Excitatory-inhibitory balance and critical period plasticity in developing visual cortex

Brain Science Institute (BSI), RIKEN, Вако, Saitama, Japan
Progress in brain research (Impact Factor: 5.1). 02/2005; 147:115-24. DOI: 10.1016/S0079-6123(04)47009-5
Source: PubMed
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    • "This E/I balance is a critical factor in regulating cortical neuronal functionality and critical periods of cortical plasticity which occur throughout development are governed by this E/I balance (Hensch and Fagiolini, 2005; Levelt and Hubener, 2012) whereby immaturity of cortical inhibition promotes plasticity while maturation of inhibitory circuits results in the decrease in plasticity associated with cortical maturation (Huang et al., 1999; Fagiolini and Hensch, 2000). Shifts in this E/I balance may also play a major role in the experience-dependent cortical plasticity, which includes plasticity induced by EE or deprivation, that occurs outside developmental critical periods (Hensch and Fagiolini, 2005; Sale et al., 2007; Benali et al., 2008; Maya Vetencourt et al., 2008; Megevand et al., 2009; Baroncelli et al., 2010b, 2011; Luz and Shamir, 2012; Maya- Vetencourt et al., 2012). Changes in neuronal function in the adult brain suggest that EE exposure causes a reactivation of forms of neuronal plasticity generally seen only in the developing, immature brain (Chang and Merzenich, 2003; Chang et al., 2005) in which inhibitory mechanisms are immature. "
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    ABSTRACT: The brain's life-long capacity for experience-dependent plasticity allows adaptation to new environments or to changes in the environment, and to changes in internal brain states such as occurs in brain damage. Since the initial discovery by Hebb (1947) that environmental enrichment (EE) was able to confer improvements in cognitive behavior, EE has been investigated as a powerful form of experience-dependent plasticity. Animal studies have shown that exposure to EE results in a number of molecular and morphological alterations, which are thought to underpin changes in neuronal function and ultimately, behavior. These consequences of EE make it ideally suited for investigation into its use as a potential therapy after neurological disorders, such as traumatic brain injury (TBI). In this review, we aim to first briefly discuss the effects of EE on behavior and neuronal function, followed by a review of the underlying molecular and structural changes that account for EE-dependent plasticity in the normal (uninjured) adult brain. We then extend this review to specifically address the role of EE in the treatment of experimental TBI, where we will discuss the demonstrated sensorimotor and cognitive benefits associated with exposure to EE, and their possible mechanisms. Finally, we will explore the use of EE-based rehabilitation in the treatment of human TBI patients, highlighting the remaining questions regarding the effects of EE.
    Frontiers in Systems Neuroscience 09/2014; 8. DOI:10.3389/fnsys.2014.00156
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    • "For example, in the auditory system a CP exists for rapid and permanent alterations of cortical sensory representations in response to sound (Eggermont, 2013; Kral, 2013), with implications that inform cochlear implantation (Kral and Sharma, 2012). Furthermore, in primary somatosensory and auditory cortices CPs are thought to be regulated via balances in excitatory/inhibitory network activity (Froemke and Jones, 2011; Xiong et al., 2011; Zhang et al., 2011), a suggestion that has been made for the modulation of the CP in V1 as well (Hensch and Fagiolini, 2005; Chen and Nedivi, 2013). While these topics present fascinating parallels with ODP, we refer readers to the citations listed above for an in-depth review. "
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    ABSTRACT: A primary goal of research on developmental critical periods is the recapitulation of a juvenile-like state of malleability in the adult brain that might enable recovery from injury. These ambitions are often framed in terms of the simple reinstatement of enhanced plasticity in the growth-restricted milieu of an injured adult brain. Here, we provide an analysis of the similarities and differences between deprivation-induced and injury-induced cortical plasticity, to provide for a nuanced comparison of these remarkably similar processes. As a first step, we review the factors that drive ocular dominance plasticity in the primary visual cortex of the uninjured brain during the critical period (CP) and in adults, to highlight processes that might confer adaptive advantage. In addition, we directly compare deprivation-induced cortical plasticity during the CP and plasticity following acute injury or ischemia in mature brain. We find that these two processes display a biphasic response profile following deprivation or injury: an initial decrease in GABAergic inhibition and synapse loss transitions into a period of neurite expansion and synaptic gain. This biphasic response profile emphasizes the transition from a period of cortical healing to one of reconnection and recovery of function. Yet while injury-induced plasticity in adult shares several salient characteristics with deprivation-induced plasticity during the CP, the degree to which the adult injured brain is able to functionally rewire, and the time required to do so, present major limitations for recovery. Attempts to recapitulate a measure of CP plasticity in an adult injury context will need to carefully dissect the circuit alterations and plasticity mechanisms involved while measuring functional behavioral output to assess their ultimate success.
    Neuroscience 04/2014; 283. DOI:10.1016/j.neuroscience.2014.04.029 · 3.33 Impact Factor
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    • "Gephyrin anchors the inhibitory GABA A receptor, and is required for the stabilization of GABAergic synapses (Yu et al., 2007). Together, the expression of PSD-95 and gephyrin can provide information about the development of excitatory and inhibitory synapses (Keith and El-Husseini, 2008) especially the E/I balance that is crucial for ocular dominance plasticity in visual cortex (Hensch and Fagiolini, 2005). "
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    ABSTRACT: TWO THEORIES HAVE INFLUENCED OUR UNDERSTANDING OF CORTICAL DEVELOPMENT: the integrated network theory, where synaptic development is coordinated across areas; and the cascade theory, where the cortex develops in a wave-like manner from sensory to non-sensory areas. These different views on cortical development raise challenges for current studies aimed at comparing detailed maturation of the connectome among cortical areas. We have taken a different approach to compare synaptic development in rat visual, somatosensory, and frontal cortex by measuring expression of pre-synaptic (synapsin and synaptophysin) proteins that regulate vesicle cycling, and post-synaptic density (PSD-95 and Gephyrin) proteins that anchor excitatory or inhibitory (E-I) receptors. We also compared development of the balances between the pairs of pre- or post-synaptic proteins, and the overall pre- to post-synaptic balance, to address functional maturation and emergence of the E-I balance. We found that development of the individual proteins and the post-synaptic index overlapped among the three cortical areas, but the pre-synaptic index matured later in frontal cortex. Finally, we applied a neuroinformatics approach using principal component analysis and found that three components captured development of the synaptic proteins. The first component accounted for 64% of the variance in protein expression and reflected total protein expression, which overlapped among the three cortical areas. The second component was gephyrin and the E-I balance, it emerged as sequential waves starting in somatosensory, then frontal, and finally visual cortex. The third component was the balance between pre- and post-synaptic proteins, and this followed a different developmental trajectory in somatosensory cortex. Together, these results give the most support to an integrated network of synaptic development, but also highlight more complex patterns of development that vary in timing and end point among the cortical areas.
    Frontiers in Neural Circuits 05/2013; 7:97. DOI:10.3389/fncir.2013.00097 · 2.95 Impact Factor
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