XB-ART-45478
Front Endocrinol (Lausanne)
2010 Jan 01;1:4. doi: 10.3389/fendo.2010.00004.
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About a snail, a toad, and rodents: animal models for adaptation research.
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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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Species referenced: Xenopus laevis
Genes referenced: adcyap1 avp bdnf cartpt cnr1 crh gabarap hpse lep ngfr npy nr3c1 nradd ntrk2 pomc snai1 tbx2 trh ucn1 vipr1
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Figure 1. Summarizing scheme of the regulation by the caudodorsal cells (CDC) of Lymnaea stagnalis of overt (visible) and covert (invisible) aspects of egg-laying behavior by, respectively, neurohemal peptide release from axon terminals in the periphery of the cerebral commissure and non-synaptic peptide release from axon collaterals in the inner part of the commissure. Overt aspects include the activation of muscles in the foot for locomotion during substrate cleaning (bottom left) and of muscles attached to the shell for shell turning (bottom right), while covert aspects include the induction of ovulation and the activation of accessory sex glands to produce an egg mass (top). For details on these aspects, see text. LC, left cerebral ganglion; LP, left pedal ganglion; MN, motor neurons; RC, right cerebral ganglion; RN, Ring neuron; RP, right pedal ganglion. | |
Figure 2. Transduction of various physiological environmental stimuli to the melanotrope cell of Xenopus laevis controlling the secretion of αMSH, via neurohemal nerve terminals in the pars nervosa and from synaptic terminals in the pars intermedia of the pituitary gland. 5HT, 5-hydroxytryptamine (serotonin); A, arginine-vasopressin receptor; ACh, acetylcholine; AVT, arginine-vasopressin; β, β-adrenergic receptor; BDNF, brain-derived neurotrophic factor; C, calcium-sensing receptor; C1, corticotropin-releasing factor receptor 1; C2, corticotropin-releasing factor receptor 2; Ca2+, calcium ion; CRF, corticotropin-releasing factor; D2, dopamine D2 receptor; DA, dopamine; Ga, GABAA receptor; Gb, GABAB receptor; GABA, γ-aminobutyric acid; M, mesotocin receptor; M1, muscarinic M1 receptor; ME, metenkephalin; Me, metenkephalin receptor; MT, mesotocin; NA, noradrenalin; NPY, neuropeptide Y; P, P75NTR receptor; PACAP, pituitary adenylyl cyclase-activating polypeptide; T, TrkB receptor; T3, thyrotropin-releasing hormone receptor 3; TRH, thyrotropin-releasing hormone; Ucn1, urocortin 1; V1, VPAC1 receptor; Y1, NPY Y1 receptor. (Modified after Roubos et al., 2005.) | |
Figure 3. Model of interactions between the npEW and the HPA-axis and other centers involved in stress adaptation and energy metabolism. Continuous lines indicate established interactions, dashed lines indicate presumed interactions; the dotted line refers to sex difference. 5HT, serotonin; ACTH, adrenocorticotrope hormone; BDNF, brain-derived neurotrophic factor; C2, corticotropin-releasing factor receptor 2; CART, cocaine- and amphetamine-regulated transcript peptide; CB, endocannabinoids; CB1, endocannabinoid receptor 1; CRF, corticotropin-releasing factor; DR, dorsal raphe nucleus; ERβ, estrogen receptor β; GABA, γ-aminobutyric acid; GC, glucocorticoids; GR, glucocorticoid receptor; IN, interneuron; LH, lateral hypothalamus; LS, lateral septum; NPY, neuropeptide Y; ObR, leptin receptor; PVN, paraventricular nucleus; Ucn1, urocortin 1; Y-1/5; neuropeptide Y receptors 1 and 5. (Slightly modified after Derks, 2010.) |
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