title: Switching of the transmitters that mediate hindbrain correlated activity in the chick embryo.
abstract: Widely propagating correlated neuronal activity is a hallmark of the developing nervous system. The activity is usually mediated by multiple transmitters, and the contribution of gap junctions has also been suggested in several systems. In some structures, such as the retina and spinal cord, it has been shown that the dominant transmitter mediating the correlated wave switches from acetylcholine to glutamate during development, although the functional significance of this phenomenon has not been clarified. An important question is whether such a transmitter switch occurs in other systems, especially in the brain. In the present study, we demonstrate that the major transmitter mediating correlated wave activity in the embryonic chick hindbrain changes from acetylcholine/gamma-aminobutyric acid (GABA)/glycine to glutamate/GABA as development proceeds. The results show for the first time that the dominant transmitter switches from acetylcholine to glutamate in a region other than the retina and spinal cord. This finding sheds more light on the role of nicotinic acetylcholine receptors in the generation of correlated wave activity, which is considered to regulate the development of the nervous system.
authors.affiliation: Department of Psychiatry, Graduate School and Faculty of Medicine, Kobe University, Kobe, Japan.
authors.forename: Hiraku
authors.initials: H
authors.lastname: Mochida
authors.forename: Katsushige
authors.initials: K
authors.lastname: Sato
authors.forename: Yoko
authors.initials: Y
authors.lastname: Momose-Sato
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D002450:Cell Communication / Q000502:physiology; D002642:Chick Embryo; D018680:Cholinergic Antagonists / Q000494:pharmacology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D009046:Motor Neurons / Q000378:metabolism; D009434:Neural Pathways / Q000196:embryology / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D018722:Nicotinic Agonists / Q000494:pharmacology; D010641:Phenotype; D012249:Rhombencephalon / Q000187:drug effects / Q000196:embryology / Q000378:metabolism*; D013331:Strychnine / Q000494:pharmacology; D009435:Synaptic Transmission / Q000502:physiology*; D014630:Vagus Nerve / Q000196:embryology / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D018680:Cholinergic Antagonists; D002800:Cholinesterase Inhibitors; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018377:Neurotransmitter Agents; D018722:Nicotinic Agonists; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D013331:Strychnine; D000109:Acetylcholine