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El derrame de glutamato suprime la inhibición mediante la activación de las mGluRs presinápticas

S J Mitchell¹, R A Silver

¹Department of Physiology, University College London, UK.

|April 13, 2000

Resumen

Los receptores metabotrópicos de glutamato (mGluR) en las terminales inhibidoras detectan el derrame de glutamato de las sinapsis excitatorias. Este derrame de glutamato inhibe la liberación de GABA, mejorando la eficacia de la señal excitatoria en el cerebro.

Área de la Ciencia:

La neurociencia es la neurociencia.
La plasticidad sináptica.
Modulación de la neurotransmisión.

Sus antecedentes:

Los receptores metabotrópicos de glutamato (mGluR) modulan la neurotransmisión, estudiados principalmente en las terminales excitatorias.
La función de los mGluRs en los terminales inhibidores sigue siendo en gran medida poco clara.
El glomérulo cerebeloso presenta una estrecha aposición de las terminales excitatorias inhibidoras GABAérgicas y glutamatérgicas.

Objetivo del estudio:

Investigar la activación de mGluR en los terminales inhibidores en el glomérulo cerebeloso.
Determinar el papel fisiológico de los mGluRs en la regulación de la liberación de GABA.
Elucidar el impacto de la actividad excitadora en la neurotransmisión inhibidora.

Principales métodos:

Registros electrofisiológicos en el glomérulo cerebeloso.
Estimulación de las fibras excitatorias del musgo.
Medición de las corrientes postsinápticas inhibidoras (IPSC).

Principales resultados:

El derrame de glutamato de las fibras de musgo excitatorio inhibe la liberación de GABA de las terminales celulares de Golgi a través de mGluRs presinápticas.
La inhibición de la liberación de GABA es dependiente de la frecuencia, alcanzando una depresión del 50% a 100 Hz.
La duración de la inhibición de la liberación de GABA se correlaciona con la actividad de la fibra de musgo.

Conclusiones:

Las mGluR en los axones de las interneuronas inhibidoras detectan la actividad de las sinapsis excitatorias vecinas.
Este mecanismo heterosináptico reduce localmente la inhibición, lo que potencialmente aumenta la eficacia de la fibra excitadora activa.
Los hallazgos revelan una nueva vía para regular la actividad del circuito neuronal a través de la comunicación intersináptica.

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