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Journal articles on the topic 'Somatosensory plasticity'

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Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Kuehn, Esther, and Burkhard Pleger. "How Visual Body Perception Influences Somatosensory Plasticity." Neural Plasticity 2018 (2018): 1–12. http://dx.doi.org/10.1155/2018/7909684.

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The study of somatosensory plasticity offers unique insights into the neuronal mechanisms that underlie human adaptive and maladaptive plasticity. So far, little attention has been paid on the specific influence of visual body perception on somatosensory plasticity and learning in humans. Here, we review evidence on how visual body perception induces changes in the functional architecture of the somatosensory system and discuss the specific influence the social environment has on tactile plasticity and learning. We focus on studies that have been published in the areas of human cognitive and clinical neuroscience and refer to animal studies when appropriate. We discuss the therapeutic potential of socially mediated modulations of somatosensory plasticity and introduce specific paradigms to induce plastic changes under controlled conditions. This review offers a contribution to understanding the complex interactions between social perception and somatosensory learning by focusing on a novel research field: socially mediated sensory plasticity.

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2

Ma, Xiaofeng, and Nobuo Suga. "Augmentation of Plasticity of the Central Auditory System by the Basal Forebrain and/or Somatosensory Cortex." Journal of Neurophysiology 89, no. 1 (January 1, 2003): 90–103. http://dx.doi.org/10.1152/jn.00968.2001.

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Auditory conditioning (associative learning) or focal electric stimulation of the primary auditory cortex (AC) evokes reorganization (plasticity) of the cochleotopic (frequency) map of the inferior colliculus (IC) as well as that of the AC. The reorganization results from shifts in the best frequencies (BFs) and frequency-tuning curves of single neurons. Since the importance of the cholinergic basal forebrain for cortical plasticity and the importance of the somatosensory cortex and the corticofugal auditory system for collicular and cortical plasticity have been demonstrated, Gao and Suga proposed a hypothesis that states that the AC and corticofugal system play an important role in evoking auditory collicular and cortical plasticity and that auditory and somatosensory signals from the cerebral cortex to the basal forebrain play an important role in augmenting collicular and cortical plasticity. To test their hypothesis, we studied whether the amount and the duration of plasticity of both collicular and cortical neurons evoked by electric stimulation of the AC or by acoustic stimulation were increased by electric stimulation of the basal forebrain and/or the somatosensory cortex. In adult big brown bats ( Eptesicus fuscus), we made the following major findings. 1) Collicular and cortical plasticity evoked by electric stimulation of the AC is augmented by electric stimulation of the basal forebrain. The amount of augmentation is larger for cortical plasticity than for collicular plasticity. 2) Collicular and cortical plasticity evoked by AC stimulation is augmented by somatosensory cortical stimulation mimicking fear conditioning. The amount of augmentation is larger for cortical plasticity than for collicular plasticity. 3) Collicular and cortical plasticity evoked by both AC and basal forebrain stimulations is further augmented by somatosensory cortical stimulation. 4) A lesion of the basal forebrain tends to reduce collicular and cortical plasticity evoked by AC stimulation. The reduction is small and statistically insignificant for collicular plasticity but significant for cortical plasticity. 5) The lesion of the basal forebrain eliminates the augmentation of collicular and cortical plasticity that otherwise would be evoked by somatosensory cortical stimulation. 6) Collicular and cortical plasticity evoked by repetitive acoustic stimuli is augmented by basal forebrain and/or somatosensory cortical stimulation. However, the lesion of the basal forebrain eliminates the augmentation of collicular and cortical plasticity that otherwise would be evoked by somatosensory cortical stimulation. These findings support the hypothesis proposed by Gao and Suga.

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3

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 reflects a single Hebbian process acting at a small set of cortical synapses.

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4

Ohashi, Hiroki, Paul L. Gribble, and David J. Ostry. "Somatosensory cortical excitability changes precede those in motor cortex during human motor learning." Journal of Neurophysiology 122, no. 4 (October 1, 2019): 1397–405. http://dx.doi.org/10.1152/jn.00383.2019.

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Motor learning is associated with plasticity in both motor and somatosensory cortex. It is known from animal studies that tetanic stimulation to each of these areas individually induces long-term potentiation in its counterpart. In this context it is possible that changes in motor cortex contribute to somatosensory change and that changes in somatosensory cortex are involved in changes in motor areas of the brain. It is also possible that learning-related plasticity occurs in these areas independently. To better understand the relative contribution to human motor learning of motor cortical and somatosensory plasticity, we assessed the time course of changes in primary somatosensory and motor cortex excitability during motor skill learning. Learning was assessed using a force production task in which a target force profile varied from one trial to the next. The excitability of primary somatosensory cortex was measured using somatosensory evoked potentials in response to median nerve stimulation. The excitability of primary motor cortex was measured using motor evoked potentials elicited by single-pulse transcranial magnetic stimulation. These two measures were interleaved with blocks of motor learning trials. We found that the earliest changes in cortical excitability during learning occurred in somatosensory cortical responses, and these changes preceded changes in motor cortical excitability. Changes in somatosensory evoked potentials were correlated with behavioral measures of learning. Changes in motor evoked potentials were not. These findings indicate that plasticity in somatosensory cortex occurs as a part of the earliest stages of motor learning, before changes in motor cortex are observed. NEW & NOTEWORTHY We tracked somatosensory and motor cortical excitability during motor skill acquisition. Changes in both motor cortical and somatosensory excitability were observed during learning; however, the earliest changes were in somatosensory cortex, not motor cortex. Moreover, the earliest changes in somatosensory cortical excitability predict the extent of subsequent learning; those in motor cortex do not. This is consistent with the idea that plasticity in somatosensory cortex coincides with the earliest stages of human motor learning.

