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The Journal of Neuroscience, May 2, 2007, 27(18):4929-4934; doi:10.1523/JNEUROSCI.5342-06.2007

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Brief Communications
Conversion of Functional Synapses into Silent Synapses in the Trigeminal Brainstem after Neonatal Peripheral Nerve Transection

Fu-Sun Lo and Reha S. Erzurumlu

Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Correspondence should be addressed to Dr. Reha S. Erzurumlu, Department of Anatomy and Neurobiology, University of Maryland, School of Medicine, 20 Penn Street, Health Science Facility II S251, Baltimore, MD 21201. Email: rerzu001{at}umaryland.edu

One of the major consequences of neonatal infraorbital nerve damage is irreversible morphological reorganization in the principal sensory nucleus (PrV) of the trigeminal nerve in the brainstem. We used the voltage-clamp technique to study synaptic transmission in the normal and the denervated PrV of neonatal rats in an in vitro brainstem preparation. Most of the synapses in the PrV are already functional at birth. Three days after peripheral deafferentation, functional synapses become silent, lacking AMPA receptor-mediated currents. Without sensory inputs from the whiskers, silent synapses persist through the second postnatal week, indicating that the maintenance of AMPA receptor function depends on sensory inputs. High-frequency (50 Hz) electrical stimulation of the afferent pathway, which mimics sensory input, restores synaptic function, whereas low-frequency (1 Hz) stimulation has no effect. Application of glycine, which promotes AMPA receptor exocytosis, also restores synaptic function. Therefore, normal synaptic function in the developing PrV requires incoming activity via sensory afferents and/or enhanced AMPA receptor exocytosis. Sensory deprivation most likely results in AMPA receptor endocytosis and/or lateral diffusion to the extrasynaptic membrane.

Key words: synaptic plasticity; AMPA receptors; NMDA receptors; principal sensory nucleus; infraorbital nerve; barrelettes

Received Dec. 11, 2006; revised April 4, 2007; accepted April 9, 2007.

Correspondence should be addressed to Dr. Reha S. Erzurumlu, Department of Anatomy and Neurobiology, University of Maryland, School of Medicine, 20 Penn Street, Health Science Facility II S251, Baltimore, MD 21201. Email: rerzu001{at}umaryland.edu






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