis, the opposite effect.[43]​ The most typical class of antidepressants administered for this disease are selective serotonin reuptake inhibitors (SSRIs) [45]​ and their efficacy may be explained by neurogenesis. In a normal brain, an increases in serotonin causes suppression of the corticotropin-releasing hormone (CRH) through connection to the hippocampus. It directly acts on the paraventricular nucleus to decrease CRH release and down regulate noroepinephrine functioning in the locus coeruleus.[43]​ Because CRH is being repressed, the decrease in neurogenesis that is associated with elevated levels of it is also being reversed. This allows for the production of more brain cells, in particular at the 5-HT1a receptor in the dentate gyrus of the hippocampus which has been shown to improve symptoms of depression. It normally takes neurons approximately three to six weeks to mature,[46]​ which is approximately the same amount of time it takes for SSRIs to take effect. This correlation strengthens the hypothesis that SSRIs act through neurogenesis to decrease the symptoms of depression.

Effects of Stress

Adult-born neurons appear to have a role in the regulation of stress.[47]​[48]​ Studies have linked neurogenesis to the beneficial actions of specific antidepressants, suggesting a connection between decreased hippocampal neurogenesis and depression.[49]​[50]​ In a pioneer study, scientists demonstrated that the behavioral benefits of antidepressant administration in mice is reversed when neurogenesis is prevented with x-irradiation techniques.[51]​ In fact, newborn neurons are more excitable than older neurons due to a differential expression of GABA receptors.[cita requerida] A plausible model, therefore, is that these neurons augment the role of the hippocampus in the negative feedback mechanism of the HPA-axis (physiological stress) and perhaps in inhibiting the amygdala (the region of brain responsible for fearful responses to stimuli).Plantilla:Vague Indeed, suppression of adult neurogenesis can lead to an increased HPA-axis stress response in mildly stressful situations.[47]​ This is consistent with numerous findings linking stress-relieving activities (learning, exposure to a new yet benign environment, and exercise) to increased levels of neurogenesis, as well as the observation that animals exposed to physiological stress (cortisol) or psychological stress (e.g. isolation) show markedly decreased levels of newborn neurons. Interestingly, under chronic stress conditions, the elevation of newborn neurons by antidepressants improves the hippocampal-dependent control on the stress response; without newborn neurons, antidepressants are unable to restore the regulation of the stress response and recovery becomes impossible.[48]​

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.[52]​ 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.[53]​ 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 glucocorticoids. It was shown that two weeks of sleep deprivation acted as a neurogenesis-inhibitor, which was reversed after return of normal sleep and even shifted to a temporary increase in normal cell proliferation.[54]​ More precisely, when levels of corticosterone are elevated, sleep deprivation inhibits this process. Nonetheless, normal levels of neurogenesis after chronic sleep deprivation return after 2 weeks, with a temporary increase of neurogenesis.[55]​ While this is recognized, overlooked is the blood glucose demand exhibited during temporary diabetic hypoglycemic states. The American Diabetes Association amongst many documents the pseudosenilia and agitation found during temporary hypoglycemic states. Much more clinical documentation is needed to competently demonstrate the link between decreased hematologic glucose and neuronal activity and mood.

Possible Use in Treating Parkinson's Disease

Parkinson's disease is a neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra. Transplantation of fetal dopaminergic precursor cells has paved the way for the possibility of a cell replacement therapy that could ameliorate clinical symptoms in affected patients.[56]​ In recent years, scientists have provided evidence for the existence of neural stem cells with the potential to produce new neurons, particularly of a dopaminergic phenotype, in the adult mammalian brain.[57]​[58]​[59]​ Experimental depletion of dopamine in rodents decreases precursor cell proliferation in both the subependymal zone and the subgranular zone.[60]​ Proliferation is restored completely by a selective agonist of D2-like (D2L) receptors.[60]​ Neural stem cells have been identified in the neurogenic brain regions, where neurogenesis is constitutively ongoing, but also in the non-neurogenic zones, such as the midbrain and the striatum, where neurogenesis is not thought to occur under normal physiological conditions.[56]​ Newer research has shown that there in fact is neurogenesis in the striatum.[61]​ A detailed understanding of the factors governing adult neural stem cells in vivo may ultimately lead to elegant cell therapies for neurodegenerative disorders such as Parkinson's disease by mobilizing autologous endogenous neural stem cells to replace degenerated neurons.[56]​

