GABAergic Interneurons Shape the Functional Maturation of the Cortex

Magueresse, Corentin Le; Monyer, Hannah

doi:10.1016/j.neuron.2013.01.011

Cited by 366 publications

(325 citation statements)

References 238 publications

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“…The increase in inhibitory signaling that initiates the onset of critical periods is mediated by activity at the GABA A receptor (Hensch, 2005). At birth, the GABA A receptor is excitatory, with a shift to inhibitory action occurring early in development (Ben-Ari et al, 2012;Le Magueresse and Monyer, 2013). Several elements of the GABAergic system continue to exhibit marked developmental change through adolescence and early adulthood (Kilb, 2012;Le Magueresse and Monyer, 2013).…”

Section: Developmental Regulation Of Fear-related Plasticitymentioning

confidence: 99%

“…At birth, the GABA A receptor is excitatory, with a shift to inhibitory action occurring early in development (Ben-Ari et al, 2012;Le Magueresse and Monyer, 2013). Several elements of the GABAergic system continue to exhibit marked developmental change through adolescence and early adulthood (Kilb, 2012;Le Magueresse and Monyer, 2013). GABAergic synapse proliferation, GABA receptor and transporter distribution, and metabolic enzyme production, all modulate GABAergic tone.…”

Section: Developmental Regulation Of Fear-related Plasticitymentioning

confidence: 99%

“…In particular, inhibitory neurotransmission in the prefrontal cortex increases throughout adolescence and does not reach peak levels until young adulthood (Kilb, 2012;Le Magueresse and Monyer, 2013). GABA signaling is not only involved in inhibitory synaptic transmission, but also regulates synapse elimination and axonal pruning (Wu et al, 2012).…”

Section: Developmental Regulation Of Fear-related Plasticitymentioning

confidence: 99%

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Sensitive Periods in Affective Development: Nonlinear Maturation of Fear Learning

Hartley

Lee

2014

Neuropsychopharmacol

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At specific maturational stages, neural circuits enter sensitive periods of heightened plasticity, during which the development of both brain and behavior are highly receptive to particular experiential information. A relatively advanced understanding of the regulatory mechanisms governing the initiation, closure, and reinstatement of sensitive period plasticity has emerged from extensive research examining the development of the visual system. In this article, we discuss a large body of work characterizing the pronounced nonlinear changes in fear learning and extinction that occur from childhood through adulthood, and their underlying neural substrates. We draw upon the model of sensitive period regulation within the visual system, and present burgeoning evidence suggesting that parallel mechanisms may regulate the qualitative changes in fear learning across development.

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Section: Developmental Regulation Of Fear-related Plasticitymentioning

confidence: 99%

Section: Developmental Regulation Of Fear-related Plasticitymentioning

confidence: 99%

Section: Developmental Regulation Of Fear-related Plasticitymentioning

confidence: 99%

See 1 more Smart Citation

Sensitive Periods in Affective Development: Nonlinear Maturation of Fear Learning

Hartley

Lee

2014

Neuropsychopharmacol

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“…Critical periods of plasticity are defined, among other things, by the maturation of GABAergic neurons [27], which make up about 25% of all cortical neurons in primates [28,29]. Although this fraction of GABAergic interneurons in the cortex is relatively constant from neurogenesis to adulthood [30], during postnatal development a subgroup of these cells expressing the Ca ++ -binding protein parvalbumin gradually accumulate extracellular matrix components around the cell body, such as chondroitin sulfate proteoglycans, forming a lattice-like structure called perineuronal net (PNN).…”

Section: Introductionmentioning

confidence: 99%

Effect of chronic stress during adolescence in prefrontal cortex structure and function

Folha

Bahia

Aguiar

et al. 2017

Behavioural Brain Research

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h i g h l i g h t s• Chronic stress impairs the development of the adolescent brain.• Chronic stress delays the maturation of extracellular structures called perineuronal nets, which stabilize synaptic contacts on inhibitory neurons, and prefrontal cortex-associated behavior.• These negative effects of chronic stress on the prefrontal cortex can theoretically occur in humans. Critical periods of plasticity (CPPs) are defined by developmental intervals wherein neuronal circuits are most susceptible to environmental influences. The CPP of the prefrontal cortex (PFC), which controls executive functions, extends up to early adulthood and, like other cortical areas, reflects the maturation of perineuronal nets (PNNs) surrounding the cell bodies of specialized inhibitory interneurons. The aim of the present work was to evaluate the effect of chronic stress on both structure and function of the adolescent's rat PFC. We subjected P28 rats to stressful situations for 7, 15 and 35 days and evaluated the spatial distribution of histochemically-labeled PNNs in both the Medial Prefrontal Cortex (MPFC) and the Orbitofrontal Cortex (OFC) and PFC-associated behavior as well. Chronic stress affects PFC development, slowing PNN maturation in both the (MPFC) and (OFC) while negatively affecting functions associated with these areas. We speculate upon the risks of prolonged exposure to stressful environments in human adolescents and the possibility of stunted development of executive functions.

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“…13 Indeed, alterations of GABAergic cell function, either during development or in the mature brain, can cause increased excitability and epilepsy. The intractable seizures observed in all three affected individuals described here could thus result from the abnormal development of the GABAergic network associated with the loss of DOCK7 function.…”

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confidence: 99%

ISDN2014_0400: Mutations in DOCK7 in individuals with epileptic encephalopathy and cortical blindness

Hamdan

Perrault

Rio

et al. 2015

Intl J of Devlp Neuroscience

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Epileptic encephalopathies are increasingly thought to be of genetic origin, although the exact etiology remains uncertain in many cases. We describe here three girls from two nonconsanguineous families affected by a clinical entity characterized by dysmorphic features, early-onset intractable epilepsy, intellectual disability, and cortical blindness. In individuals from each family, brain imaging also showed specific changes, including an abnormally marked pontobulbar sulcus and abnormal signals (T2 hyperintensities) and atrophy in the occipital lobe. Exome sequencing performed in the first family did not reveal any gene with rare homozygous variants shared by both affected siblings. It did, however, show one gene, DOCK7, with two rare heterozygous variants (c.2510delA [p.Asp837Alafs*48] and c.3709C>T [p.Arg1237*]) found in both affected sisters. Exome sequencing performed in the proband of the second family also showed the presence of two rare heterozygous variants (c.983C>G [p.Ser328*] and c.6232G>T [p.Glu2078*]) in DOCK7. Sanger sequencing confirmed that all three individuals are compound heterozygotes for these truncating mutations in DOCK7. These mutations have not been observed in public SNP databases and are predicted to abolish domains critical for DOCK7 function. DOCK7 codes for a Rac guanine nucleotide exchange factor that has been implicated in the genesis and polarization of newborn pyramidal neurons and in the morphological differentiation of GABAergic interneurons in the developing cortex. All together, these observations suggest that loss of DOCK7 function causes a syndromic form of epileptic encephalopathy by affecting multiple neuronal processes.

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GABAergic Interneurons Shape the Functional Maturation of the Cortex

Cited by 366 publications

References 238 publications

Sensitive Periods in Affective Development: Nonlinear Maturation of Fear Learning

Sensitive Periods in Affective Development: Nonlinear Maturation of Fear Learning

Effect of chronic stress during adolescence in prefrontal cortex structure and function

ISDN2014_0400: Mutations in DOCK7 in individuals with epileptic encephalopathy and cortical blindness

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