title: Slow synaptic inhibition in nucleus HVc of the adult zebra finch.
abstract: Nervous systems process information over a broad range of time scales and thus need corresponding cellular mechanisms spanning that range. In the avian song system, long integration times are likely necessary to process auditory feedback of the bird's own vocalizations. For example, in nucleus HVc, a center that contains both auditory and premotor neurons and that is thought to act as a gateway for auditory information into the song system, slow inhibitory mechanisms appear to play an important role in the processing of auditory information. These long-lasting processes include inhibitory potentials thought to shape auditory selectivity and a vocalization-induced inhibition of auditory responses lasting several seconds. To investigate the possible cellular mechanisms of these long-lasting inhibitory processes, we have made intracellular recordings from HVc neurons in slices of adult zebra finch brains and have stimulated extracellularly within HVc. A brief, high-frequency train of stimuli (50 pulses at 100 Hz) could elicit a hyperpolarizing response that lasted 2-20 sec. The slow hyperpolarization (SH) could still be elicited in the presence of glutamate receptor blockers, suggesting that it does not require polysynaptic excitation. Three major components contribute to this activity-induced SH: a long-lasting GABAB receptor-mediated IPSP, a slow afterhyperpolarization requiring action potentials but not Ca2+ influx, and a long-lasting IPSP, the neurotransmitter and receptor of which remain unidentified. These three slow hyperpolarizing events are well placed to contribute to the observed inhibition of HVc neurons after singing and could shape auditory feedback during song learning.
authors.affiliation: Division of Biology, California Institute of Technology, Pasadena, California 91125, USA.
authors.forename: M F
authors.initials: MF
authors.lastname: Schmidt
authors.forename: D J
authors.initials: DJ
authors.lastname: Perkel
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000161:Acoustic Stimulation; D000200:Action Potentials / Q000502:physiology; D000367:Age Factors; D000818:Animals; D001306:Auditory Pathways / Q000737:chemistry / Q000166:cytology / Q000502:physiology*; D001418:Baclofen / Q000494:pharmacology; D001717:Birds / Q000502:physiology*; D002104:Cadmium / Q000494:pharmacology; D005072:Evoked Potentials, Auditory / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D007858:Learning / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009943:Organophosphorus Compounds / Q000494:pharmacology; D011963:Receptors, GABA-A / Q000502:physiology; D018080:Receptors, GABA-B / Q000502:physiology; D013569:Synapses / Q000737:chemistry / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D014828:Vocalization, Animal / Q000502:physiology*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D018756:GABA Antagonists; D009943:Organophosphorus Compounds; D011963:Receptors, GABA-A; D018080:Receptors, GABA-B; D002104:Cadmium; D013779:Tetrodotoxin; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D015763:2-Amino-5-phosphonovalerate; C066430:CGP 35348; D001418:Baclofen