Neuroligin-1 is required for normal expression of LTP and associative fear memory in the amygdala of adult animals

Neuroligin-1 is a potent trigger for the de novo formation of synaptic connections, and it has recently been suggested that it is required for the maturation of functionally competent excitatory synapses. Despite evidence for the role of neuroligin-1 in specifying excitatory synapses, the underlying...

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Published in:Proceedings of the National Academy of Sciences - PNAS 2008-07, Vol.105 (26), p.9087-9092
Main Authors: Kim, Juhyun, Jung, Sang-Yong, Lee, Yeon Kyung, Park, Sangki, Choi, June-Seek, Lee, C. Justin, Kim, Hye-Sun, Choi, Yun-Beom, Scheiffele, Peter, Bailey, Craig H, Kandel, Eric R, Kim, Joung-Hun
Format: Article
Language:English
Subjects:
Amygdala
Amygdala - cytology
Amygdala - metabolism
Animal memory
Animals
Autistic disorder
Behavioral neuroscience
Biological Sciences
Brain
Cell Adhesion Molecules, Neuronal
Cells
Fear - physiology
Gene expression
Ion Channel Gating
Long term potentiation
Male
Membrane Proteins - deficiency
Membrane Proteins - metabolism
Memory
Memory - physiology
Molecular structure
Nerve Tissue Proteins - deficiency
Nerve Tissue Proteins - metabolism
Neurons
Neurosciences
Pyramidal Cells - metabolism
Rats
Rats, Sprague-Dawley
Receptors, N-Methyl-D-Aspartate - metabolism
Synapses
Synaptic Transmission
Thalamus - metabolism
Viruses
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Summary:Neuroligin-1 is a potent trigger for the de novo formation of synaptic connections, and it has recently been suggested that it is required for the maturation of functionally competent excitatory synapses. Despite evidence for the role of neuroligin-1 in specifying excitatory synapses, the underlying molecular mechanisms and physiological consequences that neuroligin-1 may have at mature synapses of normal adult animals remain unknown. By silencing endogenous neuroligin-1 acutely in the amygdala of live behaving animals, we have found that neuroligin-1 is required for the storage of associative fear memory. Subsequent cellular physiological studies showed that suppression of neuroligin-1 reduces NMDA receptor-mediated currents and prevents the expression of long-term potentiation without affecting basal synaptic connectivity at the thalamo-amygdala pathway. These results indicate that persistent expression of neuroligin-1 is required for the maintenance of NMDAR-mediated synaptic transmission, which enables normal development of synaptic plasticity and long-term memory in the amygdala of adult animals.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.0803448105