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Ostry, D. J., M. Darainy, A. A. G. Mattar, J. Wong, and P. L. Gribble. "Somatosensory Plasticity and Motor Learning." Journal of Neuroscience 30, no. 15 (April 14, 2010): 5384–93. http://dx.doi.org/10.1523/jneurosci.4571-09.2010.

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6

Wu, Calvin, Roxana A. Stefanescu, David T. Martel, and Susan E. Shore. "Tinnitus: Maladaptive auditory–somatosensory plasticity." Hearing Research 334 (April 2016): 20–29. http://dx.doi.org/10.1016/j.heares.2015.06.005.

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7

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 cause substantial cortical plasticity. Part of the reason for the lack of thalamic plasticity may lie in the synaptic properties of afferent systems to the thalamus. A second factor may lie in the differences in the organization of cortical and thalamic circuits. Many deprivation paradigms induce plasticity by decreasing phasic lateral inhibition. Since lateral inhibition appears to be far weaker in the thalamus than the cortex, sensory deprivation may not cause large enough imbalances in thalamic activity to induce plasticity in the thalamus.

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Fox, Kevin. "Experience-dependent plasticity mechanisms for neural rehabilitation in somatosensory cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 364, no. 1515 (November 27, 2008): 369–81. http://dx.doi.org/10.1098/rstb.2008.0252.

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Functional rehabilitation of the cortex following peripheral or central nervous system damage is likely to be improved by a combination of behavioural training and natural or therapeutically enhanced synaptic plasticity mechanisms. Experience-dependent plasticity studies in the somatosensory cortex have begun to reveal those synaptic plasticity mechanisms that are driven by sensory experience and might therefore be active during behavioural training. In this review the anatomical pathways, synaptic plasticity mechanisms and structural plasticity substrates involved in cortical plasticity are explored, focusing on work in the somatosensory cortex and the barrel cortex in particular.

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9

Peng, Weiqin, Tiange Yang, Jiawei Yuan, Jianpeng Huang, and Jianhua Liu. "Electroacupuncture-Induced Plasticity between Different Representations in Human Motor Cortex." Neural Plasticity 2020 (August 14, 2020): 1–8. http://dx.doi.org/10.1155/2020/8856868.

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Somatosensory stimulation can effectively induce plasticity in the motor cortex representation of the stimulated body part. Specific interactions have been reported between different representations within the primary motor cortex. However, studies evaluating somatosensory stimulation-induced plasticity between different representations within the primary motor cortex are sparse. The purpose of this study was to investigate the effect of somatosensory stimulation on the modulation of plasticity between different representations within the primary motor cortex. Twelve healthy volunteers received both electroacupuncture (EA) and sham EA at the TE5 acupoint (located on the forearm). Plasticity changes in different representations, including the map volume, map area, and centre of gravity (COG) were evaluated by transcranial magnetic stimulation (TMS) before and after the intervention. EA significantly increased the map volume of the forearm and hand representations compared to those of sham EA and significantly reduced the map volume of the face representation compared to that before EA. No significant change was found in the map volume of the upper arm and leg representations after EA, and likewise, no significant changes in map area and COG were observed. These results suggest that EA functions as a form of somatosensory stimulation to effectively induce plasticity between different representations within the primary motor cortex, which may be related to the extensive horizontal intrinsic connectivity between different representations. The cortical plasticity induced by somatosensory stimulation might be purposefully used to modulate human cortical function.

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10

Diamond, M., W. Huang, and F. Ebner. "Laminar comparison of somatosensory cortical plasticity." Science 265, no. 5180 (September 23, 1994): 1885–88. http://dx.doi.org/10.1126/science.8091215.

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11

Wu, Carolyn W. H., Peter van Gelderen, Takashi Hanakawa, Zaneb Yaseen, and Leonardo G. Cohen. "Enduring representational plasticity after somatosensory stimulation." NeuroImage 27, no. 4 (October 2005): 872–84. http://dx.doi.org/10.1016/j.neuroimage.2005.05.055.

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12

Florence, Sherre L., Neeraj Jain, and Jon H. Kaas. "Plasticity of Somatosensory Cortex in Primates." Seminars in Neuroscience 9, no. 1-2 (1997): 3–12. http://dx.doi.org/10.1006/smns.1997.0101.

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13

Michel, Niklas, Pratibha Narayanan, and Manuela Schmidt. "Age-Dependent Plasticity of Somatosensory Mechanosensation." Biophysical Journal 116, no. 3 (February 2019): 376a. http://dx.doi.org/10.1016/j.bpj.2018.11.2044.

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14

Sims, Robert E., John B. Butcher, H. Rheinallt Parri, and Stanislaw Glazewski. "Astrocyte and Neuronal Plasticity in the Somatosensory System." Neural Plasticity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/732014.

