Advances in Understanding the Molecular Mechanisms of Neuronal Polarity

Gu, Xi; Jia, Chunhong; Wang, Junhao

doi:10.1007/s12035-023-03242-w

Cited by 3 publications

(2 citation statements)

References 191 publications

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“…Netrin receptor DCC can interact with Dab1 which intensifies the speed of MPs differentiation into BPs ( Attardo et al, 2008 ; Homem et al, 2015 ; Dwyer et al, 2016 ; Zhang et al, 2018 ; Xing et al, 2021 ). The role of such factors is recently reviewed elsewhere in details ( Gu et al, 2023 ). Above mentioned molecules are required for BP to MPC transition and therefore axon determination.…”

Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of corpus callosum development: a four-step journey

Gavrish,

Kustova,

Celis Suescún

et al. 2024

Front. Neuroanat.

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The Corpus Callosum (CC) is a bundle of axons connecting the cerebral hemispheres. It is the most recent structure to have appeared during evolution of placental mammals. Its development is controlled by a very complex interplay of many molecules. In humans it contains almost 80% of all commissural axons in the brain. The formation of the CC can be divided into four main stages, each controlled by numerous intracellular and extracellular molecular factors. First, a newborn neuron has to specify an axon, leave proliferative compartments, the Ventricular Zone (VZ) and Subventricular Zone (SVZ), migrate through the Intermediate Zone (IZ), and then settle at the Cortical Plate (CP). During the second stage, callosal axons navigate toward the midline within a compact bundle. Next stage is the midline crossing into contralateral hemisphere. The last step is targeting a defined area and synapse formation. This review provides an insight into these four phases of callosal axons development, as well as a description of the main molecular players involved.

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Section: Introductionmentioning

confidence: 99%

Molecular mechanisms of corpus callosum development: a four-step journey

Gavrish,

Kustova,

Celis Suescún

et al. 2024

Front. Neuroanat.

View full text Add to dashboard Cite

show abstract

“…4,5 In addition, abnormal neuronal polarity causes a variety of neurodevelopmental disorders and ultimately leads to the death and disappearance of neuronal cells. [6][7][8] It has been reported that soluble b-amyloid (Ab) disrupts actin and microtubule (MT) dynamics in cultured hippocampal neurons by activating RhoA and inhibiting histone deacetylase 6 (HDAC6). 5 The inhibition of HDAC6 blocks the deacetylation of Acetylated Tau (AC-Tau), ultimately interfering with the maintenance of neuronal polarity.…”

Section: Introductionmentioning

confidence: 99%