title: Effective sensory modality activating an escape triggering neuron switches during early development in zebrafish.
abstract: Developing nervous systems grow to integrate sensory signals from different modalities and to respond through various behaviors. Here, we examined the development of escape behavior in zebrafish [45-170 h postfertilization (hpf)] to study how developing sensory inputs are integrated into sensorimotor circuits. Mature fish exhibit fast escape upon both auditory/vestibular (AV) and head-tactile stimuli. Newly hatched larvae, however, do not respond to AV stimuli before 75 hpf. Because AV-induced fast escape in mature fish is triggered by a pair of hindbrain neurons known as Mauthner (M) cells, we studied functional development of the M-cell circuit accounting for late acquisition of AV-induced escape. In fast escape elicited by head-directed water jet, minimum onset latency decreased throughout development (5 ms at 45-59 hpf, 3 ms after 75 hpf). After 75 hpf, lesioning the otic vesicle (OV) to eliminate AV input resulted in loss of short-latency (<5 ms) fast escape, whereas ablation of the sensory trigeminal ganglion (gV) to block head-tactile input did not. Before 75 hpf, however, fast escape persisted after OV lesion but disappeared after gV ablation. Laser ablation of the M-cell and Ca²⁺ imaging of the M-cell during escape demonstrated that M-cell firing is required to initiate short-latency fast escapes at every developmental stage and further suggest that head-tactile input activates the M-cell before 75 hpf, but that after this point AV input activates the M-cell instead. Thus, a switch in the effective sensory input to the M-cells mediates the acquisition of a novel modality for initiating fast escape.
authors.affiliation: Division of Biological Sciences, Graduate School of Science, Nagoya University, Nagoya 464-8602, Japan. kohashi-t@bio.nagoyau.ac.jp
authors.forename: Tsunehiko
authors.initials: T
authors.lastname: Kohashi
authors.forename: Natsuyo
authors.initials: N
authors.lastname: Nakata
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Oda
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways / Q000254:growth & development* / Q000502:physiology; D000367:Age Factors; D000818:Animals; D030801:Animals, Genetically Modified; D001522:Behavior, Animal / Q000502:physiology; D051959:ELAV Proteins / Q000378:metabolism; D004924:Escape Reaction / Q000502:physiology*; D049452:Green Fluorescent Proteins / Q000235:genetics; D006257:Head / Q000294:innervation; D060850:LIM-Homeodomain Proteins / Q000235:genetics; D007814:Larva; D053685:Laser Therapy / Q000379:methods; D009474:Neurons / Q000502:physiology*; D009930:Organic Chemicals / Q000378:metabolism; D010812:Physical Stimulation; D011930:Reaction Time / Q000502:physiology; D018709:Statistics, Nonparametric; D013997:Time Factors; D014157:Transcription Factors / Q000235:genetics; D012668:Trigeminal Ganglion / Q000166:cytology / Q000254:growth & development; D014276:Trigeminal Nerve / Q000502:physiology; D014722:Vestibule, Labyrinth / Q000254:growth & development* / Q000293:injuries; D015027:Zebrafish
chemical_list: D051959:ELAV Proteins; D060850:LIM-Homeodomain Proteins; C403124:Oregon Green BAPTA-dextran; D009930:Organic Chemicals; D014157:Transcription Factors; C063843:insulin gene enhancer binding protein Isl-1; D049452:Green Fluorescent Proteins