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1

Giasson, Claude J., and Christian Casanova. "Plasticity and Sensory Substitution." Canadian Journal of Optometry 71, no. 4 (August 1, 2009): 39. http://dx.doi.org/10.15353/cjo.71.654.

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Doty, R. W. "Sensory Neurons: Diversity, Development, Plasticity." Archives of Neurology 51, no. 6 (June 1, 1994): 539. http://dx.doi.org/10.1001/archneur.1994.00540180017006.

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Ptito, Maurice, Ron Kupers, Steve Lomber, and Pietro Pietrini. "Sensory Deprivation and Brain Plasticity." Neural Plasticity 2012 (2012): 1–2. http://dx.doi.org/10.1155/2012/810370.

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Calford, M. B. "Dynamic representational plasticity in sensory cortex." Neuroscience 111, no. 4 (June 2002): 709–38. http://dx.doi.org/10.1016/s0306-4522(02)00022-2.

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Ostry, David J., and Paul L. Gribble. "Sensory Plasticity in Human Motor Learning." Trends in Neurosciences 39, no. 2 (February 2016): 114–23. http://dx.doi.org/10.1016/j.tins.2015.12.006.

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Davidoff, R. "Sensory Neurons: Diversity, Development, and Plasticity." Neurology 43, no. 8 (August 1, 1993): 1633. http://dx.doi.org/10.1212/wnl.43.8.1633-d.

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Butko, Nicholas J., and Jochen Triesch. "Learning sensory representations with intrinsic plasticity." Neurocomputing 70, no. 7-9 (March 2007): 1130–38. http://dx.doi.org/10.1016/j.neucom.2006.11.006.

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Frank, Eric. "Sensory Neurons: Diversity, Development and Plasticity." Trends in Neurosciences 16, no. 12 (December 1993): 534–35. http://dx.doi.org/10.1016/0166-2236(93)90201-v.

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Fox, Kevin, Helen Wallace, and Stanislaw Glazewski. "Is there a thalamic component to experience–dependent cortical plasticity?" Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 357, no. 1428 (December 29, 2002): 1709–15. http://dx.doi.org/10.1098/rstb.2002.1169.

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Sensory deprivation and injury to the peripheral nervous system both induce plasticity in the somatosensory system of adult animals, but in different places. While injury induces plasticity at several locations within the ascending somatosensory pathways, sensory deprivation appears only to affect the somatosensory cortex. Experiments have been performed to detect experience–dependent plasticity in thalamic receptive fields, thalamic domain sizes and convergence of thalamic receptive fields onto cortical cells. So far, plasticity has not been detected with sensory deprivation paradigms that ca
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10

Desgent, Sébastien, and Maurice Ptito. "Cortical GABAergic Interneurons in Cross-Modal Plasticity following Early Blindness." Neural Plasticity 2012 (2012): 1–20. http://dx.doi.org/10.1155/2012/590725.

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Early loss of a given sensory input in mammals causes anatomical and functional modifications in the brain via a process called cross-modal plasticity. In the past four decades, several animal models have illuminated our understanding of the biological substrates involved in cross-modal plasticity. Progressively, studies are now starting to emphasise on cell-specific mechanisms that may be responsible for this intermodal sensory plasticity. Inhibitory interneurons expressing γ-aminobutyric acid (GABA) play an important role in maintaining the appropriate dynamic range of cortical excitation, i
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11

Maruska, Karen P., and Julie M. Butler. "Reproductive- and Social-State Plasticity of Multiple Sensory Systems in a Cichlid Fish." Integrative and Comparative Biology 61, no. 1 (May 10, 2021): 249–68. http://dx.doi.org/10.1093/icb/icab062.

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Synopsis Intra- and inter-sexual communications are vital to the survival and reproductive success of animals. In species that cycle in and out of breeding or other physiological condition, sensory function can be modulated to optimize communication at crucial times. Little is known, however, about how widespread this sensory plasticity is across taxa, whether it occurs in multiple senses or both sexes within a species, and what potential modulatory substances and substrates are involved. Thus, studying modulation of sensory communication in a single species can provide valuable insights for u
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12

Bell, C. C., V. Z. Han, Y. Sugawara, and K. Grant. "Synaptic plasticity in the mormyrid electrosensory lobe." Journal of Experimental Biology 202, no. 10 (May 15, 1999): 1339–47. http://dx.doi.org/10.1242/jeb.202.10.1339.