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Changing the whisker complement on a rodent’s snout can lead to two forms of experience-dependent plasticity (EDP) in the neurons of the barrel cortex, where whiskers are somatotopically represented. One form, termed coding plasticity, concerns changes in synaptic transmission and connectivity between neurons. This is thought to underlie learning and memory processes and so adaptation to a changing environment. The second, called homeostatic plasticity, serves to maintain a restricted dynamic range of neuronal activity thus preventing its saturation or total downregulation. Current explanatory models of cortical EDP are almost exclusively neurocentric. However, in recent years, increasing evidence has emerged on the role of astrocytes in brain function, including plasticity. Indeed, astrocytes appear as necessary partners of neurons at the core of the mechanisms of coding and homeostatic plasticity recorded in neurons. In addition to neuronal plasticity, several different forms of astrocytic plasticity have recently been discovered. They extend from changes in receptor expression and dynamic changes in morphology to alteration in gliotransmitter release. It is however unclear how astrocytic plasticity contributes to the neuronal EDP. Here, we review the known and possible roles for astrocytes in the barrel cortex, including its plasticity.

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Miller, Luke E., Matthew R. Longo, and Ayse P. Saygin. "Tool Use Modulates Somatosensory Cortical Processing in Humans." Journal of Cognitive Neuroscience 31, no. 12 (December 2019): 1782–95. http://dx.doi.org/10.1162/jocn_a_01452.

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Tool use leads to plastic changes in sensorimotor body representations underlying tactile perception. The neural correlates of this tool-induced plasticity in humans have not been adequately characterized. This study used ERPs to investigate the stage of sensory processing modulated by tool use. Somatosensory evoked potentials, elicited by median nerve stimulation, were recorded before and after two forms of object interaction: tool use and hand use. Compared with baseline, tool use—but not use of the hand alone—modulated the amplitude of the P100. The P100 is a mid-latency component that indexes the construction of multisensory models of the body and has generators in secondary somatosensory and posterior parietal cortices. These results mark one of the first demonstrations of the neural correlates of tool-induced plasticity in humans and suggest that tool use modulates relatively late stages of somatosensory processing outside primary somatosensory cortex. This finding is consistent with what has been observed in tool-trained monkeys and suggests that the mechanisms underlying tool-induced plasticity have been preserved across primate evolution.

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Dykes, R. W. "Mechanisms controlling neuronal plasticity in somatosensory cortex." Canadian Journal of Physiology and Pharmacology 75, no. 5 (May 1, 1997): 535–45. http://dx.doi.org/10.1139/y97-089.

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17

Ray, Saikat, Miao Li, Stefan Paul Koch, Susanne Mueller, Philipp Boehm-Sturm, Hong Wang, Michael Brecht, and Robert Konrad Naumann. "Seasonal plasticity in the adult somatosensory cortex." Proceedings of the National Academy of Sciences 117, no. 50 (November 30, 2020): 32136–44. http://dx.doi.org/10.1073/pnas.1922888117.

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Seasonal cycles govern life on earth, from setting the time for the mating season to influencing migrations and governing physiological conditions like hibernation. The effect of such changing conditions on behavior is well-appreciated, but their impact on the brain remains virtually unknown. We investigate long-term seasonal changes in the mammalian brain, known as Dehnel’s effect, where animals exhibit plasticity in body and brain sizes to counter metabolic demands in winter. We find large seasonal variation in cellular architecture and neuronal activity in the smallest terrestrial mammal, the Etruscan shrew, Suncus etruscus. Their brain, and specifically their neocortex, shrinks in winter. Shrews are tactile hunters, and information from whiskers first reaches the somatosensory cortex layer 4, which exhibits a reduced width (−28%) in winter. Layer 4 width (+29%) and neuron number (+42%) increase the following summer. Activity patterns in the somatosensory cortex show a prominent reduction of touch-suppressed neurons in layer 4 (−55%), the most metabolically active layer. Loss of inhibitory gating occurs with a reduction in parvalbumin-positive interneurons, one of the most active neuronal subtypes and the main regulators of inhibition in layer 4. Thus, a reduction in neurons in layer 4 and particularly parvalbumin-positive interneurons may incur direct metabolic benefits. However, changes in cortical balance can also affect the threshold for detecting sensory stimuli and impact prey choice, as observed in wild shrews. Thus, seasonal neural adaptation can offer synergistic metabolic and behavioral benefits to the organism and offer insights on how neural systems show adaptive plasticity in response to ecological demands.

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18

Goldenkoff, Elana R., Heather R. McGregor, Joshua Mergos, Puyan Gholizadeh, John Bridenstine, Matt J. N. Brown, and Michael Vesia. "Reversal of Visual Feedback Modulates Somatosensory Plasticity." Neuroscience 452 (January 2021): 335–44. http://dx.doi.org/10.1016/j.neuroscience.2020.10.033.

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19

Medina, Jared, and Brenda Rapp. "Rapid Experience-Dependent Plasticity following Somatosensory Damage." Current Biology 24, no. 6 (March 2014): 677–80. http://dx.doi.org/10.1016/j.cub.2014.01.070.

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20

Darainy, Mohammad, Shahabeddin Vahdat, and David J. Ostry. "Neural Basis of Sensorimotor Plasticity in Speech Motor Adaptation." Cerebral Cortex 29, no. 7 (July 6, 2018): 2876–89. http://dx.doi.org/10.1093/cercor/bhy153.

