Neuronal Plasticity: Beyond the Critical Period

Hübener, Mark; Bonhoeffer, Tobias

doi:10.1016/j.cell.2014.10.035

Cited by 204 publications

(165 citation statements)

References 115 publications

Supporting

Mentioning

154

Contrasting

Unclassified

Order By: Relevance

“…All we now know is clearly compatible with the view that we are dealing mainly with biological processes, which may constitute natural kinds even while their functional roles vary when used in organisms which need to meet rather different environmental challenges, especially over evolutionary timescales. Well-known observations concerning the plasticity of the brain (Hübener and Bonhoeffer 2014) show how wide this degree of variation can be. Thus, the same biological mechanism can be used to realize rather different cognitive functions, which certainly is a challenge for the natural kind view of cognitive processes.…”

Section: Theoretical Evaluation and Conclusionmentioning

confidence: 98%

What are cognitive processes? An example-based approach

Newen

2015

Synthese

View full text Add to dashboard Cite

The question "What are cognitive processes?" can be understood variously as meaning "What is the nature of cognitive processes?", "Can we distinguish epistemically cognitive processes from physical and biochemical processes on the one hand, and from mental or conscious processes on the other?", and "Can we establish a fruitful notion of cognitive process?" The present aim is to deliver a positive answer to the last question by developing criteria for what would count as a paradigmatic exemplar of a cognitive process, and then to offer the comparator (or feedforward) mechanism as a convincing paradigmatic example. Thus, the paper argues, given the current state of science, we can indeed establish a fruitful scientific notion of a cognitive process. Nevertheless, it is left open whether the example-based characterization ends up as merely highlighting a fruitful convention within the early-twentyfirst century interdisciplinary investigation of intelligent behaviour in humans, animals, and robots, or whether the examples determine a natural kind or a property cluster.

show abstract

Section: Theoretical Evaluation and Conclusionmentioning

confidence: 98%

What are cognitive processes? An example-based approach

Newen

2015

Synthese

View full text Add to dashboard Cite

show abstract

“…One implication of these observations is that a rather restricted period during development determines its reactivity to the external world for the rest of its life. Recent studies attempt to prolong this critical period by drugs and behavioral manipulations (9)(10)(11). It is proposed that PS may use similar mechanisms, which modulate the onor offset and duration of developmental critical periods, particularly with respect to limbic and prefrontal cortical regions (Fig.…”

Section: Introductionmentioning

confidence: 99%

Stress In Utero: Prenatal Programming of Brain Plasticity and Cognition

Bock

Wainstock

Braun

et al. 2015

Biological Psychiatry

210

177

View full text Add to dashboard Cite

“…S3A). A specific level of inhibition is thought to control the opening of the critical period, whereas increased, mature levels of inhibition reduce or terminate it in adulthood (45,46). Furthermore, reduction of PV + firing can extend the critical period for OD plasticity (67), as can manipulations in adult animals that reduce intracortical inhibition (68,69).…”

Section: Interneuron-specific Mecp2 Deletion Prolongs Experience-depementioning

confidence: 99%

“…Analysis of alterations in visual responses and neuronal information processing in MeCP2 mutant mice thus provides both a mechanistic understanding of visual deficits in RTT as well as sensitive assays of changes in synaptic integration and neuronal circuits. Furthermore, visual cortical plasticity is influenced by maturation of excitation and inhibition in cortical circuits (44)(45)(46)(47), and the initiation and termination of critical period plasticity in V1 of MeCP2 mutant mice is a sensitive indicator of the level of inhibition in cortical circuits.…”

Section: Significancementioning

confidence: 99%

Jointly reduced inhibition and excitation underlies circuit-wide changes in cortical processing in Rett syndrome

Banerjee

Rikhye

Breton-Provencher

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

154

202

View full text Add to dashboard Cite

Rett syndrome (RTT) arises from loss-of-function mutations in methyl-CpG binding protein 2 gene (Mecp2), but fundamental aspects of its physiological mechanisms are unresolved. Here, by whole-cell recording of synaptic responses in MeCP2 mutant mice in vivo, we show that visually driven excitatory and inhibitory conductances are both reduced in cortical pyramidal neurons. The excitation-to-inhibition (E/I) ratio is increased in amplitude and prolonged in time course. These changes predict circuit-wide reductions in response reliability and selectivity of pyramidal neurons to visual stimuli, as confirmed by two-photon imaging. and increases KCC2 expression to normalize the KCC2/NKCC1 ratio. Thus, loss of MeCP2 in the brain alters both excitation and inhibition in brain circuits via multiple mechanisms. Loss of MeCP2 from a specific interneuron subtype contributes crucially to the cell-specific and circuit-wide deficits of RTT. The joint restoration of inhibition and excitation in cortical circuits is pivotal for functionally correcting the disorder.MeCP2 | E/I balance | parvalbumin neurons | IGF1 | chloride transporters S ynaptic excitation (E) and inhibition (I), along with the neuronal balance of excitation and inhibition (E/I), is key to the function of brain circuits, and is often disrupted in neurodevelopmental disorders, including autism spectrum disorders (ASDs) (1-3). Rett syndrome (RTT) is a severe neurodevelopmental and adult disorder that arises from sporadic loss-of-function mutations in the X-linked (Xq28) methyl-CpG binding protein 2 gene (Mecp2) encoding the protein MeCP2 (4-7). MeCP2 is a critical regulator of brain development and adult neural function (8), and arrested brain maturation due to synaptic dysfunction is one of the hallmarks of RTT (3). However, the effects of MeCP2 on excitatory and inhibitory synaptic mechanisms in vivo, and on neuronal and circuit function underlying RTT pathophysiology, are unknown.MeCP2 is ubiquitously expressed in multiple cell types and subregions of the brain (4, 6, 9), including inhibitory interneurons, and has cell-autonomous as well as non-cell-autonomous effects (10); thus, it has been particularly challenging to identify its role in cell-specific brain circuits. Anatomically diverse inhibitory interneuron subtypes with distinct physiological signatures influence different aspects of neocortical function and behavior (11,12). Soma-targeting parvalbumin-expressing (PV + ) and dendritetargeting somatostatin-expressing (SOM + ) interneurons are the two major nonoverlapping populations of interneurons in mice that target cortical pyramidal neurons (13). Inhibition by PV + and SOM + neurons powerfully influences neuronal responses and circuit computations in visual cortex (14-17). Deletion of MeCP2 from all forebrain GABAergic interneurons recapitulates key aspects of RTT (18), demonstrating that altered inhibitory function is an important facet of RTT pathophysiology. Indeed, a major phenotype of MeCP2 reduction in individuals with RTT and in mouse models is ...

show abstract

Neuronal Plasticity: Beyond the Critical Period

Cited by 204 publications

References 115 publications

What are cognitive processes? An example-based approach

What are cognitive processes? An example-based approach

Stress In Utero: Prenatal Programming of Brain Plasticity and Cognition

Jointly reduced inhibition and excitation underlies circuit-wide changes in cortical processing in Rett syndrome

Contact Info

Product

Resources

About