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The mormyrid electrosensory lateral line lobe (ELL) is one of several different sensory structures in fish that behave as adaptive sensory processors. These structures generate negative images of predictable features in the sensory inflow which are added to the actual inflow to minimize the effects of predictable sensory features. The negative images are generated through a process of association between centrally originating predictive signals and sensory inputs from the periphery. In vitro studies in the mormyrid ELL show that pairing of parallel fiber input with Na+ spikes in postsynaptic c
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13

Scheyltjens, Isabelle, and Lutgarde Arckens. "The Current Status of Somatostatin-Interneurons in Inhibitory Control of Brain Function and Plasticity." Neural Plasticity 2016 (2016): 1–20. http://dx.doi.org/10.1155/2016/8723623.

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The mammalian neocortex contains many distinct inhibitory neuronal populations to balance excitatory neurotransmission. A correct excitation/inhibition equilibrium is crucial for normal brain development, functioning, and controlling lifelong cortical plasticity. Knowledge about how the inhibitory network contributes to brain plasticity however remains incomplete. Somatostatin- (SST-) interneurons constitute a large neocortical subpopulation of interneurons, next to parvalbumin- (PV-) and vasoactive intestinal peptide- (VIP-) interneurons. Unlike the extensively studied PV-interneurons, acknow
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14

Phan, Mimi L., and Kasia M. Bieszczad. "Sensory Cortical Plasticity Participates in the Epigenetic Regulation of Robust Memory Formation." Neural Plasticity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/7254297.

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Neuroplasticity remodels sensory cortex across the lifespan. A function of adult sensory cortical plasticity may be capturing available information during perception for memory formation. The degree of experience-dependent remodeling in sensory cortex appears to determine memory strength and specificity for important sensory signals. A key open question is how plasticity is engaged to induce different degrees of sensory cortical remodeling. Neural plasticity for long-term memory requires the expression of genes underlying stable changes in neuronal function, structure, connectivity, and, ultim
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15

Zochodne, Douglas W. "Diabetes and the plasticity of sensory neurons." Neuroscience Letters 596 (June 2015): 60–65. http://dx.doi.org/10.1016/j.neulet.2014.11.017.

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Jamann, Nora, Merryn Jordan, and Maren Engelhardt. "Activity-Dependent Axonal Plasticity in Sensory Systems." Neuroscience 368 (January 2018): 268–82. http://dx.doi.org/10.1016/j.neuroscience.2017.07.035.

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Gundersen, Brigitta. "Context-dependent plasticity in a sensory circuit." Nature Neuroscience 16, no. 10 (September 25, 2013): 1366. http://dx.doi.org/10.1038/nn1013-1366.

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Das, Aniruddha. "Plasticity in adult sensory cortex: a review." Network: Computation in Neural Systems 8, no. 2 (January 1997): R33—R76. http://dx.doi.org/10.1088/0954-898x_8_2_001.

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Depner, Manfred, Konstantin Tziridis, Andreas Hess, and Holger Schulze. "Sensory cortex lesion triggers compensatory neuronal plasticity." BMC Neuroscience 15, no. 1 (2014): 57. http://dx.doi.org/10.1186/1471-2202-15-57.

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20

Moore, David R. "Stroke recovery and sensory plasticity: Common mechanisms?" Developmental Psychobiology 54, no. 3 (March 13, 2012): 326–31. http://dx.doi.org/10.1002/dev.20627.

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Chapman, Ben B., Lesley J. Morrell, Colin R. Tosh, and Jens Krause. "Behavioural consequences of sensory plasticity in guppies." Proceedings of the Royal Society B: Biological Sciences 277, no. 1686 (January 6, 2010): 1395–401. http://dx.doi.org/10.1098/rspb.2009.2055.

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22

Edeline, JM. "Does Hebbian synaptic plasticity explain learning-induced sensory plasticity in adult mammals?" Journal of Physiology-Paris 90, no. 3-4 (January 1996): 271–76. http://dx.doi.org/10.1016/s0928-4257(97)81437-4.

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Feldman, Daniel E., and Michael Brecht. "Map Plasticity in Somatosensory Cortex." Science 310, no. 5749 (November 3, 2005): 810–15. http://dx.doi.org/10.1126/science.1115807.

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Sensory maps in neocortex are adaptively altered to reflect recent experience and learning. In somatosensory cortex, distinct patterns of sensory use or disuse elicit multiple, functionally distinct forms of map plasticity. Diverse approaches—genetics, synaptic and in vivo physiology, optical imaging, and ultrastructural analysis—suggest a distributed model in which plasticity occurs at multiple sites in the cortical circuit with multiple cellular/synaptic mechanisms and multiple likely learning rules for plasticity. This view contrasts with the classical model in which the map plasticity refl
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24

Forster, H. V. "Invited Review: Plasticity in the control of breathing following sensory denervation." Journal of Applied Physiology 94, no. 2 (February 1, 2003): 784–94. http://dx.doi.org/10.1152/japplphysiol.00602.2002.

