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      About a Snail, a Toad, and Rodents: Animal Models for Adaptation Research

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          Abstract

          Neural adaptation mechanisms have many similarities throughout the animal kingdom, enabling to study fundamentals of human adaptation in selected animal models with experimental approaches that are impossible to apply in man. This will be illustrated by reviewing research on three of such animal models, viz. (1) the egg-laying behavior of a snail, Lymnaea stagnalis: how one neuron type controls behavior, (2) adaptation to the ambient light condition by a toad, Xenopus laevis: how a neuroendocrine cell integrates complex external and neural inputs, and (3) stress, feeding, and depression in rodents: how a neuronal network co-ordinates different but related complex behaviors. Special attention is being paid to the actions of neurochemical messengers, such as neuropeptide Y, urocortin 1, and brain-derived neurotrophic factor. While awaiting new technological developments to study the living human brain at the cellular and molecular levels, continuing progress in the insight in the functioning of human adaptation mechanisms may be expected from neuroendocrine research using invertebrate and vertebrate animal models.

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          Most cited references 275

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          Sex differences in HPA axis responses to stress: a review.

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            Limits to evolution at range margins: when and why does adaptation fail?

            What stops populations expanding into new territory beyond the edge of a range margin? Recent models addressing this problem have brought together population genetics and population ecology, and some have included interactions among species at range edges. Here, we review these models of adaptation at environmental or parapatric margins, and discuss the contrasting effects of migration in either swamping local adaptation, or supplying the genetic variation that is necessary for adaptation to continue. We illustrate how studying adaptation at range margins (both with and without hybridization) can provide insight into the genetic and ecological factors that limit evolution more generally, especially in response to current rates of environmental change.
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              The induction of pain: an integrative review.

               José Millán (1998)
              The highly disagreeable sensation of pain results from an extraordinarily complex and interactive series of mechanisms integrated at all levels of the neuroaxis, from the periphery, via the dorsal horn to higher cerebral structures. Pain is usually elicited by the activation of specific nociceptors ('nociceptive pain'). However, it may also result from injury to sensory fibres, or from damage to the CNS itself ('neuropathic pain'). Although acute and subchronic, nociceptive pain fulfils a warning role, chronic and/or severe nociceptive and neuropathic pain is maladaptive. Recent years have seen a progressive unravelling of the neuroanatomical circuits and cellular mechanisms underlying the induction of pain. In addition to familiar inflammatory mediators, such as prostaglandins and bradykinin, potentially-important, pronociceptive roles have been proposed for a variety of 'exotic' species, including protons, ATP, cytokines, neurotrophins (growth factors) and nitric oxide. Further, both in the periphery and in the CNS, non-neuronal glial and immunecompetent cells have been shown to play a modulatory role in the response to inflammation and injury, and in processes modifying nociception. In the dorsal horn of the spinal cord, wherein the primary processing of nociceptive information occurs, N-methyl-D-aspartate receptors are activated by glutamate released from nocisponsive afferent fibres. Their activation plays a key role in the induction of neuronal sensitization, a process underlying prolonged painful states. In addition, upon peripheral nerve injury, a reduction of inhibitory interneurone tone in the dorsal horn exacerbates sensitized states and further enhance nociception. As concerns the transfer of nociceptive information to the brain, several pathways other than the classical spinothalamic tract are of importance: for example, the postsynaptic dorsal column pathway. In discussing the roles of supraspinal structures in pain sensation, differences between its 'discriminative-sensory' and 'affective-cognitive' dimensions should be emphasized. The purpose of the present article is to provide a global account of mechanisms involved in the induction of pain. Particular attention is focused on cellular aspects and on the consequences of peripheral nerve injury. In the first part of the review, neuronal pathways for the transmission of nociceptive information from peripheral nerve terminals to the dorsal horn, and therefrom to higher centres, are outlined. This neuronal framework is then exploited for a consideration of peripheral, spinal and supraspinal mechanisms involved in the induction of pain by stimulation of peripheral nociceptors, by peripheral nerve injury and by damage to the CNS itself. Finally, a hypothesis is forwarded that neurotrophins may play an important role in central, adaptive mechanisms modulating nociception. An improved understanding of the origins of pain should facilitate the development of novel strategies for its more effective treatment.
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                Author and article information

                Affiliations
                simpleDepartment of Cellular Animal Physiology, Faculty of Science, Donders Institute for Brain, Cognition and Behaviour, Centre for Neuroscience, Radboud University Nijmegen Nijmegen, Netherlands
                Author notes

                Edited by: Billy K. Chow, University of Hong Kong, China

                Reviewed by: Maria M. Malagon, University of Cordoba, Spain; J. C. Cardoso, University of Algarve, Portugal

                *Correspondence: Eric W. Roubos, Department of Cellular Animal Physiology, Faculty of Science, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen, P.O. Box 9010, 6500 GL Nijmegen, Netherlands. e-mail: roubos@ 123456science.ru.nl
                This article was submitted to Frontiers in Neuroendocrine Science, a specialty of Frontiers in Endocrinology.
                Journal
                Front Endocrinol (Lausanne)
                Front Endocrinol (Lausanne)
                Front. Endocrin.
                Frontiers in Endocrinology
                Frontiers Research Foundation
                1664-2392
                20 September 2010
                20 October 2010
                2010
                : 1
                3355873
                22649351
                10.3389/fendo.2010.00004
                Copyright © 2010 Roubos, Jenks, Xu, Kuribara, Scheenen and Kozicz.

                This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

                Counts
                Figures: 3, Tables: 0, Equations: 0, References: 278, Pages: 18, Words: 19512
                Categories
                Endocrinology
                Review Article

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