Talk:Sensory - Touch Development
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Cite this page: Hill, M.A. (2026, September 4) Embryology Sensory - Touch Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Sensory_-_Touch_Development |
2011
A Shift in Sensory Processing that Enables the Developing Human Brain to Discriminate Touch from Pain
Curr Biol. 2011 Sep 7.
Fabrizi L, Slater R, Worley A, Meek J, Boyd S, Olhede S, Fitzgerald M. Source Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, UK. Abstract When and how infants begin to discriminate noxious from innocuous stimuli is a fundamental question in neuroscience [1]. However, little is known about the development of the necessary cortical somatosensory functional prerequisites in the intact human brain. Recent studies of developing brain networks have emphasized the importance of transient spontaneous and evoked neuronal bursting activity in the formation of functional circuits [2, 3]. These neuronal bursts are present during development and precede the onset of sensory functions [4, 5]. Their disappearance and the emergence of more adult-like activity are therefore thought to signal the maturation of functional brain circuitry [2, 4]. Here we show the changing patterns of neuronal activity that underlie the onset of nociception and touch discrimination in the preterm infant. We have conducted noninvasive electroencephalogram (EEG) recording of the brain neuronal activity in response to time-locked touches and clinically essential noxious lances of the heel in infants aged 28-45 weeks gestation. We show a transition in brain response following tactile and noxious stimulation from nonspecific, evenly dispersed neuronal bursts to modality-specific, localized, evoked potentials. The results suggest that specific neural circuits necessary for discrimination between touch and nociception emerge from 35-37 weeks gestation in the human brain.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID 21906948
2010
Identification of epidermal progenitors for the Merkel cell lineage
Development. 2010 Dec;137(23):3965-71. Epub 2010 Nov 1.
Woo SH, Stumpfova M, Jensen UB, Lumpkin EA, Owens DM. Source Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA. Abstract Epithelial stem cells in adult mammalian skin are known to maintain epidermal, follicular and sebaceous lineages during homeostasis. Recently, Merkel cell mechanoreceptors were identified as a fourth lineage derived from the proliferative layer of murine skin epithelium; however, the location of the stem or progenitor population for Merkel cells remains unknown. Here, we have identified a previously undescribed population of epidermal progenitors that reside in the touch domes of hairy skin, termed touch dome progenitor cells (TDPCs). TDPCs are epithelial keratinocytes and are distinguished by their unique co-expression of α6 integrin, Sca1 and CD200 surface proteins. TDPCs exhibit bipotent progenitor behavior as they give rise to both squamous and neuroendocrine epidermal lineages, whereas the remainder of the α6(+) Sca1(+) CD200(-) epidermis does not give rise to Merkel cells. Finally, TDPCs possess a unique transcript profile that appears to be enforced by the juxtaposition of TDPCs with Merkel cells within the touch dome niche.
PMID 21041368
2009
Epidermal progenitors give rise to Merkel cells during embryonic development and adult homeostasis
J Cell Biol. 2009 Oct 5;187(1):91-100. Epub 2009 Sep 28.
Van Keymeulen A, Mascre G, Youseff KK, Harel I, Michaux C, De Geest N, Szpalski C, Achouri Y, Bloch W, Hassan BA, Blanpain C. Source Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Université Libre de Bruxelles, Brussels B-1070, Belgium.
Abstract
Merkel cells (MCs) are located in the touch-sensitive area of the epidermis and mediate mechanotransduction in the skin. Whether MCs originate from embryonic epidermal or neural crest progenitors has been a matter of intense controversy since their discovery >130 yr ago. In addition, how MCs are maintained during adulthood is currently unknown. In this study, using lineage-tracing experiments, we show that MCs arise through the differentiation of epidermal progenitors during embryonic development. In adults, MCs undergo slow turnover and are replaced by cells originating from epidermal stem cells, not through the proliferation of differentiated MCs. Conditional deletion of the Atoh1/Math1 transcription factor in epidermal progenitors results in the absence of MCs in all body locations, including the whisker region. Our study demonstrates that MCs arise from the epidermis by an Atoh1-dependent mechanism and opens new avenues for study of MC functions in sensory perception, neuroendocrine signaling, and MC carcinoma.
PMID 19786578
2004
Pacinian corpuscle development involves multiple Trk signaling pathways
Dev Dyn. 2004 Nov;231(3):551-63.
Sedý J, Szeder V, Walro JM, Ren ZG, Nanka O, Tessarollo L, Sieber-Blum M, Grim M, Kucera J. Source Institute of Anatomy, Charles University, First Faculty of Medicine, U nemocnice 3, 128-00 Prague, Czech Republic. Abstract The development of crural Pacinian corpuscles was explored in neonatal mutant mice lacking nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) or neurotrophin-4 (NT4), or their cognate Trk receptors. Deficits of the corpuscles and their afferents were greatest in NT3, less in BDNF, and least in NT4 null mice. Deletion of NGF or p75(NTR) genes had little or no impact. No Pacinian corpuscles were present in NT3;BDNF and NT3;NT4 double or NT3;BDNF;NT4 triple null mice. Deficits were larger in NT3 than TrkC mutants and were comparable to deficits observed in TrkB or TrkA mutants. Afferents of all corpuscles coexpressed TrkA and TrkB receptors, and some afferents coexpressed all three Trk receptors. Our results suggest that multiple neurotrophins, in particular NT3, regulate the density of crural Pacinian corpuscles, most likely by regulating the survival of sensory neurons. In addition, NT3/TrkB and/or NT3/TrkA signaling plays a greater role than NT3/TrkC signaling in afferents to developing Pacinian corpuscles. (c) 2004 Wiley-Liss, Inc.
PMID 15376326
Mouse (129/Balb/c)
- crural Pacinian corpuscles took place over a 3-day period between embryonic day (E) 16.5 and postnatal day (P) 0 (with the delivery occurring on day E19)
- NT3 is the principal neurotrophin responsible for the development of afferents to Pacinian corpuscles
