title: The impact of early environmental interventions on structural plasticity of the axon initial segment in neocortex.
abstract: Plasticity of the axon initial segment (AIS) is a newly discovered type of structural plasticity that regulates cell excitability. AIS plasticity has been reported to happen during normal development of neocortex and also in a few pathological conditions involving disruption of the inhibition/excitation balance. Here we report on the impact of early environmental interventions on structural plasticity of AIS in the mouse neocortex. C57BL/6 mice were raised in standard or enriched environment (EE) from birth up to the time of experiments and were injected with saline or MK-801 [N-Methyl-D-Aspartate (NMDA) receptor antagonist, 1 mg/kg] on postnatal days (P) 6-10. We used Ankyrin G immunoreactivity to mark the AIS of cortical neurons in two sub-regions of frontal cortex (frontal association area, FrA and secondary motor cortex, M2) and in the secondary visual cortex (V2). In 1-month-old mice, the mean AIS length differed between three areas, with the shortest AISs being observed in V2. Postnatal MK-801 or EE led to shortening of AIS only in the frontal areas. However, exposure to EE restored AIS shortening induced by MK-801. Chronic postnatal MK-801 results in structural plasticity of AIS exclusive to the frontal cortex. EE may modify underlying neuronal mechanisms resulting in restoration of AIS length.
authors.affiliation: Neuroscience Research Center, Neuropharmacology Institute, Kerman University of Medical Sciences, Kerman, Iran.
authors.forename: Masoumeh
authors.initials: M
authors.lastname: Nozari
authors.affiliation: Laboratory for Neurogenetics, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan.
authors.forename: Toshimitsu
authors.initials: T
authors.lastname: Suzuki
authors.affiliation: Neuroscience Program, Monash Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia.|Australian Research Council, Centre of Excellence for Integrative Brain Function, Monash University Node, Clayton, Victoria, Australia.
authors.forename: Marcello G P
authors.initials: MG
authors.lastname: Rosa
authors.affiliation: Laboratory for Neurogenetics, RIKEN Brain Science Institute, Wako-shi, Saitama, Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Yamakawa
authors.affiliation: Neuroscience Program, Monash Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australia.
authors.forename: Nafiseh
authors.initials: N
authors.lastname: Atapour
mesh_terms: D000818:Animals; D000071040:Axon Initial Segment / Q000187:drug effects / Q000502:physiology*; D016291:Dizocilpine Maleate / Q000008:administration & dosage / Q000494:pharmacology*; D004777:Environment; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D019579:Neocortex / Q000187:drug effects / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D016291:Dizocilpine Maleate
keywords: NMDA receptor antagonist; axon initial segment; enriched environment; plasticity; schizophrenia