Developmental changes in activity-dependent plasticity of maturation-related neuronal phenotypes
- 1Department of System Neurophysiology, Wakayama Medical University , ,
Abstract
Immaturity of neurons in the adult hippocampal dentate gyrus (DG) has been implicated in the pathophysiology of neuropsychiatric disorders. Pseudo-immaturity of DG neurons can be induced by neuronal hyperexcitation in adulthood. This "dematuration," a reversal of maturation, could lead to aberrant neuronal maturation, if activated during development. However, it has not been directly tested whether dematuration can be induced in developing neurons. In the present study, we examined the effect of electroconvulsive treatment (ECT) on DG neurons of mice at several different developmental stages. Electrophysiological recordings were made using hippocampal slices. We analyzed frequency facilitation, a form of short-term synaptic plasticity, at the DG output mossy fiber synapses as an index of functional maturity of DG neurons. ECT had no significant effects on mossy fiber synaptic transmission at early postnatal ages, but it significantly reduced frequency facilitation at the postnatal age of ≥4 weeks, suggesting the induction of dematuration. Neuronal maturation marker analysis confirmed this result. The development of responsiveness to ECT was accompanied by maturation of N-methyl-D-aspartate receptor functions at the excitatory synaptic input onto DG neurons. Our results demonstrate that neuronal dematuration by ECT becomes inducible in postnatal 4 weeks in the DG of mice. Neuronal hyperexcitation such as seizures or alterations in N-methyl-D-aspartate receptor signaling around this developmental stage might affect proper maturation of DG neurons, thereby possibly increasing a risk of neuropsychiatric disorders.
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BibTeX
@article{kobayashi2026developmental,
title = {{Developmental changes in activity-dependent plasticity of maturation-related neuronal phenotypes}},
author = {Katsunori Kobayashi and Hiroki Imbe},
journal = {Frontiers in synaptic neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fnsyn.2026.1926357},
url = {https://europepmc.org/article/PMC/PMC13716739},
note = {CC BY},
}
RIS
TY - JOUR
TI - Developmental changes in activity-dependent plasticity of maturation-related neuronal phenotypes
AU - Katsunori Kobayashi
AU - Hiroki Imbe
PY - 2026
DA - 2026/10/15
JO - Frontiers in synaptic neuroscience
DO - 10.3389/fnsyn.2026.1926357
UR - https://europepmc.org/article/PMC/PMC13716739
AB - Immaturity of neurons in the adult hippocampal dentate gyrus (DG) has been implicated in the pathophysiology of neuropsychiatric disorders. Pseudo-immaturity of DG neurons can be induced by neuronal hyperexcitation in adulthood. This "dematuration," a reversal of maturation, could lead to aberrant neuronal maturation, if activated during development. However, it has not been directly tested whether dematuration can be induced in developing neurons. In the present study, we examined the effect of electroconvulsive treatment (ECT) on DG neurons of mice at several different developmental stages. Electrophysiological recordings were made using hippocampal slices. We analyzed frequency facilitation, a form of short-term synaptic plasticity, at the DG output mossy fiber synapses as an index of functional maturity of DG neurons. ECT had no significant effects on mossy fiber synaptic transmission at early postnatal ages, but it significantly reduced frequency facilitation at the postnatal age of ≥4 weeks, suggesting the induction of dematuration. Neuronal maturation marker analysis confirmed this result. The development of responsiveness to ECT was accompanied by maturation of N-methyl-D-aspartate receptor functions at the excitatory synaptic input onto DG neurons. Our results demonstrate that neuronal dematuration by ECT becomes inducible in postnatal 4 weeks in the DG of mice. Neuronal hyperexcitation such as seizures or alterations in N-methyl-D-aspartate receptor signaling around this developmental stage might affect proper maturation of DG neurons, thereby possibly increasing a risk of neuropsychiatric disorders.
SN - 1663-3563
ER -