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The purpose of this manuscript is to review the results of studies on the recovery or plasticity following a denervation- or lesion-induced change in breathing. Carotid body denervation (CBD), lung denervation (LD), cervical (CDR) and thoracic (TDR) dorsal rhizotomy, dorsal spinal column lesions, and lesions at pontine, medullary, and spinal sites all chronically alter breathing. The plasticity after these is highly variable, ranging from near complete recovery of the peripheral chemoreflex in rats after CBD to minimal recovery of the Hering-Breuer inflation reflex in ponies after LD. The degr
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25

Mihail, Sandra M., Andi Wangzhou, Kumud K. Kunjilwar, Jamie K. Moy, Gregory Dussor, Edgar T. Walters, and Theodore J. Price. "MNK-eIF4E signalling is a highly conserved mechanism for sensory neuron axonal plasticity: evidence from Aplysia californica." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1785 (September 23, 2019): 20190289. http://dx.doi.org/10.1098/rstb.2019.0289.

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Injury to sensory neurons causes an increase in the excitability of these cells leading to enhanced action potential generation and a lowering of spike threshold. This type of sensory neuron plasticity occurs across vertebrate and invertebrate species and has been linked to the development of both acute and persistent pain. Injury-induced plasticity in sensory neurons relies on localized changes in gene expression that occur at the level of mRNA translation. Many different translation regulation signalling events have been defined and these signalling events are thought to selectively target s
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26

Maya-Vetencourt, José Fernando, and Nicola Origlia. "Visual Cortex Plasticity: A Complex Interplay of Genetic and Environmental Influences." Neural Plasticity 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/631965.

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The central nervous system architecture is highly dynamic and continuously modified by sensory experience through processes of neuronal plasticity. Plasticity is achieved by a complex interplay of environmental influences and physiological mechanisms that ultimately activate intracellular signal transduction pathways regulating gene expression. In addition to the remarkable variety of transcription factors and their combinatorial interaction at specific gene promoters, epigenetic mechanisms that regulate transcription have emerged as conserved processes by which the nervous system accomplishes
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27

Romashchenko, A. V., Р. Е. Kireeva, M. В. Sharapova, Т. A. Zapara, and A. S. Ratushnyak. "Learning-induced sensory plasticity of mouse olfactory epithelium." Vavilov Journal of Genetics and Breeding 22, no. 8 (January 3, 2019): 1070–77. http://dx.doi.org/10.18699/vj18.452.

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Traditionally, studies of the neurobiology of learning and memory focus on the circuitry that interfaces between sensory inputs and behavioral outputs, such as the amygdala and cerebellum. However, evidence is accumulating that some forms of learning can in fact drive stimulus­specifc changes very early in sensory systems, including not only primary sensory cortices but also precortical structures and even the peripheral sensory organs themselves. In this study, we investigated the effect of olfactory associative training on the functional activity of olfactory epithelium neurons in response to
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28

Fallon, James B., Dexter R. F. Irvine, and Robert K. Shepherd. "Cochlear implants and brain plasticity." Hearing Research 238, no. 1-2 (April 2008): 110–17. http://dx.doi.org/10.1016/j.heares.2007.08.004.

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Franosch, Jan-Moritz P., Sebastian Urban, and J. Leo van Hemmen. "Supervised Spike-Timing-Dependent Plasticity: A Spatiotemporal Neuronal Learning Rule for Function Approximation and Decisions." Neural Computation 25, no. 12 (December 2013): 3113–30. http://dx.doi.org/10.1162/neco_a_00520.

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How can an animal learn from experience? How can it train sensors, such as the auditory or tactile system, based on other sensory input such as the visual system? Supervised spike-timing-dependent plasticity (supervised STDP) is a possible answer. Supervised STDP trains one modality using input from another one as “supervisor.” Quite complex time-dependent relationships between the senses can be learned. Here we prove that under very general conditions, supervised STDP converges to a stable configuration of synaptic weights leading to a reconstruction of primary sensory input.
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30

Jiang, Mingchen C., Sherif M. Elbasiouny, William F. Collins, and C. J. Heckman. "The transformation of synaptic to system plasticity in motor output from the sacral cord of the adult mouse." Journal of Neurophysiology 114, no. 3 (September 2015): 1987–2004. http://dx.doi.org/10.1152/jn.00337.2015.

