Perinatal changes in epidermal innervation in rat and mouse

Fitzgerald, M. J. T.

doi:10.1002/cne.901260103

Cited by 32 publications

(15 citation statements)

References 14 publications

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“…have affected neuronal transport in two ways: nerve section, which totally interrupts all transport as well as impulse conduction, and colchicine application which, as measured by its effect on cholinesterase and catecholamine flow, partially interrupts fast axoplasmic transport, but does not affect impulse conduction (Aguilar et al 1973;M. Holmes, C. Turner, J. A Fried, E. Cooper and J.…”

Section: Resultsmentioning

confidence: 99%

“…Ramon y Cajal (1919) pointed out that sprouting of nerves during primary development occurs only when the nerves arrive at their targettissues, in the case of epithelium at least; his suggestion to explain this phenomenon is analogous to our hypothesis, namely that a sprouting stimulus derives from the target-tissue, and becomes eventually neutralized by factors released from the nerve. The findings of Fitzgerald (1961) on the development of the innervation of the pig snout suggest that a targettissue can be matched throughout its growth by an appropriate increase in the nerve endings without a change in the number of parent axons; the density of innervation stays constant. More target-tissue would presumably make more sprouting stimulus, so inducing sprouting until the equilibrium state is reached.…”

Section: Other Examples Of Collateral Sproutingmentioning

confidence: 99%

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The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

Cooper¹,

Diamond²,

Turner³

1977

The Journal of Physiology

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SUMMARYWe have shown that when one of the spinal nerves supplying the salamander hind limb is cut or treated with colchicine, the fields of the remaining nerves enlarge in area; whereas nerve section produces Wallerian degeneration, the colchicine-treated nerves conducted action potentials normally and their peripheral fields remained unchanged in area (Aguilar, Bisby, Cooper & Diamond, 1973). Since colchicine-treatment reduced neuronal transport, and nerve-section eliminated it, we proposed that nerve sprouting is regulated by factors normally conveyed to the endings by axoplasmic transport.1. We have now investigated the effects of colchicine on the thresholds and distribution of individual mechanosensory endings in the skin. If reduction of neuronal transport were enough to cause the threshold to be increased to the point of total unresponsiveness, then this could be a sign of an early stage of degeneration in those terminals. It could then be hypothesized that products of degeneration were providing a stimulus for adjacent nerves to sprout.2. Quantitative physiological studies of the effects of colchicine doses known to interfere with fast axoplasmic transport, indicate that in some experiments the terminal field of the treated nerve was invaded by sprouting fibres from neighbouring axons, when its own endings were unchanged in number, distribution and sensory thresholds. In other experiments the colchicine-treated nerve endings showed an increase in threshold but their function was otherwise unchanged; a similar adjacent nerve sprouting occurred. In a final group, colchicine caused total unresponsiveness of some endings of the treated nerve.3. When a region of skin was partially denervated by nerve section, the

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Section: Resultsmentioning

confidence: 99%

Section: Other Examples Of Collateral Sproutingmentioning

confidence: 99%

The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

Cooper¹,

Diamond²,

Turner³

1977

The Journal of Physiology

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“…Axons reach trunk skin by El3 but do not reach the most distal skin in the toes until as late as E 19 (Reynolds et al,199 1). Sensory axons do not immediately innervate targets in the skin but form a dense plexus in the epidermis that persists for the next several days (Fitzgerald, 1967;Reynolds et al, 1991). Most of these fibers then withdraw from the epidermis between PND 5 and 10 to innervate structures such as hair follicles in the dermis, with withdrawal of more rostra1 innervation occurring in advance of that of more caudal innervation.…”

