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El análogo de la acetilcolina estimula la síntesis de ADN en las células derivadas del cerebro a través de subtipos

A Ashkenazi¹, J Ramachandran, D J Capon

¹Department of Molecular Biology, Genentech, Incorporated, South San Francisco, California 94080.

|July 13, 1989

Resumen

La acetilcolina estimula la síntesis de ADN en el desarrollo de las células gliales del cerebro a través de los receptores muscarínicos de acetilcolina (mAChR). La expresión del subtipo de receptor dicta la respuesta de proliferación, lo que sugiere un papel clave para la acetilcolina en la regulación del crecimiento de las células astrogliales.

Área de la Ciencia:

La neurociencia es la neurociencia.
Biología celular Biología celular.
Biología del desarrollo Biología del desarrollo.

Sus antecedentes:

La proliferación de células neuronales cesa temprano en el desarrollo del cerebro de los mamíferos.
La proliferación y diferenciación de las células gliales ocurren principalmente durante el período perinatal.
La señalización de acetilcolina, específicamente la hidrólisis de fosfoinositida (PI), alcanza sus picos en el cerebro perinatal.

Objetivo del estudio:

Para investigar si el carbacol, un análogo de la acetilcolina, puede inducir la síntesis de ADN celular en las células cerebrales perinatales.
Determinar el papel de los receptores muscarínicos de acetilcolina (mAChR) en la mediación de la proliferación celular inducida por el carbacol.
Explorar cómo la expresión del subtipo mAChR influye en la respuesta proliferativa a la acetilcolina.

Principales métodos:

Los astrocitos primarios del cerebro de rata perinatal fueron tratados con carbacol.
El efecto del carbacol en la síntesis del ADN se evaluó en varias líneas celulares derivadas del cerebro y en células del ovario del hámster chino (CHO) que expresan mAChRs recombinantes.
Se analizó la correlación entre la expresión del subtipo mAChR, la activación de la hidrólisis de PI y la síntesis de ADN.

Principales resultados:

El carbacol estimuló significativamente la síntesis de ADN en los astrocitos primarios de una manera dependiente de la edad.
El carbacol demostró efectos mitogénicos en las líneas celulares de astrocitoma, neuroblastoma y células CHO que expresan mAChRs.
La proliferación celular se correlacionó con la eficiencia de los subtipos de mAChR en la activación de la hidrólisis de PI.

Conclusiones:

La acetilcolina juega un papel crucial en la regulación del crecimiento de las células astrogliales durante el desarrollo del cerebro.
La especificidad de la proliferación celular inducida por la acetilcolina está determinada por la expresión de subtipos específicos de mAChR que activan la hidrólisis de PI.
Este estudio pone de relieve una nueva vía de señalización que regula la proliferación de células gliales en el cerebro en desarrollo de los mamíferos.

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