Environmental enrichment differentially modifies specific components of sensory-evoked activity in rat barrel cortex as revealed by simultaneous electrophysiological recordings and optical imaging in vivo
“…Similar to studies in auditory cortex, generic EE (i.e., non-specific enrichment) results in reorganized cortical topographic maps, decreased receptive field sizes, increased response selectivity and increased sensory evoked potentials in the somatosensory cortex (Xerri et al, 1996; Coq and Xerri, 1998; Polley et al, 2004; Devonshire et al, 2010). One interesting effect demonstrated here is that EE effects on receptive field sizes and responses to stimulation of the main topographic input to the neurons may be laminar selective (an effect that does not appear to have been explored in auditory cortex).…”
Section: Neuronal Functional Changes Associated With Exposure To Eementioning
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.
“…Similar to studies in auditory cortex, generic EE (i.e., non-specific enrichment) results in reorganized cortical topographic maps, decreased receptive field sizes, increased response selectivity and increased sensory evoked potentials in the somatosensory cortex (Xerri et al, 1996; Coq and Xerri, 1998; Polley et al, 2004; Devonshire et al, 2010). One interesting effect demonstrated here is that EE effects on receptive field sizes and responses to stimulation of the main topographic input to the neurons may be laminar selective (an effect that does not appear to have been explored in auditory cortex).…”
Section: Neuronal Functional Changes Associated With Exposure To Eementioning
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.
“…Because of its accessibility and behavioral relevance, the trigeminal system in rodents has been a frequent target for these studies. In rodents exposed to this type of environment, the somatosensory cortex exhibits increases in cortical thickness and volume, dendrite number and length, and number and/or size of spines, synapses, glial cells and capillaries (Diamond 1988;MachĂn et al 2004;Nithianantharajah et al 2004;Rema et al 2006;Landers et al 2011), as well as refinements of topographic maps and potentiation of sensory responses (Frostig 2006;Devonshire et al 2010).…”
Section: Effects Of Exposure To Sensory Enrichmentmentioning
Lasting modifications of sensory input induce structural and functional changes in the brain, but the involvement of primary sensory neurons in this plasticity has been practically ignored. Here, we examine qualitatively and quantitatively the central axonal terminations of a population of trigeminal ganglion neurons, whose peripheral axons innervate a single mystacial vibrissa. Vibrissa follicles are heavily innervated by myelinated and unmyelinated fibers that exit the follicle mainly through a single deep vibrissal nerve. We made intraneural injections of a mixture of cholera-toxin B (CTB) and isolectin B4, tracers for myelinated and unmyelinated fibers, respectively, in three groups of young adult rats: controls, animals subjected to chronic haptic touch deprivation by unilateral whisker trimming, and rats exposed for 2Â months to environmental enrichment. The regional and laminar pattern of terminal arborizations in the trigeminal nuclei of the brain stem did not show gross changes after sensory input modification. However, there were significant and widespread increases in the number and size of CTB-labeled varicosities in the enriched condition, and a prominent expansion in both parameters in laminae III-IV of the caudal division of the spinal nucleus in the whisker trimming condition. No obvious changes were detected in IB4-labeled terminals in laminae I-II. These results show that a prolonged exposure to changes in sensory input without any neural damage is capable of inducing structural changes in terminals of primary afferents in mature animals, and highlight the importance of peripheral structures as the presumed earliest players in sensory experience-dependent plasticity.
“…To examine this question, in vivo chronic imaging has proven useful for assessing the large-scale spatial dynamics of network response properties12 and for quantifying changes in those responses to sensory deprivation1345 or enrichment67. In parallel, behavioural and lesion experiments have been implemented to elucidate the psychophysical properties of sensory processing and the biological loci and function of neuronal elements involved891011.…”
Lesion experiments suggest that odour input to the olfactory bulb contains significant redundant signal such that rodents can discern odours using minimal stimulus-related information. Here we investigate the dependence of odour-quality perception on the integrity of glomerular activity by comparing odour-evoked activity maps before and after epithelial lesions. Lesions prevent mice from recognizing previously experienced odours and differentially delay discrimination learning of unrecognized and novel odour pairs. Poor recognition results not from mice experiencing an altered concentration of an odour but from perception of apparent novel qualities. Consistent with this, relative intensity of glomerular activity following lesions is altered compared with maps recorded in shams and by varying odour concentration. Together, these data show that odour recognition relies on comprehensively matching input patterns to a previously generated stimulus template. When encountering novel odours, access to all glomerular activity ensures rapid generation of new templates to perform accurate perceptual judgements.
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