The impact of early environmental interventions on structural plasticity of the axon initial segment in neocortex. Issue 1 (30th July 2016)

• Record Type: Journal Article
• Authors: Nozari, Masoumeh; Suzuki, Toshimitsu; Rosa, Marcello G. P.; Yamakawa, Kazuhiro; Atapour, Nafiseh
• Is Part Of: Developmental psychobiology. Volume 59:Issue 1(2017)
• Page Start: 39
• Page End: 47
• Publication Date: 2016-07-30
• Subjects: axon initial segment -- enriched environment -- NMDA receptor antagonist -- plasticity -- schizophrenia; Psychobiology -- Periodicals; 155
• DOI: 10.1002/dev.21453
• Languages: English
• ISSNs: 0012-1630

Abstract

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.