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Abstract When we speak, we get correlated sensory feedback from speech sounds and from the muscles and soft tissues of the vocal tract. Here we dissociate the contributions of auditory and somatosensory feedback to identify brain networks that underlie the somatic contribution to speech motor learning. The technique uses a robotic device that selectively alters somatosensory inputs in combination with resting-state fMRI scans that reveal learning-related changes in functional connectivity. A partial correlation analysis is used to identify connectivity changes that are not explained by the time course of activity in any other learning-related areas. This analysis revealed changes related to behavioral improvements in movement and separately, to changes in auditory perception: Speech motor adaptation itself was associated with connectivity changes that were primarily in non-motor areas of brain, specifically, to a strengthening of connectivity between auditory and somatosensory cortex and between presupplementary motor area and the inferior parietal lobule. In contrast, connectively changes associated with alterations to auditory perception were restricted to speech motor areas, specifically, primary motor cortex and inferior frontal gyrus. Overall, our findings show that during adaptation, somatosensory inputs result in a broad range of changes in connectivity in areas associated with speech motor control and learning.

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Jacobs, M., A. Premji, and A. J. Nelson. "Plasticity-Inducing TMS Protocols to Investigate Somatosensory Control of Hand Function." Neural Plasticity 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/350574.

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Hand function depends on sensory feedback to direct an appropriate motor response. There is clear evidence that somatosensory cortices modulate motor behaviour and physiology within primary motor cortex. However, this information is mainly from research in animals and the bridge to human hand control is needed. Emerging evidence in humans supports the notion that somatosensory cortices modulate motor behaviour, physiology and sensory perception. Transcranial magnetic stimulation (TMS) allows for the investigation of primary and higher-order somatosensory cortices and their role in control of hand movement in humans. This review provides a summary of several TMS protocols in the investigation of hand control via the somatosensory cortices. TMS plasticity inducing protocols reviewed include paired associative stimulation, repetitive TMS, theta-burst stimulation as well as other techniques that aim to modulate cortical excitability in sensorimotor cortices. Although the discussed techniques may modulate cortical excitability, careful consideration of experimental design is needed to isolate factors that may interfere with desired results of the plasticity-inducing protocol, specifically events that may lead to metaplasticity within the targeted cortex.

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Muret, Dollyane, Sébastien Daligault, Hubert R. Dinse, Claude Delpuech, Jérémie Mattout, Karen T. Reilly, and Alessandro Farnè. "Neuromagnetic correlates of adaptive plasticity across the hand-face border in human primary somatosensory cortex." Journal of Neurophysiology 115, no. 4 (April 1, 2016): 2095–104. http://dx.doi.org/10.1152/jn.00628.2015.

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It is well established that permanent or transient reduction of somatosensory inputs, following hand deafferentation or anesthesia, induces plastic changes across the hand-face border, supposedly responsible for some altered perceptual phenomena such as tactile sensations being referred from the face to the phantom hand. It is also known that transient increase of hand somatosensory inputs, via repetitive somatosensory stimulation (RSS) at a fingertip, induces local somatosensory discriminative improvement accompanied by cortical representational changes in the primary somatosensory cortex (SI). We recently demonstrated that RSS at the tip of the right index finger induces similar training-independent perceptual learning across the hand-face border, improving somatosensory perception at the lips (Muret D, Dinse HR, Macchione S, Urquizar C, Farnè A, Reilly KT. Curr Biol 24: R736–R737, 2014). Whether neural plastic changes across the hand-face border accompany such remote and adaptive perceptual plasticity remains unknown. Here we used magnetoencephalography to investigate the electrophysiological correlates underlying RSS-induced behavioral changes across the hand-face border. The results highlight significant changes in dipole location after RSS both for the stimulated finger and for the lips. These findings reveal plastic changes that cross the hand-face border after an increase, instead of a decrease, in somatosensory inputs.

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Juliano, S. L., D. E. Eslin, and M. Tommerdahl. "Developmental regulation of plasticity in cat somatosensory cortex." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1706–16. http://dx.doi.org/10.1152/jn.1994.72.4.1706.

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1. The neocortical response to deprivation of somatic sensory input in young animals of different ages was compared with the same manipulation in adults. The response was measured through the use of 2-deoxyglucose (2DG) mapping. Although several features of the cortical response were similar in animals of all ages, the metabolic patterns evoked by somatic stimulation differed substantially from each other at all ages. 2. When adult cats receive a digit amputation and survive from 2 to 8 wk, the pattern of stimulus-evoked metabolic uptake expands dramatically in the somatosensory cortex contralateral to the deprived forepaw. Comparisons between the normal and experimental somatosensory cortices reveal that the distribution of activity on the experimental side was roughly an expanded version of the normal pattern. 3. Unilateral digit amputations of digit 2 were conducted on kittens 2, 4, or 6 wk old. They survived until 3–4 mo and then received a 2DG experiment, during which digit 3 was stimulated bilaterally. Evaluation of the evoked metabolic pattern indicated substantial differences from the activity elicited in adults undergoing identical manipulations. 4. The individual patches of activity that made up the metabolic pattern were similar in intensity in both hemispheres when the digit amputation was conducted at either 2, 4, or 6 wk. After a digit amputation at 2 wk, the patches were significantly narrower in the experimental hemisphere; after a digit amputation at 6 wk, the patches were significantly wider in the hemisphere receiving from the deprived forepaw. 5. Two-dimensional maps of 2DG uptake in areas 3b and 1 of the somatosensory cortex reveal that after a digit amputation at 2, 4, or 6 wk, the distribution of activity in the hemisphere receiving from the digit amputation was more dispersed and widespread than in the normal hemisphere. The dispersed pattern of uptake was not an expanded version of the normal pattern, but scattered over a wider region of somatosensory cortex. This observation is similar to the normal pattern of evoked activity seen in developing animals. 6. The total area of 2DG uptake in the somatosensory cortex contralateral to a digit amputation conducted at 2 or 4 wk was not greater than that in the normal hemisphere, even though it was more widespread. After a digit amputation at 6 wk, however, the area of evoked activity was greater in the experimental hemisphere but not of the magnitude as the same manipulation in an adult.(ABSTRACT TRUNCATED AT 400 WORDS)

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24

Clarey, Janine C., Rowan Tweedale, and Michael B. Calford. "Interhemispheric Modulation of Somatosensory Receptive Fields: Evidence for Plasticity in Primary Somatosensory Cortex." Cerebral Cortex 6, no. 2 (1996): 196–206. http://dx.doi.org/10.1093/cercor/6.2.196.

