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La exposición repetida a la cocaína in vivo facilita la inducción de LTP en las neuronas de dopamina del cerebro

Qing-song Liu¹, Lu Pu, Mu-ming Poo

¹Division of Neurobiology, Department of Molecular and Cell Biology, Helen Wills Neuroscience Institute, University of California, Berkeley, California 94720, USA. qsliu@berkeley.edu

|October 14, 2005

Resumen

La exposición repetida a la cocaína aumenta la plasticidad sináptica en las neuronas dopaminérgicas del área tegmental ventral (VTA) al reducir la inhibición del receptor GABA. Esto facilita la potenciación a largo plazo (LTP), ayudando potencialmente a la formación de la memoria asociada a las drogas.

Área de la Ciencia:

La neurociencia es la neurociencia.
Neurofarmacología y Neurofarmacología.
Investigación de adicciones Investigación de adicciones.

Sus antecedentes:

Las drogas de abuso alteran los circuitos neuronales, contribuyendo a la adicción.
La plasticidad sináptica de las neuronas de dopamina del área tegmental ventral (VTA) está implicada en las modificaciones del circuito inducidas por fármacos.

Objetivo del estudio:

Para investigar los efectos de la exposición repetida a la cocaína en la plasticidad sináptica en las neuronas de dopamina VTA de la rata.
Determinar el papel de la inhibición mediada por el receptor GABA (A) en los cambios sinápticos inducidos por la cocaína.

Principales métodos:

In vivo, la administración repetida de cocaína en ratas.
Las grabaciones electrofisiológicas en las rebanadas del cerebro medio para evaluar la potenciación a largo plazo (LTP) inducción.
Manipulación farmacológica de la actividad del receptor GABA (A) utilizando bicuculina, picrotoxina y diazepam.

Principales resultados:

La exposición repetida a la cocaína facilitó la inducción de LTP en las sinapsis excitatorias en las neuronas de dopamina del VTA.
Esta facilitación se relacionó con una reducción inducida por la cocaína en la inhibición mediada por el receptor GABA (A).
La inhibición GABAérgica mejorada impidió la LTP inducida por la cocaína, mientras que la inhibición reducida fue necesaria para su inducción en ratas ingenuas.
El tratamiento con cocaína disminuyó la amplitud de corriente sináptica mediada por GABA y aumentó la probabilidad de inicio de picos en las neuronas dopaminérgicas del VTA.

Conclusiones:

La exposición repetida a la cocaína aumenta la plasticidad sináptica en las neuronas dopaminérgicas del VTA.
La inhibición reducida del receptor GABA (A) es un mecanismo clave que subyace a esta mejora de la plasticidad.
La plasticidad sináptica VTA inducida por la cocaína puede desempeñar un papel en la formación de recuerdos asociados a las drogas.

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