"Sensitive periods are commonly conceptualized as epochs of time during which a system is highly plastic and open to environmental restructuring or attunement (e.g., Hensch, 2005d; Werker & Hensch, 2015). A classic example of sensitive period plasticity is the organization of ocular dominance columns in the visual cortex that occurs in numerous species including rats and humans (see Hensch, 2005b, for reviews of this literature; Wiesel & Hubel, 1963). While sensitive periods have traditionally been examined in sensory domains, it is clear that sensitive periods occur throughout the brain in a region specific, analytical level (i.e., molecules to circuits), and time dependent manner. "
[Show abstract][Hide abstract] ABSTRACT: Early experiences critically shape the structure and function of the brain. Perturbations in typical/species-expected early experiences are known to have profound neural effects, especially in regions important for emotional responding. Parental care is one species-expected stimulus that plays a fundamental role in the development of emotion neurocircuitry. Emerging evidence across species suggests that phasic variation in parental presence during the sensitive period of childhood affects the recruitment of emotional networks on a moment-to-moment basis. Also, it appears that increasing independence from caregivers cues the termination of the sensitive period for environmental input into emotion network development. In this review, we examine how early parental care, the central nervous system, and behaviour come together to form a 'neuro-environmental loop', contributing to the formation of stable emotion regulation circuits. To achieve this end, we focus on the interaction of parental care and the developing amygdala-medial prefrontal cortex (mPFC) network-which is at the core of human emotional functioning. Using this model, we discuss how individual or group variations in parental-independence, across chronic and brief timescales, might contribute to neural and emotional phenotypes that have implications for long-term mental health.Neuropsychopharmacology accepted article preview online, 21 July 2015. doi:10.1038/npp.2015.204.
Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 07/2015; DOI:10.1038/npp.2015.204 · 7.83 Impact Factor
"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. "
[Show abstract][Hide abstract] 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
"These critical periods are limited to specific windows of time that are different for each sensory system. In the visual system, the primary visual cortex is subjected to a critical period for ocular dominance plasticity during which connections from a weak or absent eye can be permanently overtaken by the strong eye
2. The integrated action between inhibitory and excitatory circuits determines critical period onset, with a major role being played by the maturation of fast-spiking parvalbumin (FSPV) interneurons
3. We have shown that Otx2 homeoprotein helps determine critical period timing by signaling FSPV cells in mice
4. Conditional knock-down in heterozygous floxed mice just prior to normal critical period timing is sufficient to delay onset, while cortical infusion of recombinant Otx2 protein accelerates both onset and closure
[Show abstract][Hide abstract] ABSTRACT: Plasticity in the visual cerebral cortex is regulated by the internalization of Otx2 homeoprotein into parvalbumin neurons in cortical layers II/III and IV. However the
Otx2 locus is not active in these neurons and the protein is imported from external sources, including the choroid plexus. Because Otx1 and Otx2 may have redundant functions, we wanted to verify if part of the staining in parvalbumin neurons corresponds to Otx1 transported from cortical layer V neurons. It is demonstrated here that Otx staining in layer IV cells is maintained in
Otx1-null mice. The immunoprecipitation of extracts from finely dissected granular and supragranular cortex (layers I-IV) gave immunoblots with a band corresponding to Otx2 and not Otx1. Moreover, high-resolution mass spectrometry analysis after immunoprecipitation identifies two peptides within the Otx2 homeodomain. One of these peptides is specific for Otx2 and is not found in Otx1. These results unambiguously establish that the staining in parvalbumin neurons revealed with the anti-Otx2 antibodies used in our previous studies identifies non-cell autonomous Otx2.
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