Version June 2024
| Factor | Consequence |
| Input resistance and time constant: Increased in immature neurons | Small inputs result in relatively large voltage changes |
| Voltage-gated ion channels: Earlier maturation of sodium and calcium channels, delayed development of potassium channels | Longer action potentials, shorter refractory periods, increased neuron firing |
| Synapse development: Excitatory synapses appear before inhibitory synapses | Relative predominance of excitation over inhibition early in development |
| Synapse development: Over expression of excitatory synapses during critical period | Corresponds to window of heightened seizure susceptibility |
| Developmental changes in glutamate receptor subunits: NR2B/NR2A ratio favors prolonged depolarizing responses; NR2D relative over expression reduces Mg++ block | Favor relative hyperexcitability |
| Late appearance of functional inhibitory synapses | Along with other factors favoring excitation, contributes to neuronal excitatory drive and lack of functional inhibition |
| Developmental changes in GABAA receptor function and Cl– gradient due to differential development of the K+/Cl– co-transporters | GABA is depolarizing early in life, enhancing excitability |
| Developmental changes in GABAA receptor subunits | Partially accounts for developmental differences in inhibitory effectiveness and benzodiazepine responsiveness |
| Developmental sensitivity to glutamate toxicity | Less glutamate-induced excitotoxicity early in development |
| Immature GABAA binding pattern in substantia nigra | Proconvulsant effect |
| Electrical synapses: More common early in development | Mechanism for enhanced synchrony of neuronal networks |
| Immature homeostatic mechanisms: NaK-ATPase, glial K+ regulation, K+/Cl– co-transporters | Prolonged exposure to elevated extracellular K+ leads to further neuronal depolarization |
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