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Kole, Koen. "Experience-dependent plasticity of neurovascularization." Journal of Neurophysiology 114, no. 4 (October 2015): 2077–79. http://dx.doi.org/10.1152/jn.00972.2014.

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Experience powerfully shapes structural and functional organization of neurons during development and in adulthood. Recent experiments in the mouse primary somatosensory cortex now suggest that experience is also a critical factor in shaping neurovasculature and promoting angiogenesis. These results support the universality of brain plasticity and show that all structural cellular components in the brain, from neuron and glia to epithelia, are shaped by experience.

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Terranova, C., V. Rizzo, F. Morgante, R. Maggio, A. Calamuneri, G. Chillemi, P. Girlanda, and A. Quartarone. "Spatial Integration of Somatosensory Inputs during Sensory-Motor Plasticity Phenomena Is Normal in Focal Hand Dystonia." Neural Plasticity 2018 (October 10, 2018): 1–7. http://dx.doi.org/10.1155/2018/4135708.

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Background. Surround inhibition is a system that sharpens sensation by creating an inhibitory zone around the central core of activation. In the motor system, this mechanism probably contributes to the selection of voluntary movements, and it seems to be lost in dystonia. Objectives. To explore if sensory information is abnormally processed and integrated in focal hand dystonia (FHD) and if surround inhibition phenomena are operating during sensory-motor plasticity and somatosensory integration in normal humans and in patients with FHD. Methods. We looked at the MEP facilitation obtained after 5 Hz repetitive paired associative stimulation of median (PAS M), ulnar (PAS U), and median + ulnar nerve (PAS MU) stimulation in 8 normal subjects and 8 FHD. We evaluated the ratio MU/(M + U) ∗ 100 and the spatial and temporal somatosensory integration recording the somatosensory evoked potentials (SEPs) evoked by a dual nerve input. Results. FHD had two main abnormalities: first, the amount of facilitation was larger than normal subjects; second, the spatial specificity was lost. The MU/(M + U) ∗ 100 ratio was similar in healthy subjects and in FHD patients, and the somatosensory integration was normal in this subset of patients. Conclusions. The inhibitory integration of somatosensory inputs and the somatosensory inhibition are normal in patients with focal dystonia as well as lateral surrounding inhibition phenomena during sensory-motor plasticity in FHD.

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Schlaggar, Bradley L., Kevin Fox, and Dennis M. O'Leary. "Postsynaptic control of plasticity in developing somatosensory cortex." Nature 364, no. 6438 (August 1993): 623–26. http://dx.doi.org/10.1038/364623a0.

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Hadoush, Hikmat, Toru Sunagawa, Kazuyoshi Nakanishi, and Mitsuo Ochi. "Somatosensory cortical plasticity after toe-to-index transfer." NeuroReport 23, no. 17 (December 2012): 1000–1005. http://dx.doi.org/10.1097/wnr.0b013e32835a649e.

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Kole, Koen, Wim Scheenen, Paul Tiesinga, and Tansu Celikel. "Cellular diversity of the somatosensory cortical map plasticity." Neuroscience & Biobehavioral Reviews 84 (January 2018): 100–115. http://dx.doi.org/10.1016/j.neubiorev.2017.11.015.

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Foeller, Elisabeth, and Daniel E. Feldman. "Synaptic basis for developmental plasticity in somatosensory cortex." Current Opinion in Neurobiology 14, no. 1 (February 2004): 89–95. http://dx.doi.org/10.1016/j.conb.2004.01.011.

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Galvez, R. "Vibrissa-Signaled Eyeblink Conditioning Induces Somatosensory Cortical Plasticity." Journal of Neuroscience 26, no. 22 (May 31, 2006): 6062–68. http://dx.doi.org/10.1523/jneurosci.5582-05.2006.

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32

Wolters, Alexander, Arne Schmidt, Axel Schramm, Daniel Zeller, Markus Naumann, Erwin Kunesch, Reiner Benecke, Karlheinz Reiners, and Joseph Classen. "Timing-dependent plasticity in human primary somatosensory cortex." Journal of Physiology 565, no. 3 (June 15, 2005): 1039–52. http://dx.doi.org/10.1113/jphysiol.2005.084954.

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Orczyk, John J., and Preston E. Garraghty. "Reconciling Homeostatic and Use-Dependent Plasticity in the Context of Somatosensory Deprivation." Neural Plasticity 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/290819.

