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Somatosensory system

About: Somatosensory system is a research topic. Over the lifetime, 6371 publications have been published within this topic receiving 316900 citations.


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Journal ArticleDOI
TL;DR: It is reported that visual deprivation produces opposite changes in synaptic function in primary visual and somatosensory cortices in rats, which are rapidly reversed by visual experience.
Abstract: Lack of a sensory input not only alters the cortical circuitry subserving the deprived sense, but also produces compensatory changes in the functionality of other sensory modalities. Here we report that visual deprivation produces opposite changes in synaptic function in primary visual and somatosensory cortices in rats, which are rapidly reversed by visual experience. This type of bidirectional cross-modal plasticity is associated with changes in synaptic AMPA receptor subunit composition.

201 citations

Journal ArticleDOI
TL;DR: The findings confirm the notion that pain intensity processing is distributed over several brain areas, and suggest that the intensity coding of a noxious stimulus occurs already at the earliest stage of perception processing, in the operculoinsular region and, possibly, the primary somatosensory area.

200 citations

Journal ArticleDOI
TL;DR: Analysis of the evoked potentials produced by electrical stimulation in MSN suggests that the somatosensory inputs activate the granule cell system of the DCN molecular layer, and molecular layer interneurons are a second possible source of inhibition to principal cells.
Abstract: 1. Single units and evoked potentials were recorded in dorsal cochlear nucleus (DCN) in response to electrical stimulation of the somatosensory dorsal column and spinal trigeminal nuclei (together called MSN for medullary somatosensory nuclei) and for tactile somatosensory stimuli. Recordings were from paralyzed decerebrate cats. 2. DCN principal cells (type IV units) were strongly inhibited by electrical stimulation (single 50-microA bipolar pulse) in MSN or by somatosensory stimulation. Units recorded in the fusiform cell and deep layers of DCN were inhibited, suggesting that the inhibition affects both types of principal cells (i.e., both fusiform and giant cells). 3. Interneurons (type II units) that inhibit principal cells were only weakly inhibited by electrical stimulation and were never excited, demonstrating that the inhibitory effect on principal cells does not pass through the type II circuit. In the vicinity of the DCN/PVCN (posteroventral cochlear nucleus) boundary, units were encountered that were excited by electrical stimulation in MSN; some of these neurons responded to sound, and some did not. Their response properties are consistent with the hypothesis that they are deep-layer inhibitory interneurons conveying somatosensory information to the DCN. 4. Analysis of the evoked potentials produced by electrical stimulation in MSN suggests that the somatosensory inputs activate the granule cell system of the DCN molecular layer. A model based on previous work by Klee and Rall was used to show that the distribution of evoked potentials in DCN can be explained as resulting from radial currents produced in the DCN molecular and fusiform-cell layers by synchronous activation of granule cells inputs to fusiform and cartwheel cells. Current-source density analysis of the evoked potentials is consistent with this model. Thus molecular layer interneurons (cartwheel and stellate cells) are a second possible source of inhibition to principal cells. 5. With lower stimulus levels (20 microA) and pulse-pair stimuli (50- to 100-ms interstimulus interval), three components of the inhibitory response can be recognized in both fusiform cell layer and deep layer type IV units: a short-latency inhibition that begins before the start of the evoked potential; a longer-latency inhibition whose timing corresponds to the evoked potential; and an excitatory component that occurs on the rising phase of the evoked potential. The excitatory component is usually overwhelmed by the inhibitory components and could be derived from granule cell inputs; the long-latency inhibitory component could be derived from cartwheel cells or the hypothesized deep-layer inhibitory interneurons.(ABSTRACT TRUNCATED AT 400 WORDS)

200 citations

Journal ArticleDOI
TL;DR: A computer model based on the process of neuronal group selection has been constructed that accounts for reported results on map plasticity in somatosensory cortex and provides several insights into the mechanisms of such changes, as well as a series of predictions about cortical behavior for further experimental test.
Abstract: Recent experimental evidence from the somatosensory, auditory, and visual systems documents the existence of functional plasticity in topographic map organization in adult animals. This evidence suggests that an ongoing competitive organizing process controls the locations of map borders and the receptive field properties of neurons. A computer model based on the process of neuronal group selection has been constructed that accounts for reported results on map plasticity in somatosensory cortex. The simulations construct a network of locally connected excitatory and inhibitory cells that receives topographic projections from 2 receptor sheets corresponding to the glabrous and dorsal surfaces of the hand (a typical simulation involves approximately 1500 cells, 70,000 intrinsic and 100,000 extrinsic connections). Both intrinsic and extrinsic connections undergo activity-dependent modifications according to a synaptic rule based on heterosynaptic interactions. Repeated stimulation of the receptor sheet resulted in the formation of neuronal groups-local sets of strongly interconnected neurons in the network. Cells in most groups were found to have similar receptive fields: they were exclusively glabrous or dorsal despite equal numbers of anatomical connections from both surfaces. The sharpness of map borders was due to the sharpness of the underlying group structure; shifts in the locations of these borders resulted from competition between groups. Following perturbations of the input, the network underwent changes similar to those observed experimentally in monkey somatosensory cortex. Repeated local tapping on the receptor sheet resulted in a large increase in the magnification factor of the stimulated region. Transection of the connections from a glabrous region resulted in the organization of a new representation of corresponding dorsal region. The detailed simulations provide several insights into the mechanisms of such changes, as well as a series of predictions about cortical behavior for further experimental test.

200 citations

Journal ArticleDOI
01 Mar 2013-Pain
TL;DR: It is demonstrated that an extreme anterior position within SI (area 3a) receives input originating predominantly from unmyelinated nociceptors, distinguishing it from posterior SI (areas 3b and 1), long recognized as receiving input predominantly from myelinated afferents, including nocICEptors.
Abstract: The intensity and submodality of pain are widely attributed to stimulus encoding by peripheral and subcortical spinal/trigeminal portions of the somatosensory nervous system. Consistent with this interpretation are studies of surgically anesthetized animals, demonstrating that relationships between nociceptive stimulation and activation of neurons are similar at subcortical levels of somatosensory projection and within the primary somatosensory cortex (in cytoarchitectural areas 3b and 1 of somatosensory cortex, SI). Such findings have led to characterizations of SI as a network that preserves, rather than transforms, the excitatory drive it receives from subcortical levels. Inconsistent with this perspective are images and neurophysiological recordings of SI neurons in lightly anesthetized primates. These studies demonstrate that an extreme anterior position within SI (area 3a) receives input originating predominantly from unmyelinated nociceptors, distinguishing it from posterior SI (areas 3b and 1), long recognized as receiving input predominantly from myelinated afferents, including nociceptors. Of particular importance, interactions between these subregions during maintained nociceptive stimulation are accompanied by an altered SI response to myelinated and unmyelinated nociceptors. A revised view of pain coding within SI cortex is discussed, and potentially significant clinical implications are emphasized.

199 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20241
2023463
2022986
2021238
2020233
2019234