Neurexin-neuroligin transsynaptic interaction mediates learning-related synaptic remodeling and long-term facilitation in aplysia.
Neuron
; 70(3): 468-81, 2011 May 12.
Article
em En
| MEDLINE
| ID: mdl-21555073
Neurexin and neuroligin, which undergo heterophilic interactions with each other at the synapse, are mutated in some patients with autism spectrum disorder, a set of disorders characterized by deficits in social and emotional learning. We have explored the role of neurexin and neuroligin at sensory-to-motor neuron synapses of the gill-withdrawal reflex in Aplysia, which undergoes sensitization, a simple form of learned fear. We find that depleting neurexin in the presynaptic sensory neuron or neuroligin in the postsynaptic motor neuron abolishes both long-term facilitation and the associated presynaptic growth induced by repeated pulses of serotonin. Moreover, introduction into the motor neuron of the R451C mutation of neuroligin-3 linked to autism spectrum disorder blocks both intermediate-term and long-term facilitation. Our results suggest that activity-dependent regulation of the neurexin-neuroligin interaction may govern transsynaptic signaling required for the storage of long-term memory, including emotional memory that may be impaired in autism spectrum disorder.
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Base de dados:
MEDLINE
Assunto principal:
Células Receptoras Sensoriais
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Moléculas de Adesão Celular Neuronais
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Potenciação de Longa Duração
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Receptores de Superfície Celular
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Proteínas de Membrana
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Neurônios Motores
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Proteínas do Tecido Nervoso
Idioma:
En
Ano de publicação:
2011
Tipo de documento:
Article