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The concept of homeostatic plasticity postulates that neurons maintain relatively stable rates of firing despite changing inputs. Homeostatic and use-dependent plasticity mechanisms operate concurrently, although they have different requirements for induction. Depriving central somatosensory neurons of their primary activating inputs reduces activity and results in compensatory changes that favor excitation. Both a reduction of GABAergic inhibition and increase in glutamatergic excitatory transmission are observed in input-deprived cortex. Topographic reorganization of the adult somatosensory cortex is likely driven by both homeostatic and use-dependent mechanisms. Plasticity is induced by changes in the strengths of synaptic inputs, as well as changes in temporal correlation of neuronal activity. However, there is less certainty regarding thein vivocontribution of homeostatic mechanisms asin vitroexperiments rely on manipulations that create states that do not normally occur in the living nervous system. Homeostatic plasticity seems to occur, but morein vivoresearch is needed to determine mechanisms.In vitroresearch is also needed but should better conform to conditions that might occur naturallyin vivo.

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Marik, Sally A., and Peter W. Hickmott. "Plasticity of Horizontal Connections at a Functional Border in Adult Rat Somatosensory Cortex." Neural Plasticity 2009 (2009): 1–15. http://dx.doi.org/10.1155/2009/294192.

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Horizontal connections in superficial cortical layers integrate information across sensory maps by connecting related functional columns. It has been hypothesized that these connections mediate cortical reorganization via synaptic plasticity. However, it is not known if the horizontal connections from discontinuous cortical regions can undergo plasticity in the adult. Here we located the border between two discontinuous cortical representations in vivo and used either pairing or low-frequency stimulation to induce synaptic plasticity in the horizontal connections surrounding this border in vitro. Individual neurons revealed significant and diverse forms of synaptic plasticity for horizontal connections within a continuous representation and discontinuous representations. Interestingly, both enhancement and depression were observed following both plasticity paradigms. Furthermore, plasticity was not restricted by the border's presence. Depolarization in the absence of synaptic stimulation also produced synaptic plasticity, but with different characteristics. These experiments suggest that plasticity of horizontal connections may mediate functional reorganization.

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Bliem, Barbara, J. Florian M. Müller-Dahlhaus, Hubert R. Dinse, and Ulf Ziemann. "Homeostatic Metaplasticity in the Human Somatosensory Cortex." Journal of Cognitive Neuroscience 20, no. 8 (August 2008): 1517–28. http://dx.doi.org/10.1162/jocn.2008.20106.

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Long-term potentiation (LTP) and long-term depression (LTD) are regulated by homeostatic control mechanisms to maintain synaptic strength in a physiological range. Although homeostatic metaplasticity has been demonstrated in the human motor cortex, little is known to which extent it operates in other cortical areas and how it links to behavior. Here we tested homeostatic interactions between two stimulation protocols—paired associative stimulation (PAS) followed by peripheral high-frequency stimulation (pHFS)—on excitability in the human somatosensory cortex and tactile spatial discrimination threshold. PAS employed repeated pairs of electrical stimulation of the right median nerve followed by focal transcranial magnetic stimulation of the left somatosensory cortex at an interstimulus interval of the individual N20 latency minus 15 msec or N20 minus 2.5 msec to induce LTD- or LTP-like plasticity, respectively [Wolters, A., Schmidt, A., Schramm, A., Zeller, D., Naumann, M., Kunesch, E., et al. Timing-dependent plasticity in human primary somatosensory cortex. Journal of Physiology, 565, 1039–1052, 2005]. pHFS always consisted of 20-Hz trains of electrical stimulation of the right median nerve. Excitability in the somatosensory cortex was assessed by median nerve somatosensory evoked cortical potential amplitudes. Tactile spatial discrimination was tested by the grating orientation task. PAS had no significant effect on excitability in the somatosensory cortex or on tactile discrimination. However, the direction of effects induced by subsequent pHFS varied with the preconditioning PAS protocol: After PASN20-15, excitability tended to increase and tactile spatial discrimination threshold decreased. After PASN20-2.5, excitability decreased and discrimination threshold tended to increase. These interactions demonstrate that homeostatic metaplasticity operates in the human somatosensory cortex, controlling both cortical excitability and somatosensory skill.

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McGregor, Heather R., Joshua G. A. Cashaback, and Paul L. Gribble. "Somatosensory perceptual training enhances motor learning by observing." Journal of Neurophysiology 120, no. 6 (December 1, 2018): 3017–25. http://dx.doi.org/10.1152/jn.00313.2018.

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Action observation activates brain regions involved in sensory-motor control. Recent research has shown that action observation can also facilitate motor learning; observing a tutor undergoing motor learning results in functional plasticity within the motor system and gains in subsequent motor performance. However, the effects of observing motor learning extend beyond the motor domain. Converging evidence suggests that observation also results in somatosensory functional plasticity and somatosensory perceptual changes. This work has raised the possibility that the somatosensory system is also involved in motor learning that results from observation. Here we tested this hypothesis using a somatosensory perceptual training paradigm. If the somatosensory system is indeed involved in motor learning by observing, then improving subjects' somatosensory function before observation should enhance subsequent motor learning by observing. Subjects performed a proprioceptive discrimination task in which a robotic manipulandum moved the arm, and subjects made judgments about the position of their hand. Subjects in a Trained Learning group received trial-by-trial feedback to improve their proprioceptive perception. Subjects in an Untrained Learning group performed the same task without feedback. All subjects then observed a learning video showing a tutor adapting her reaches to a left force field. Subjects in the Trained Learning group, who had superior proprioceptive acuity before observation, benefited more from observing learning than subjects in the Untrained Learning group. Improving somatosensory function can therefore enhance subsequent observation-related gains in motor learning. This study provides further evidence in favor of the involvement of the somatosensory system in motor learning by observing. NEW & NOTEWORTHY We show that improving somatosensory performance before observation can improve the extent to which subjects learn from watching others. Somatosensory perceptual training may prime the sensory-motor system, thereby facilitating subsequent observational learning. The findings of this study suggest that the somatosensory system supports motor learning by observing. This finding may be useful if observation is incorporated as part of therapies for diseases affecting movement, such as stroke.