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.[62]​ However, new born cells in aged animals are functionally integrated.[63]​ 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.[64]​

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 aging mice. The same study demonstrates an enhancement in learning of the "runner" (physically active) mice.[65]​[66]​ Recent research has shown that Insulin-like growth factor 1 may be the mediator of exercise-induced neurogenesis.[67]​ 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.[67]​ 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.[68]​ 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.

Regulation

Summary of the signalling pathways in the neural stem cell microenvironment.

Many factors may affect the rate of hippocampal neurogenesis. Exercise and an enriched environment have been shown to promote the survival of neurons and the successful integration of newborn cells into the existing hippocampus.[65]​[69]​[70]​[71]​ Another factor is central nervous system injury since neurogenesis occurs after cerebral ischemia,[72]​ epileptic seizures,[73]​ and bacterial meningitis.[74]​ On the other hand, conditions such as chronic stress and aging can result in a decreased neuronal proliferation.[75]​[76]​[77]​ 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.[27]​

Epigenetic regulation also plays a large role in neurogenesis. DNA methylation is critical in the fate-determination of adult neural stem cells in the subventricular zone for post-natal neurogenesis through the regulation of neuronic genes such as Dlx2, Neurog2, and Sp8. Many microRNAs such as miR-124 and miR-9 have been shown to influence cortical size and layering during development.[78]​

Adult neural stem cells

Artículo principal: Neural stem cell

Neural stem cells (NSCs) are the self-renewing, multipotent cells that generate the main phenotypes of the nervous system.

Effects of cannabinoids

Some studies have shown that the use of cannabinoids results in the growth of new nerve cells in the hippocampus from both embryonic and adult stem cells. In 2005 a clinical study of rats at the University of Saskatchewan showed regeneration of nerve cells in the hippocampus.[79]​ Studies have shown that a synthetic drug resembling THC, the main psychoactive ingredient in marijuana, provides some protection against brain inflammation, which might result in better memory at an older age. This is due to receptors in the system that can also influence the production of new neurons.[80]​ Nonetheless, a study directed at Rutgers University demonstrated how synchronization of action potentials in the hippocampus of rats was altered after THC administration. Lack of synchronization corresponded with impaired performance in a standard test of memory.[81]​ Recent studies indicate that a natural cannabinoid of cannabis, cannabidiol (CBD), increases adult neurogenesis while having no effect on learning. THC however impaired learning and had no effect on neurogenesis.[82]​ A greater CBD to THC ratio in hair analyses of cannabis users correlates with protection against gray matter reduction in the right hippocampus.[83]​ CBD has also been observed to attenuate the deficits in prose recall and visuo-spatial associative memory of those currently under the influence of cannabis,[84]​[85]​ implying neuroprotective effects against heavy THC exposure. Neurogenesis might play a role in its neuroprotective effects, but further research is required.

See also

References

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  79. ↑ Wen Jiang; Yun Zhang; Lan Xiao; Jamie Van Cleemput; Shao-Ping Ji; Guang Bai; Xia Zhang (1 de noviembre de 2005). «Cannabinoids promote embryonic and adult hippocampus neurogenesis and produce anxiolytic- and antidepressant-like effects». Journal of Clinical Investigation 115 (11): 3104-16. PMC 1253627. PMID 16224541. doi:10.1172/JCI25509. Consultado el 2 de marzo de 2011. 
  80. ↑ 11-19-2008 Ohio State study: Scientists are high on idea that marijuana reduces memory impairment. OSU.edu
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Notes

Plantilla:Development of nervous system Plantilla:Neurotrophinergics

[[Category:Neurobiology]] [[Category:Embryology of nervous system]] [[Category:Neuropsychology]] [[Category:Stem cells]]

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