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.
| Original language | English |
|---|---|
| Pages (from-to) | 39-47 |
| Number of pages | 9 |
| Journal | Developmental Psychobiology |
| Volume | 59 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 2017 |
Keywords
- Axon initial segment
- Enriched environment
- NMDA receptor antagonist
- Plasticity
- Schizophrenia
Cite this
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The impact of early environmental interventions on structural plasticity of the axon initial segment in neocortex. / Nozari, Masoumeh; Suzuki, Toshimitsu; Rosa, Marcello G. P.; Yamakawa, Kazuhiro; Atapour, Nafiseh.
In: Developmental Psychobiology, Vol. 59, No. 1, 01.2017, p. 39-47.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - The impact of early environmental interventions on structural plasticity of the axon initial segment in neocortex
AU - Nozari, Masoumeh
AU - Suzuki, Toshimitsu
AU - Rosa, Marcello G. P.
AU - Yamakawa, Kazuhiro
AU - Atapour, Nafiseh
PY - 2017/1
Y1 - 2017/1
N2 - 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.
AB - 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.
KW - Axon initial segment
KW - Enriched environment
KW - NMDA receptor antagonist
KW - Plasticity
KW - Schizophrenia
UR - http://www.scopus.com/inward/record.url?scp=84979735704&partnerID=8YFLogxK
U2 - 10.1002/dev.21453
DO - 10.1002/dev.21453
M3 - Article
AN - SCOPUS:84979735704
VL - 59
SP - 39
EP - 47
JO - Developmental Psychobiology
JF - Developmental Psychobiology
SN - 0012-1630
IS - 1
ER -