Developmental genetic programs and activity-dependent mechanisms instruct neocortical area mapping

Simi, Alessandro; Studer, Michèle

doi:10.1016/j.conb.2018.06.007

Cited by 32 publications

(32 citation statements)

References 49 publications

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“…Furthermore, different studies, using in vivo models, indicate that synaptic activity promotes dendritic arbor elaboration and stabilization (Foa et al , ; Cline and Haas, ). The effects of neuronal activity and molecular mechanisms on dendritic morphology may be site‐ and context‐dependent and may differ between animal species and between brain regions (McAllister, ; Simi and Studer, ).…”

Section: Il1rapl1 Knockout Micementioning

confidence: 99%

The Synaptic and Neuronal Functions of the X‐Linked Intellectual Disability Protein Interleukin‐1 Receptor Accessory Protein Like 1 (IL1RAPL1)

Montani

Gritti

Beretta

et al. 2018

Developmental Neurobiology

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Since the first observation that described a patient with a mutation in IL1RAPL1 gene associated with intellectual disability in 1999, the function of IL1RAPL1 has been extensively studied by a number of laboratories. In this review, we summarize all the major data describing the synaptic and neuronal functions of IL1RAPL1 and recapitulate most of the genetic deletion identified in humans and associated to intellectual disability (ID) and autism spectrum disorders (ASD). All the data clearly demonstrate that IL1RAPL1 is a synaptic adhesion molecule localized at the postsynaptic membrane. Mutations in IL1RAPL1 gene cause either the absence of the protein or the production of a dysfunctional protein. More recently it has been demonstrated that IL1RAPL1 regulated dendrite formation and mediates the activity of IL‐1β on dendrite morphology. All these data will possibly contribute to identifying therapies for patients carrying mutations in IL1RAPL1 gene.

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Section: Il1rapl1 Knockout Micementioning

confidence: 99%

The Synaptic and Neuronal Functions of the X‐Linked Intellectual Disability Protein Interleukin‐1 Receptor Accessory Protein Like 1 (IL1RAPL1)

Montani

Gritti

Beretta

et al. 2018

Developmental Neurobiology

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“…Changes in the size of individual neocortical areas or hippocampal fields cause behavioral, cognitive, and memory deficits in mice and humans (Caronia, Wilcoxon, Feldman, & Grove, ; Cooper et al, ; Leingartner et al, ; Rubenstein, ; Scearce‐Levie et al, ; Zola‐Morgan, Squire, & Amaral, ). Despite considerable investigation, however, the mechanisms that subdivide the cortical primordium are still far from understood (O'Leary, Chou, & Sahara, ; O'Leary & Sahara, ; Simi & Studer, ).…”

Section: Introductionmentioning

confidence: 99%

A model of neocortical area patterning in the lissencephalic mouse may hold for larger gyrencephalic brains

Jones

Guadiana

Grove

2019

J of Comparative Neurology

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In the mouse, two telencephalic signaling centers orchestrate embryonic patterning of the cerebral cortex. From the rostral patterning center in the telencephalon, the Fibroblast Growth Factor, FGF8, disperses as a morphogen to establish the rostral to caudal axis of the neocortical area map.FGF8 coordinates with Wnt3a from the cortical hem to regulate graded expression of transcription factors that position neocortical areas, and control hippocampal development. Whether similar signaling centers pattern the much larger cortices of carnivore and primate species, however, is unclear. The limited dispersion range of FGF8 and Wnt3a is inconsistent with patterning larger cortical primordia. Yet the implication that different mechanisms organize cortex in different mammals flies in the face of the tenet that developmental patterning mechanisms are conserved across vertebrate species. In the present study, both signaling centers were identified in the ferret telencephalon, as were expression gradients of the patterning transcription factor genes regulated by FGF8 and Wnt3a. Notably, at the stage corresponding to the peak period of FGF8 signaling in the mouse neocortical primordium (NP), the NP was the same size in ferret and mouse, which would allow morphogen patterning of the ferret NP. Subsequently, the size of ferret neocortex shot past that of the mouse. Images from online databases further suggest that NP growth in humans, too, is slowed in early cortical development. We propose that if early growth in larger brains is held back, mechanisms that pattern the neocortical area map in the mouse could be conserved across mammalian species. K E Y W O R D Scerebral cortex, embryonic patterning, Ferret, FGF8, morphogen, mouse, neocortical area map, RRID:AB_514497, RRID:SCR 003070, Wnt3a

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“…The area-and cell-type specific organization of the mammalian neocortex is a process involving coordinated interactions between cell intrinsic genetic programs and neural activity, an essential feature in specifying the composition and organization of neural circuits during all stages of development (Jabaudon, 2017;Simi and Studer, 2018). Before experience shapes neuronal circuits via sensory-driven activity, the developing cortex is genetically primed to establish patterns of local spontaneous activity, which autonomously synchronizes large groups of neurons independently of sensory stimulation and contributes to the development of neuronal circuits (Luhmann and Khazipov, 2018;Andreae and Burrone, 2018;Kirischuk et al, 2017;Anton-Bolanos et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

“…Functioning in a dose-, context-and time-dependent manner, these signaling pathways modulate gradient expression of area patterning genes, such as Pax6, Sp8, Emx2 and Nr2f1 (also known as COUP-TFI), among others. These transcriptional regulators cooperatively regulate cell identity specification in cortical progenitors and early postmitotic neurons, building a rough primordial areal map, known as a protomap, which will be refined by sensory-evoked activity during postnatal stages (Simi and Studer, 2018). Alterations in genetic dosage of these factors alter the size and position of primordial area maps with severe consequences in cell-type specification and circuit formation (Greig et al, 2013;Jabaudon, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Alterations in genetic dosage of these factors alter the size and position of primordial area maps with severe consequences in cell-type specification and circuit formation (Greig et al, 2013;Jabaudon, 2017). Although the interaction between cortical patterning genes and onset of spontaneous activity during primary area mapping has been hypothesized (Simi and Studer, 2018), there is still no clear evidence on how this interaction is perpetrated.…”

Section: Introductionmentioning

confidence: 99%

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COUP-TFI/Nr2f1 orchestrates intrinsic neuronal activity during cortical area patterning

Pino

Tocco

Magrinelli

et al. 2019

Preprint

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Early intrinsic cortical activity regulated by Nr2f1. 2 ABSTRACTThe formation of functional cortical maps in the cerebral cortex results from a timely regulated interaction between intrinsic genetic mechanisms and electrical activity. To understand how transcriptional regulation influences network activity and neuronal excitability within the neocortex, we used mice deficient for the area mapping gene Nr2f1(also known as COUP-TFI), a key determinant of somatosensory area specification during development. We found that cortical loss of Nr2f1 impacts on spontaneous network activity and synchronization at perinatal stages. In addition, we observed alterations in the intrinsic excitability and morphological features of layer V pyramidal neurons.Accordingly, we identified distinct voltage-gated ion channels regulated by Nr2f1 that might directly influence intrinsic bioelectrical properties during critical time windows of somatosensory cortex specification. Together, our data suggest a tight link between Nr2f1 and neuronal excitability in the developmental sequence that ultimately sculpts the emergence of cortical network activity within the immature neocortex.

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Developmental genetic programs and activity-dependent mechanisms instruct neocortical area mapping

Cited by 32 publications

References 49 publications

The Synaptic and Neuronal Functions of the X‐Linked Intellectual Disability Protein Interleukin‐1 Receptor Accessory Protein Like 1 (IL1RAPL1)

The Synaptic and Neuronal Functions of the X‐Linked Intellectual Disability Protein Interleukin‐1 Receptor Accessory Protein Like 1 (IL1RAPL1)

A model of neocortical area patterning in the lissencephalic mouse may hold for larger gyrencephalic brains

COUP-TFI/Nr2f1 orchestrates intrinsic neuronal activity during cortical area patterning

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