Early and transient increase in spontaneous synaptic inputs to the rat facial motoneurons after axotomy in isolated brainstem slices of rats.
Section of motor nerve fibers (axotomy) elicits a variety of morphofunctional responses in the motoneurons in the motor nuclei. Later than the fifth post-operational day after section of the facial nerve, synapse elimination occurs in the facial motoneuron pool, leading to gradual abolishment of synaptic input-driven activities of the axotomized motoneurons. However, it remains unknown how the amount of synaptic input changes during this period between the axotomy and the synaptic elimination. Here we examined a hypothesis that axotomy of the motoneurons itself modifies the synaptic inputs to the motoneurons. One day after axotomy, the postsynaptic currents, mostly mediated by non-N-methyl-D-aspartic acid (non-NMDA) receptors, recorded from the axotomized facial motoneurons in the acute slice preparations of the rats were of higher frequency and larger amplitude than those in the intact motoneurons. This difference was not observed after the third post-operational day and appeared earlier than the changes in the electrophysiological properties and increase in the number of dead neurons in the axotomized motor nucleus. The larger postsynaptic current frequency of the axotomized motoneurons was observed both in the absence and in the presence of tetrodotoxin citrate, suggesting that increased excitability and facilitated release underlie the postsynaptic current frequency increase. These results suggest that synaptic re-organization occurs in the synapses of motoneurons at an early stage following axotomy.
Laboratory of Neurophysiology, Department of Neuroscience, Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo 105-8461, Japan.
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R
Ikeda
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F
Kato
D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn; D019771:Axotomy / Q000379:methods; D001933:Brain Stem / Q000166:cytology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D020220:Facial Nerve Injuries / Q000503:physiopathology*; D005260:Female; D007839:Functional Laterality; D007150:Immunohistochemistry / Q000379:methods; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques / Q000379:methods; D051381:Rats; D017208:Rats, Wistar; D026941:Sodium Channel Blockers / Q000494:pharmacology; D013266:Stilbamidines / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D016708:Synaptophysin / Q000378:metabolism; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D018691:Excitatory Amino Acid Antagonists; D026941:Sodium Channel Blockers; D013266:Stilbamidines; D016708:Synaptophysin; D013779:Tetrodotoxin; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione