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Simons Initiative for the Developing Brain
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Simons Initiative for the Developing Brain
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Paper Chain Countdown

In celebration of SIDB’s 5th year anniversary on the 1st April 2022, during March we showcased a paper published from across SIDB every day on Twitter.  For our final week we showcased two papers a day!

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'Radically truncated MeCP2 rescues Rett syndrome-like neurological defects’ - Bird lab

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‘Cell type-specific translation profiling reveals a novel strategy for treating fragile X syndrome’ - Osterweil lab

This study details the first cell-type-specific translation profile of Fragile X Syndrome (FX) mouse model (Fmr1-/y ) neurons. Surprisingly, it was shown that many over-translating mRNAs are protective rather than pathological. One example of this is muscarnic receptor M4, which can be positively modulated to correct aberrant plasticity and audiogenic seizures in the Fmr1-/y mouse. This shows that cell type-specific translation profiling can identify new disease mechanisms and novel therapeutic targets for FX.

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‘Architecture of the mouse brain synaptome' - Grant lab

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‘Altered dendritic spine function and integration in a mouse model of fragile X syndrome' - Kind lab

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Paper abstract

‘Stellate cells in the medial entorhinal cortex are required for spatial learning' - Nolan lab

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Paper abstract

‘Cortical neurons derived from human pluripotent stem cells lacking FMRP display altered spontaneous firing patterns' - Wyllie lab

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Paper abstract

‘FMRP sustains presynaptic function via control of activity-dependent bulk endocytosis' - Cousin lab

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‘The Impact of Visual Cues, Reward, and Motor Feedback on the Representation of Behaviorally Relevant Spatial Locations in Primary Visual Cortex' - Rochefort lab

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Paper abstract

‘A cerebellar-thalamocortical pathway drives behavioral context-dependent movement initiation' - Duguid lab

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Paper visual abstract

‘Pax6 loss alters the morphological and electrophysiological development of mouse prethalamic neurons' - Price lab

The PAX6 gene is essential for normal brain development. It controls the activities of hundreds of other genes and its mutation has catastrophic effects. For example, in humans, mutations of both copies of PAX6 cause death before or shortly after birth and mutations in one copy cause eye defects, structural brain defects and intellectual disabilities. One well-documented reason these problems occur is that PAX6 is essential for normal cell proliferation in the embryonic brain. This might not be the whole story, however. PAX6 might also be important for ensuring that the neurons that are made function properly. We set out to discover whether this is the case. We found that mutating PAX6 at the time when newborn brain cells are becoming neurons altered how they developed their shapes. It also resulted in them becoming hyperactive, generating more electrical activity in response to the same amount of stimulation. Most studies on PAX6 have focussed on its actions in dividing cells. Our results revealed previously unknown roles for it in maturing neurons in the developing brain. They show how the same gene can have different functions at different stages of a cell’s development, providing interesting insights into the mechanisms of normal and abnormal brain development.  

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Paper abstract

‘Recapitulation of the EEF1A2 D252H neurodevelopmental disorder-causing missense mutation in mice reveals a toxic gain of function' - Abbott lab

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‘Locus coeruleus and dopaminergic consolidation of everyday memory' - Morris lab

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‘The Developmental Shift of NMDA Receptor Composition Proceeds Independently of GluN2 Subunit-Specific GluN2 C-Terminal Sequences' - Hardingham lab

  • Mutating the GluN2B CaMKII site affects phosphorylation of its C-terminal domain 
  • The developmental changes in NMDAR composition and synaptogenesis occur normally 
  • Changes in NMDAR composition do not require distinct GluN2 C-terminal domains 
  • Developmental changes in NMDAR composition are primarily sensitive to GluN2A levels.

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‘Medial septal GABAergic neurons reduce seizure duration upon optogenetic closed-loop stimulation' - Gonzalez-Sulser lab

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‘Expression of Genes in the 16p11.2 Locus during Development of the Human Fetal Cerebral Cortex' - Pratt lab

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‘Sustained correction of associative learning deficits following brief, early treatment in a rat model of Fragile X Syndrome' - Wood and Kind labs

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‘The lateral septum mediates kinship behavior in the rat' - Clemens lab

Evolutionary theory and behavioral biology suggest that kinship is an organizing principle of social behavior. The neural mechanisms that mediate kinship behavior, were not previously known. Lesion effects, developmental changes and the ordered representation of response preferences according to kinship—an organization we refer to as nepotopy—point to a key role of the lateral septum in organizing mammalian kinship behavior.

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‘A mutation-led search for novel functional domains in MeCP' - Bird lab

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‘NMDA receptor activity bidirectionally controls active decay of long-term spatial memory in the dorsal hippocampus' - Hardt lab

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Paper visual abstract

‘Neocortex saves energy by reducing coding precision during food scarcity' - Rochefort lab

Padamsey et al. show that under food restriction, mouse visual cortical neurons save ATP by decreasing excitatory currents. Compensatory mechanisms preserve spike rate but decrease coding precision of visual information.

Supplementation with the fat mass- regulated hormone leptin restores coding precision.

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Paper abstract

‘Grid cells are modulated by local head direction' - Nolan lab

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‘Autism in Fragile X Syndrome; A Functional MRI Study of Facial Emotion-Processing' - Stanfield lab

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‘Dissociation of Brain Activation in Autism and Schizotypal Personality Disorder During Social Judgments' - Stanfield lab

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'Telencephalic outputs from the medial entorhinal cortex are copied directly to the hippocampus' - Sürmeli lab

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'A brainwide atlas of synapses across the mouse lifespan' - Grant lab

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'Input-output relationship of CA1 pyramidal neurons reveals intact homeostatic mechanisms in a mouse model of Fragile X syndrome' - Booker and Kind labs

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'Neuronal non-CG methylation is an essential target for MeCP2 function' - Bird lab

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