Maturation of synaptic transmission at end-bulb synapses of the cochlear nucleus.
Neurons of the avian nucleus magnocellularis transmit phase-locked action potentials of the auditory nerve in a pathway that contributes to sound localization based on interaural timing differences. We studied developmental changes in synaptic transmission that enable the end-bulb synapse to function as a synaptic relay. In chick, although the auditory system begins to function early in embryonic development, maturation of audition around the time of hatching suggested that synaptic transmission in the cochlear nucleus of young chicks may undergo further developmental changes. Synaptic physiology was investigated via patch-clamp recordings from bushy cells in brainstem slices during stimulation of auditory nerve fibers at 35 degrees C. Compared with embryonic synapses (embryonic day 18), post-hatch chicks (post-hatch days 1-11) exhibited high probability of firing a well timed postsynaptic action potential during high-frequency stimulation of the auditory nerve. Improvements in reliability and timing of postsynaptic spikes were accompanied by a developmental increase in steady-state EPSCs during stimulus trains and a decline in the extent of synaptic depression. Synchrony of EPSCs during stimulus trains improved with age. An increased pool of synaptic vesicles, lower release probability, larger and faster transmitter quanta, and reduced AMPA receptor desensitization contributed to these changes. Together, these factors improve the ability of cochlear nucleus magnocellularis neurons to faithfully transmit timing information encoded by the auditory nerve.
Brenowitz
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Neuroscience Training Program, University of Wisconsin, Madison, Wisconsin 53706, USA.
Trussell
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D000200:Action Potentials / Q000502:physiology; D000375:Aging / Q000502:physiology; D000818:Animals; D001306:Auditory Pathways / Q000196:embryology / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002642:Chick Embryo; D002645:Chickens; D003056:Cochlear Nerve / Q000502:physiology; D017626:Cochlear Nucleus / Q000196:embryology / Q000502:physiology*; D004558:Electric Stimulation / Q000379:methods; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D018755:GABA Agonists / Q000494:pharmacology; D058786:GABA-B Receptor Agonists; D018698:Glutamic Acid / Q000494:pharmacology; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D018697:Nootropic Agents / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D011760:Pyrrolidinones / Q000494:pharmacology; D018091:Receptors, AMPA / Q000187:drug effects / Q000378:metabolism; D018080:Receptors, GABA-B / Q000502:physiology; D012684:Sensory Thresholds / Q000502:physiology; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013572:Synaptic Vesicles / Q000187:drug effects / Q000378:metabolism
D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D058786:GABA-B Receptor Agonists; D018697:Nootropic Agents; D011760:Pyrrolidinones; D018091:Receptors, AMPA; D018080:Receptors, GABA-B; D018698:Glutamic Acid; C036466:aniracetam; D002118:Calcium