1,721,197 research outputs found
Erasing fear memories
No full textEvents that are associated with trauma
and fear often leave memories that
reoccur spontaneously, leading to
excessive fear, anxiety, and, in some cases,
posttraumatic stress disorder. Such relapses
of fear memories constitute a major clinical
problem, and their elimination is a major
cornerstone of psychological therapy. Many
neurobiological studies are therefore
focused on understanding
how fear memories are controlled. On page 1258 of this issue,
Gogolla et al. take an important
step in the field by determining
that the extracellular environment
in a particular region of the
brain—the amygdala—is responsible
for making fear memories
erasure-resistan
Perilesional treatment with chondroitinase ABC and motor training promote functional recovery after stroke in rats
Full text linkIschemic stroke insults may lead to chronic functional limitations that adversely affect patient movements. Partial motor recovery is thought to be sustained by neuronal plasticity, particularly in areas close to the lesion site. It is still unknown if treatments acting exclusively on cortical plasticity of perilesional areas could result in behavioral amelioration. We tested whether enhancing plasticity in the ipsilesional cortex using local injections of chondroitinase ABC (ChABC) could promote recovery of skilled motor function in a focal cortical ischemia of forelimb motor cortex in rats. Using the skilled reaching test, we found that acute and delayed ChABC treatment induced recovery of impaired motor skills in treated rats. vGLUT1, vGLUT2, and vGAT staining indicated that functional recovery after acute ChABC treatment was associated with local plastic modification of the excitatory cortical circuitry positive for VGLUT2. ChABC effects on vGLUT2 staining were present only in rats undergoing behavioral training. Thus, the combination of treatments targeting the CSPG component of the extracellular matrix in perilesional areas and rehabilitation could be sufficient to enhance functional recovery from a focal stroke. © 2013 The Author
From pupil to the brain : new insights for studying cortical plasticity through pupillometry
Full text linkPupil size variations have been associated with changes in brain activity patterns related with specific cognitive factors, such as arousal, attention, and mental effort. The locus coeruleus (LC), a key hub in the noradrenergic system of the brain, is considered to be a key regulator of cognitive control on pupil size, with changes in pupil diameter corresponding to the release of norepinephrine (NE). Advances in eye-tracking technology and open-source software have facilitated accurate pupil size measurement in various experimental settings, leading to increased interest in using pupillometry to track the nervous system activation state and as a potential biomarker for brain disorders. This review explores pupillometry as a non-invasive and fully translational tool for studying cortical plasticity starting from recent literature suggesting that pupillometry could be a promising technique for estimating the degree of residual plasticity in human subjects. Given that NE is known to be a critical mediator of cortical plasticity and arousal, the review includes data revealing the importance of the LC-NE system in modulating brain plasticity and pupil size. Finally, we will review data suggesting that pupillometry could provide a quantitative and complementary measure of cortical plasticity also in preclinical studies
Orchestrating the Matrix: the role of Glial Cells and Systemic Signals in Perineuronal Net Dynamics
No full textSynaptic plasticity and signaling in rett syndrome
Full text linkRett syndrome (RTT) is a disorder that is caused in the majority of cases by mutations in the gene methyl-CpG-binding protein-2 (MeCP2). Children with RTT are generally characterized by normal development up to the first year and a half of age, after which they undergo a rapid regression marked by a deceleration of head growth, the onset of stereotyped hand movements, irregular breathing, and seizures. Animal models of RTT with good construct and face validity are available. Their analysis showed that homeostatic regulation of MeCP2 gene is necessary for normal CNS functioning and that multiple complex pathways involving different neuronal and glial cell types are disrupted in RTT models. However, it is increasingly clear that RTT pathogenetic mechanisms converge at synaptic level impairing synaptic transmission and plasticity. We review novel findings showing how specific synaptic mechanisms and related signaling pathways are affected in RTT models. © 2013 Wiley Periodicals, Inc
A Richness that Cures
Full text linkA study in Nature by Fischer et al. shows that environmental enrichment or increasing histone acetylation rescue the ability to form new memories and re-establish access to remote memories even in the presence of brain degeneration. Chromatin remodeling may be the final gate environmental enrichment opens to enhance plasticity and represents a promising target for therapeutical intervention in neurodegenerative diseases
Extracellular Matrix and Visual Cortical Plasticity Freeing the Synapse
No full textAbstractThe effects of monocular deprivation (MD) on the ocular dominance of visual cortical neurons are a paradigmatic example of experience-dependent plasticity. Here we review recent data showing that extracellular matrix (ECM) plays an important role in the control of experience-dependent plasticity both in the developing and adult visual cortex
Vision in mice with neuronal redundancy due to inhibition of developmental cell death
No full textTransgenic mice overexpressing bcl-2, due to inhibition of naturally occurring cell death, have much larger brains and optic nerves as compared to wild-type mice. Since developmental cell death is believed to exert a crucial role in establishing the mature neural circuitry and function, we asked the question of whether basic aspects of vision were altered in bcl-2 mice. Local visually evoked potentials (VEPs) in response to patterned stimuli were recorded from the primary visual cortex. The representation of the vertical meridian was displaced by about 15% in the bcl-2 mouse, accounting for brain expansion. However, visual acuity, contrast threshold, and response latency were normal, indicating that compensatory mechanisms can ensure normal basic properties of vision in spite of marked neuronal redundancy
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