Abstract
BackgroundBoth human and animal data indicate that disruption of the endogenously slow maturation of temporal association cortical (TeA) networks is associated with abnormal higher order cognitive development. However, the neuronal mechanisms underlying the endogenous maturation delay of the TeA are poorly understood.ResultsHere we report a novel form of developmental plasticity that is present in the TeA. It was found that deep layer TeA neurons, but not hippocampal or primary visual neurons, exist in a protracted ’embryonic-like’ state through a mechanism involving reduced somato-dendritic communication and a non-excitable somatic membrane. This mechanism of neural inactivity is present in intact tissue and shows a remarkable transition into an active somato-dendritically coupled state. The quantity of decoupled cells diminishes in a protracted and age-dependent manner, continuing into adolescence.ConclusionsBased on our data, we propose a model of neural plasticity through which protracted compartmentalization and decoupling in somato-dendritic signalling plays a key role in controlling how excitable neurons are incorporated into recurrent cortical networks independent of neurogenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12915-016-0270-5) contains supplementary material, which is available to authorized users.
Highlights
Both human and animal data indicate that disruption of the endogenously slow maturation of temporal association cortical (TeA) networks is associated with abnormal higher order cognitive development
Given that neurite outgrowth is commonly used as an index of neural maturation [25], we first evaluated the developmental trajectory of temporal association cortex (TeA) neurite growth
Hippocampal and primary visual cortex (Oc1) cultures were prepared under identical conditions to serve as positive controls, and cells were transfected with green fluorescent protein (GFP) for morphological quantification
Summary
Both human and animal data indicate that disruption of the endogenously slow maturation of temporal association cortical (TeA) networks is associated with abnormal higher order cognitive development. Electrophysiological recordings and functional imaging have shown that the TeA lacks significant excitability and functional connectivity during the first month of postnatal life [1, 20], and accelerating TeA maturation during early postnatal development can disrupt normal behavioural development [20, 21] These observations are in line with data consistently reporting that electrical activity is not required for the establishment of basic neuronal morphology [22,23,24]. These findings suggest that neurobiological processes that support independently regulated neuronal morphological and electrophysiological maturation may provide an important additional mechanism of protracted functional cortical maturation
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