Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors
- Input-specific synaptic plasticity in the amygdala is regulated by neuroligin-1 via postsynaptic NMDA receptors
- 정상용; 김주현; 권오빈; 정정훈; 안경만; 정아영; 이창준; 최윤범; Craig Bailey; Eric Kandel; 김정훈
- STD-LTP; thalamic pathway; cortical pathway; autism
- Issue Date
- Proceedings of the National Academy of Sciences of the United States of America
- VOL 107, NO 10, 4710-4715
- Despite considerable evidence for a critical role of neuroligin-1 in the
specification of excitatory synapses, the cellular mechanisms and
physiological roles of neuroligin-1 in mature neural circuits are
poorly understood. In mutant mice deficient in neuroligin-1, or adult
rats in which neuroligin-1 was depleted, we have found that
neuroligin-1 stabilizes the NMDA receptors residing in the postsynapticmembrane
ofamygdala principal neurons, whichallows for
a normal range of NMDA receptor-mediated synaptic transmission.
We observed marked decreases in NMDA receptor-mediated synaptic
currents at afferent inputs to the amygdala of neuroligin-1
knockout mice. However, the knockout mice exhibited a significant
impairment in spike-timing-dependent long-term potentiation
(STD-LTP) at the thalamic but not the cortical inputs to theamygdala.
Subsequent electrophysiological analyses indicated that STD-LTP in
the cortical pathway is largely independent of activation of postsynaptic
NMDA receptors. These findings suggest that neuroligin-1
can modulate, in a pathway-specific manner, synaptic plasticity in
the amygdala circuits of adult animals, likely by regulating the
abundance of postsynaptic NMDA receptors.
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