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Schwindt, Wolfram, Michael Burke, Frank Pillekamp, Heiko J. Luhmann, and Mathias Hoehn. "Functional Magnetic Resonance Imaging and Somatosensory Evoked Potentials in Rats with a Neonatally Induced Freeze Lesion of the Somatosensory Cortex." Journal of Cerebral Blood Flow & Metabolism 24, no. 12 (December 2004): 1409–18. http://dx.doi.org/10.1097/01.wcb.0000143535.84012.ca.

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Brain plasticity is an important mechanism for functional recovery from a cerebral lesion. The authors aimed to visualize plasticity in adult rats with a neonatal freeze lesion in the somatosensory cortex using functional magnetic resonance imaging (fMRI), and hypothesized activation outside the primary projection area. A freeze lesion was induced in the right somatosensory cortex of newborn Wistar rats (n = 12). Sham-operated animals (n = 7) served as controls. After 6 or 7 months, a neurologic examination was followed by recording of somatosensory evoked potentials (SSEPs) and magnetic resonance experiments (anatomical images, fMRI with blood oxygen level–dependent contrast and perfusion-weighted imaging) with electrical forepaw stimulation under α-chloralose anesthesia. Lesioned animals had no obvious neurologic deficits. Anatomical magnetic resonance images showed a malformed cortex or hyperintense areas (cysts) in the lesioned hemisphere. SSEPs were distorted and smaller in amplitude, and fMRI activation was significantly weaker in the lesioned hemisphere. Only in a few animals were cortical areas outside the primary sensory cortex activated. The results are discussed in respect to an apparent absence of plasticity, loss of excitable tissue, the excitability of the lesioned hemisphere, altered connectivity, and a disturbed coupling of increased neuronal activity to the hemodynamic response.

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Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. "Role of the Basal Forebrain Cholinergic Projection in Somatosensory Cortical Plasticity." Journal of Neurophysiology 79, no. 6 (June 1, 1998): 3216–28. http://dx.doi.org/10.1152/jn.1998.79.6.3216.

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Sachdev, Robert N. S., Shao-Ming Lu, Ron G. Wiley, and Ford F. Ebner. Role of the basal forebrain cholinergic projection in somatosensory cortical plasticity. J. Neurophysiol. 79: 3216–3228, 1998. Trimming all but two whiskers in adult rats produces a predictable change in cortical cell-evoked responses characterized by increased responsiveness to the two intact whiskers and decreased responsiveness to the trimmed whiskers. This type of synaptic plasticity in rat somatic sensory cortex, called “whisker pairing plasticity,” first appears in cells above and below the layer IV barrels. These are also the cortical layers that receive the densest cholinergic inputs from the nucleus basalis. The present study assesses whether the cholinergic inputs to cortex have a role in regulating whisker pairing plasticity. To do this, cholinergic basal forebrain fibers were eliminated using an immunotoxin specific for these fibers. A monoclonal antibody to the low-affinity nerve growth factor receptor 192 IgG, conjugated to the cytotoxin saporin, was injected into cortex to eliminate cholinergic fibers in the barrel field. The immunotoxin reduces acetylcholine esterase (AChE)-positive fibers in S1 cortex by >90% by 3 wk after injection. Sham-depleted animals in which either saporin alone or saporin unconjugated to 192 IgG is injected into the cortex produces no decrease in AChE-positive fibers in cortex. Sham-depleted animals show the expected plasticity in barrel column neurons. In contrast, no plasticity develops in the ACh-depleted, 7-day whisker-paired animals. These results support the conclusion that the basal forebrain cholinergic projection to cortex is an important facilitator of synaptic plasticity in mature cortex.

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Bak, Myeong Seong, Haney Park, and Sun Kwang Kim. "Neural Plasticity in the Brain during Neuropathic Pain." Biomedicines 9, no. 6 (May 31, 2021): 624. http://dx.doi.org/10.3390/biomedicines9060624.

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Neuropathic pain is an intractable chronic pain, caused by damage to the somatosensory nervous system. To date, treatment for neuropathic pain has limited effects. For the development of efficient therapeutic methods, it is essential to fully understand the pathological mechanisms of neuropathic pain. Besides abnormal sensitization in the periphery and spinal cord, accumulating evidence suggests that neural plasticity in the brain is also critical for the development and maintenance of this pain. Recent technological advances in the measurement and manipulation of neuronal activity allow us to understand maladaptive plastic changes in the brain during neuropathic pain more precisely and modulate brain activity to reverse pain states at the preclinical and clinical levels. In this review paper, we discuss the current understanding of pathological neural plasticity in the four pain-related brain areas: the primary somatosensory cortex, the anterior cingulate cortex, the periaqueductal gray, and the basal ganglia. We also discuss potential treatments for neuropathic pain based on the modulation of neural plasticity in these brain areas.