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Synaptic plasticity is fundamental in shaping the output of neural networks. The transformation of synaptic plasticity at the cellular level into plasticity at the system level involves multiple factors, including behavior of local networks of interneurons. Here we investigate the synaptic to system transformation for plasticity in motor output in an in vitro preparation of the adult mouse spinal cord. System plasticity was assessed from compound action potentials (APs) in spinal ventral roots, which were generated simultaneously by the axons of many motoneurons (MNs). Synaptic plasticity was
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31

Polley, Daniel B., Andrea R. Hillock, Christopher Spankovich, Maria V. Popescu, David W. Royal, and Mark T. Wallace. "Development and Plasticity of Intra- and Intersensory Information Processing." Journal of the American Academy of Audiology 19, no. 10 (November 2008): 780–98. http://dx.doi.org/10.3766/jaaa.19.10.6.

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The functional architecture of sensory brain regions reflects an ingenious biological solution to the competing demands of a continually changing sensory environment. While they are malleable, they have the constancy necessary to support a stable sensory percept. How does the functional organization of sensory brain regions contend with these antithetical demands? Here we describe the functional organization of auditory and multisensory (i.e., auditory-visual) information processing in three sensory brain structures: (1) a low-level unisensory cortical region, the primary auditory cortex (A1);
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Feldman, Daniel E. "A New Critical Period for Sensory Map Plasticity." Neuron 31, no. 2 (August 2001): 171–73. http://dx.doi.org/10.1016/s0896-6273(01)00363-4.

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Krupa, D. J., A. A. Ghazanfar, and M. A. L. Nicolelis. "Immediate thalamic sensory plasticity depends on corticothalamic feedback." Proceedings of the National Academy of Sciences 96, no. 14 (July 6, 1999): 8200–8205. http://dx.doi.org/10.1073/pnas.96.14.8200.

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Undem, B. J. "Inflammation-induced sensory nerve plasticity in the airways." Clinical & Experimental Allergy Reviews 1, no. 2 (July 2001): 93–95. http://dx.doi.org/10.1046/j.1472-9725.2001.00015.x.

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Cafferty, W. B. J., E. J. Bradbury, M. Lidierth, M. Jones, P. J. Duffy, S. Pezet, and S. B. McMahon. "Chondroitinase ABC-Mediated Plasticity of Spinal Sensory Function." Journal of Neuroscience 28, no. 46 (November 12, 2008): 11998–2009. http://dx.doi.org/10.1523/jneurosci.3877-08.2008.

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Bach-y-Rita, P. "Brain Plasticity as a Basis of Sensory Substitution." Neurorehabilitation and Neural Repair 1, no. 2 (January 1, 1987): 67–71. http://dx.doi.org/10.1177/136140968700100202.

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GRAZIADEI, P. P. C., and G. A. MONTI GRAZIADEI. "Neurogenesis and Plasticity of the Olfactory Sensory Neurons." Annals of the New York Academy of Sciences 457, no. 1 Hope for a Ne (December 1985): 127–42. http://dx.doi.org/10.1111/j.1749-6632.1985.tb20802.x.

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Halligan, Peter W., John C. Marshall, and Derick T. Wade. "Sensory disorganization and perceptual plasticity after limb amputation." NeuroReport 5, no. 11 (June 1994): 1341–45. http://dx.doi.org/10.1097/00001756-199406000-00012.

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Cooper, Emily A., and Allyson P. Mackey. "Sensory and cognitive plasticity: implications for academic interventions." Current Opinion in Behavioral Sciences 10 (August 2016): 21–27. http://dx.doi.org/10.1016/j.cobeha.2016.04.008.

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Mamassian, Pascal. "Sensory Plasticity: When Eye Movements Change Visual Appearance." Current Biology 26, no. 1 (January 2016): R24—R26. http://dx.doi.org/10.1016/j.cub.2015.11.008.

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Perez-Borrego, Y., V. Soto-Leon, J. Aguilar, G. Foffani, M. Rotondi, S. Bestmann, and A. Oliviero. "Studying plasticity of sensory function: insight from pregnancy." Experimental Brain Research 209, no. 2 (January 4, 2011): 311–16. http://dx.doi.org/10.1007/s00221-010-2532-8.

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Morrone, Maria Concetta. "Brain Development: Critical Periods for Cross-Sensory Plasticity." Current Biology 20, no. 21 (November 2010): R934—R936. http://dx.doi.org/10.1016/j.cub.2010.09.052.

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LeMessurier, Amy M., and Daniel E. Feldman. "Plasticity of population coding in primary sensory cortex." Current Opinion in Neurobiology 53 (December 2018): 50–56. http://dx.doi.org/10.1016/j.conb.2018.04.029.