Section: Discussionmentioning

confidence: 99%

On the role of nerve growth factor in the development of myelinated nociceptors

1992

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We have previously demonstrated that administration of antisera against NGF (anti-NGF) can have profound effects on developing primary afferents (Ritter et al., 1991). Chronic administration of anti-NGF to rats beginning on the day of birth results in a severe depletion of cutaneous A delta high-threshold mechanoreceptors (HTMRs) from the sural nerve. Here we have carried out further experiments in order to define the period of time over which this change in the cutaneous afferent population can be produced, and to investigate a possible mechanism for the change. Treatment with anti-NGF from postnatal day (PND) 0–14 resulted in a depletion of cutaneous A delta HTMRs from the sural nerve and also a 20% loss of sensory neurons. However, treatment from PND 2–14 produced an identical deficit of HTMRs without any accompanying cell death. Thus, the depletion of cutaneous A delta HTMRs can be achieved in the absence of cell death induced by anti-NGF treatment. It was also found that a 7 d treatment from PND 4–11 was sufficient to reproduce this effect, but that 7 d treatments earlier (PND 2–9) or later (PND 7–14) within the first 2 weeks were much less effective. This critical period, PND 4–11, corresponds to a period of anatomical change in the innervation of the skin, from epidermal innervation to primarily dermal innervation (Fitzgerald, 1967; Reynolds et al., 1991). In every case where anti-NGF treatment reduced the proportion of HTMRs, there was a reciprocal increase in the proportion of sensitive A delta hair follicle (D-hair) afferents. We hypothesize that in the absence of NGF, developing cutaneous A delta HTMRs do not die but innervate novel targets in the dermis and become D-hair afferents instead.

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“…Arthur and Shelley (1959) and Fitzgerald (1961) suggested that free nerve endings that extend into the epidermis (Sect. 1.2.4) serve as sensory afferents.…”

Section: Suggested Biological Relevance Of Electrodermal Phenomenamentioning

confidence: 99%

Electrodermal Activity

Boucsein

2012

1,481

1,589

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except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights.Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) Foreword to the Second EditionAs noted by David Lykken in the foreword to the first edition of this book, electrodermal activity was observed for the first time in Germany. A quartercentury later the scientific study of psychology also originated in Germany. Over time, however, the focus of psychological research, including the then new field of psychophysiology, shifted to the United States and Great Britain. This trend to the dominance of the United States and Great Britain was prolonged by the devastation of World War II and its aftermath in Germany (and elsewhere in continental Europe). Slowly at first and then more rapidly, German psychological science, including psychophysiology, recovered. For several decades German psychophysiologists have been a major force in psychophysiology. With the publication of the first English edition of this book in 1992, it became essential for electrodermal researchers worldwide again to learn from our German colleagues.When I came into psychophysiology in the mid-1960s, electrodermal activity was the most common system studied. Because of its popularity, a large literature had emerged on the physiological mechanisms producing these changes in the electrical properties of the skin and on the best methodology for recording them. Major reviews and/or chapters had been published or soon were to be published by Peter Venables and Irene Martin, Robert Edelberg, and David Lykken. Later reviews and articles were published by Venables and Margaret Christie, and by me. A chapter in 1990 by Michael Dawson, Anne Schell, and Diane Filion was especially noteworthy for its coverage of the psychological applications of electrodermal measures.Note that all these publications were journal articles and chapters and that most of them focused almost entirely on mechanisms and methodology. The publication of this book, first in German and then in English, provided the first book on electrodermal activity, and one that extensively covers psychological applications as well as mechanisms and methodology. Again to quote David Lykken back in 1992, "The return of German scholarship to what I shall loftily call the high table of psychophysiology is exemplified by this fine book, the most comprehensive treatise on the electrodermal system to appear in any language . . ." I completely agree with v that evaluation. Professor Boucsein's outstanding scholarship has produced a book of such breadth of coverage ...

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Perinatal changes in epidermal innervation in rat and mouse

Cited by 32 publications

References 14 publications

The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

The effects of nerve section and of colchicine treatment on the density of mechanosensory nerve endings in salamander skin.

On the role of nerve growth factor in the development of myelinated nociceptors

Electrodermal Activity

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