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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, implemented by activity-dependent plasticity in parvalbumin interneuron circuits. These processes interact with Hebbian synaptic plasticity to maintain cortical firing rates during learned adjustments in sensory representations. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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Huang, Lianyan, Jianhua Jin, Kai Chen, Sikun You, Hongyang Zhang, Alexandra Sideris, Monica Norcini, et al. "BDNF produced by cerebral microglia promotes cortical plasticity and pain hypersensitivity after peripheral nerve injury." PLOS Biology 19, no. 7 (July 22, 2021): e3001337. http://dx.doi.org/10.1371/journal.pbio.3001337.

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Peripheral nerve injury–induced mechanical allodynia is often accompanied by abnormalities in the higher cortical regions, yet the mechanisms underlying such maladaptive cortical plasticity remain unclear. Here, we show that in male mice, structural and functional changes in the primary somatosensory cortex (S1) caused by peripheral nerve injury require neuron-microglial signaling within the local circuit. Following peripheral nerve injury, microglia in the S1 maintain ramified morphology and normal density but up-regulate the mRNA expression of brain-derived neurotrophic factor (BDNF). Using in vivo two-photon imaging and Cx3cr1CreER;Bdnfflox mice, we show that conditional knockout of BDNF from microglia prevents nerve injury–induced synaptic remodeling and pyramidal neuron hyperactivity in the S1, as well as pain hypersensitivity in mice. Importantly, S1-targeted removal of microglial BDNF largely recapitulates the beneficial effects of systemic BDNF depletion on cortical plasticity and allodynia. Together, these findings reveal a pivotal role of cerebral microglial BDNF in somatosensory cortical plasticity and pain hypersensitivity.

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Elliott, T., C. I. Howarth, and N. R. Shadbolt. "Axonal Processes and Neural Plasticity. II: Adult Somatosensory Maps." Cerebral Cortex 6, no. 6 (1996): 789–93. http://dx.doi.org/10.1093/cercor/6.6.789.

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Mogilner, A., J. A. Grossman, U. Ribary, M. Joliot, J. Volkmann, D. Rapaport, R. W. Beasley, and R. R. Llinas. "Somatosensory cortical plasticity in adult humans revealed by magnetoencephalography." Proceedings of the National Academy of Sciences 90, no. 8 (April 15, 1993): 3593–97. http://dx.doi.org/10.1073/pnas.90.8.3593.

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Borsook, David, Lino Becerra, Scott Fishman, Annabel Edwards, Candice L. Jennings, Milan Stojanovic, Lito Papinicolas, Vilayanur S. Ramachandran, R. Gilberto Gonzalez, and Hans Breiter. "Acute plasticity in the human somatosensory cortex following amputation." NeuroReport 9, no. 6 (April 1998): 1013–17. http://dx.doi.org/10.1097/00001756-199804200-00011.

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Zehr, E. Paul. "Training-induced adaptive plasticity in human somatosensory reflex pathways." Journal of Applied Physiology 101, no. 6 (December 2006): 1783–94. http://dx.doi.org/10.1152/japplphysiol.00540.2006.

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Erzurumlu, Reha S. "Somatosensory cortical plasticity: recruiting silenced barrels by active whiskers." Experimental Neurology 184, no. 2 (December 2003): 565–69. http://dx.doi.org/10.1016/s0014-4886(03)00396-0.

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Pantev, Christo, Claudia Lappe, Sibylle C. Herholz, and Laurel Trainor. "Auditory-Somatosensory Integration and Cortical Plasticity in Musical Training." Annals of the New York Academy of Sciences 1169, no. 1 (July 2009): 143–50. http://dx.doi.org/10.1111/j.1749-6632.2009.04588.x.

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Ergenzinger, E. R., M. M. Glasier, J. O. Hahm, and T. P. Pons. "Cortically induced thalamic plasticity in the primate somatosensory system." Nature Neuroscience 1, no. 3 (July 1998): 226–29. http://dx.doi.org/10.1038/673.

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Garraghty, Preston E., and Naser Muja. "NMDA receptors and plasticity in adult primate somatosensory cortex." Journal of Comparative Neurology 367, no. 2 (April 1, 1996): 319–26. http://dx.doi.org/10.1002/(sici)1096-9861(19960401)367:2<319::aid-cne12>3.0.co;2-l.

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Foeller, Elisabeth, Tansu Celikel, and Daniel E. Feldman. "Inhibitory Sharpening of Receptive Fields Contributes to Whisker Map Plasticity in Rat Somatosensory Cortex." Journal of Neurophysiology 94, no. 6 (December 2005): 4387–400. http://dx.doi.org/10.1152/jn.00553.2005.

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The role of inhibition in sensory cortical map plasticity is not well understood. Here we tested whether inhibition contributes to expression of receptive field plasticity in developing rat somatosensory (S1) cortex. In normal rats, microiontophoresis of gabazine (SR 95531), a competitive γ-aminobutyric acid (GABA)-A receptor antagonist, preferentially disinhibited surround whisker responses relative to principal whisker responses, indicating that GABAA inhibition normally acts to sharpen whisker tuning. Plasticity was induced by transiently depriving adolescent rats of all but one whisker; this causes layer 2/3 (L2/3) receptive fields to shift away from the deprived principal whisker and toward the spared surround whisker. In units with shifted receptive fields, gabazine preferentially disinhibited responses to the deprived principal whisker, unlike in controls, suggesting that GABAA inhibition was acting to preferentially suppress these responses relative to spared whisker responses. This effect was not observed for L2/3 units that did not express receptive field plasticity or in layer 4, where receptive field plasticity did not occur. Thus GABAA inhibition promoted expression of sensory map plasticity by helping to sharpen receptive fields around the spared input.

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