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Ebner, F. F., V. Rema, R. Sachdev, and F. J. Symons. "Activity-Dependent Plasticity in Adult Somatic Sensory Cortex." Seminars in Neuroscience 9, no. 1-2 (1997): 47–58. http://dx.doi.org/10.1006/smns.1997.0105.

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Hokland, Jørn, and Beatrix Vereijken. "Can robots without Hebbian plasticity make good models of adaptive behaviour?" Behavioral and Brain Sciences 24, no. 6 (December 2001): 1060–62. http://dx.doi.org/10.1017/s0140525x01330121.

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No. Animals' primary problem is the shaping of movements, guided by and adapting to sensory signals. This requires a narrower class of biorobotic models than that spanned by Webb's dimensions and examples. We claim that all model variables and mechanisms must have real counterparts, input vectors must model known sensor fields, internal state vectors and transformations must model neurophysiological processes, and output vectors must model coordinated muscle signals.
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46

Witten, Ilana B., Eric I. Knudsen, and Haim Sompolinsky. "A Hebbian Learning Rule Mediates Asymmetric Plasticity in Aligning Sensory Representations." Journal of Neurophysiology 100, no. 2 (August 2008): 1067–79. http://dx.doi.org/10.1152/jn.00013.2008.

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In the brain, mutual spatial alignment across different sensory representations can be shaped and maintained through plasticity. Here, we use a Hebbian model to account for the synaptic plasticity that results from a displacement of the space representation for one input channel relative to that of another, when the synapses from both channels are equally plastic. Surprisingly, although the synaptic weights for the two channels obeyed the same Hebbian learning rule, the amount of plasticity exhibited by the respective channels was highly asymmetric and depended on the relative strength and wid
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47

Kraft, Andrew W., Adam Q. Bauer, Joseph P. Culver, and Jin-Moo Lee. "Sensory deprivation after focal ischemia in mice accelerates brain remapping and improves functional recovery through Arc-dependent synaptic plasticity." Science Translational Medicine 10, no. 426 (January 31, 2018): eaag1328. http://dx.doi.org/10.1126/scitranslmed.aag1328.

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Recovery after stroke, a major cause of adult disability, is often unpredictable and incomplete. Behavioral recovery is associated with functional reorganization (remapping) in perilesional regions, suggesting that promoting this process might be an effective strategy to enhance recovery. However, the molecular mechanisms underlying remapping after brain injury and the consequences of its modulation are poorly understood. Focal sensory loss or deprivation has been shown to induce remapping in the corresponding brain areas through activity-regulated cytoskeleton-associated protein (Arc)–mediate
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48

Kilgard, M. P., J. L. Vazquez, N. D. Engineer, and P. K. Pandya. "Experience dependent plasticity alters cortical synchronization." Hearing Research 229, no. 1-2 (July 2007): 171–79. http://dx.doi.org/10.1016/j.heares.2007.01.005.

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Beckmann, Daniela, Mirko Feldmann, Olena Shchyglo, and Denise Manahan-Vaughan. "Hippocampal Synaptic Plasticity, Spatial Memory, and Neurotransmitter Receptor Expression Are Profoundly Altered by Gradual Loss of Hearing Ability." Cerebral Cortex 30, no. 8 (March 20, 2020): 4581–96. http://dx.doi.org/10.1093/cercor/bhaa061.

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Abstract Sensory information comprises the substrate from which memories are created. Memories of spatial sensory experience are encoded by means of synaptic plasticity in the hippocampus. Hippocampal dependency on sensory information is highlighted by the fact that sudden and complete loss of a sensory modality results in an impairment of hippocampal function that persists for months. Effects are accompanied by extensive changes in the expression of neurotransmitter receptors in cortex and hippocampus, consistent with a substantial adaptive reorganization of cortical function. Whether gradual
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50

Gainey, Melanie A., and Daniel E. Feldman. "Multiple shared mechanisms for homeostatic plasticity in rodent somatosensory and visual cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1715 (March 5, 2017): 20160157. http://dx.doi.org/10.1098/rstb.2016.0157.

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We compare the circuit and cellular mechanisms for homeostatic plasticity that have been discovered in rodent somatosensory (S1) and visual (V1) cortex. Both areas use similar mechanisms to restore mean firing rate after sensory deprivation. Two time scales of homeostasis are evident, with distinct mechanisms. Slow homeostasis occurs over several days, and is mediated by homeostatic synaptic scaling in excitatory networks and, in some cases, homeostatic adjustment of pyramidal cell intrinsic excitability. Fast homeostasis occurs within less than 1 day, and is mediated by rapid disinhibition, i
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