Video Experimental Relacionado
Updated: Feb 13, 2026
06:09
Transplantation of Chemogenetically Engineered Cortical Interneuron Progenitors into Early Postnatal Mouse Brains
Published on: August 26, 2019
6.5K
La muerte celular intrínsecamente determinada de las interneuronas corticales en desarrollo
Derek G Southwell1, Mercedes F Paredes, Rui P Galvao
1Neuroscience Graduate Program, University of California, San Francisco, California 94143, USA. dereksouthwell@gmail.com
Nature
|October 9, 2012
Resumen
Los números de interneuronas corticales están determinados por factores intrínsecos, no por señales externas. Alrededor del 40% de estas neuronas secretoras de ácido γ-aminobutírico (GABA) sufren muerte celular programada durante el desarrollo.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Biología del desarrollo Biología del desarrollo.
- Biología celular Biología celular.
Sus antecedentes:
- Los circuitos inhibidores corticales dependen de las interneuronas secretoras de ácido γ-aminobutírico (GABA) que se originan en el cerebro anterior ventral.
- Los mecanismos que determinan el número final de interneuronas corticales, a pesar de sus orígenes de desarrollo distantes, siguen sin estar claros.
- La hipótesis neurotrófica sugiere sobreproducción y posterior eliminación a través de la competencia por señales tróficas externas.
Objetivo del estudio:
- Para investigar la muerte celular del desarrollo de las interneuronas corticales de ratón.
- Para determinar si la supervivencia de las interneuronas está regulada por factores tróficos extrínsecos o por mecanismos intrínsecos.
- Explorar el papel de Bax y TrkB en la supervivencia de las interneuronas y la regulación de la población.
Principales métodos:
- Estudios in vivo e in vitro del desarrollo de las interneuronas corticales en ratones.
- Experimentos de trasplante para evaluar la supervivencia y muerte celular en diferentes condiciones.
- Análisis de la apoptosis dependiente de Bax y las vías de señalización de TrkB.
Principales resultados:
- Aproximadamente el 40% de las interneuronas corticales en desarrollo se someten a apoptosis Bax-dependiente postnatalmente.
- Los precursores de interneuronas trasplantados en la corteza o cultivados in vitro exhibieron muerte celular en tiempos de desarrollo similares.
- Las tasas de muerte celular fueron constantes en un rango de 200 veces el tamaño de los trasplantes y no se vieron afectadas por la interrupción de TrkB.
- El trasplante aumentó el número de interneuronas, pero no aumentó proporcionalmente la frecuencia de los eventos sinápticos inhibidores.
Conclusiones:
- La muerte celular de las interneuronas corticales parece estar determinada intrínsecamente, ya sea de forma celular autónoma o a través de la competencia a nivel de población entre las interneuronas.
- Las señales tróficas extrínsecas no parecen ser los principales reguladores de la supervivencia de las interneuronas.
- Los hallazgos desafían la hipótesis neurotrófica tradicional para el control de la población de interneuronas.
Videos de Conceptos Relacionados
02:18Intrinsically Disordered Proteins
19.6K
Intrinsically disordered proteins are a group of proteins that do not fold into specific three-dimensional structures. Their structural flexibility allows them to complement ordered proteins to perform functions that are inaccessible to rigid structures. They are more common in eukaryotes than prokaryotes and may either be exclusively intrinsically disordered or hybrid proteins, consisting of a mix of ordered and disordered regions. The absence of a rigid structure in these proteins can be...
19.6K
02:18Intrinsically Disordered Proteins
2.9K
No description available
2.9K
01:18Autophagic Cell Death
4.6K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.6K
01:30Overview of Cell Death
10.2K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
10.2K
01:20Extrinsic and Intrinsic Pathways of Hemostasis
13.2K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
13.2K
01:31The Intrinsic Apoptotic Pathway
8.7K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
8.7K