Acceleration of Ambystoma Tigrinum Metamorphosis by Corticotropin-Releasing Hormone 1 1,2 GRAHAM C

Total Page:16

File Type:pdf, Size:1020Kb

Acceleration of Ambystoma Tigrinum Metamorphosis by Corticotropin-Releasing Hormone 1 1,2 GRAHAM C JOURNAL OF EXPERIMENTAL ZOOLOGY 293:94–98 (2002) RAPID COMMUNICATION Acceleration of Ambystoma tigrinum Metamorphosis by Corticotropin-Releasing Hormone 1 1,2 GRAHAM C. BOORSE AND ROBERT J. DENVER * 1Department of Ecology and Evolutionary Biology,The University of Michigan, AnnArbor,Michigan48109-1048 2 Department of Molecular,Cellular and Developmental Biology,The University of Michigan, Ann Arbor,Michigan 48109-1048 ABSTRACT Previous work of others and ours has shown that corticotropin-releasing hormone (CRH) is a positive stimulus for thyroid and interrenal hormone secretion in amphibian larvae and that activation of CRH neurons may mediate environmental e¡ects on the timing of metamorphosis. These studies have investigated CRH actions in anurans (frogs and toads), whereas there is currently no information regarding the actions of CRH on metamorphosis of urodeles (salamanders and newts). We tested the hypothesis that CRH can accelerate metamorphosis of tiger salamander (Ambystoma tigrinum) larvae. We injected tiger salamander larvae with ovine CRH (oCRH; 1 mg/day; i.p.) and mon- itored e¡ects on metamorphosis by measuring the rate of gill resorption. oCRH-injected larvae com- pleted metamorphosis earlier than saline-injected larvae.There was no signi¢cant di¡erence between uninjected and saline-injected larvae. Mean time to reach 50% reduction in initial gill length was 6.9 days for oCRH-injected animals, 11.9 days for saline-injected animals, and 14.1 days for uninjected controls. At the conclusion of the experiment (day 15), all oCRH-injected animals had completed metamorphosis, whereas by day 15, only 50% of saline-injected animals and 33% of uninjected animals had metamorphosed. Our results show that exogenous oCRH can accelerate metamorphosis in urodele larvae as it does in anurans. These ¢ndings suggest that the neuroendocrine mechanisms controlling metamorphosis are evolutionarilyconserved across amphibiantaxa. J.Exp.Zool.293:94^98, 2002. r 2002 Wiley-Liss, Inc. Thyrotropin-releasing hormone (TRH), the neu- terrenal (adrenal) axes (Denver and Licht, ’89a; rohormone that regulates pituitary thyroid-stimu- Denver,’99). lating hormone (TSH) secretion in mammals, is Several lines of evidence support a physiological expressed in the tadpole hypothalamus (see Denver, role for CRH in regulating TSH secretion in anur- ’96), but lacks the ability to stimulateTSH secretion ans (frogs and toads). For example, CRH stimulated in the tadpole (Denver and Licht,’89a; see Kikuya- the secretion of thyrotropic bioactivity (Denver,’88; ma et al.,’93; Denver,’96) or in the neotenic axolotl Denver and Licht, ’89a; Jacobs and Kuhn, ’92) and (Darras and Kuhn,’83; Jacobs and Kuhn,’87). How- immunoreactive TSH b subunit (Denver, unpub- ever, TRH is active in stimulating thyroid activity lished results) by cultured tadpole and adult frog in adult frogs (Darras and Kuhn, ’82; Denver, ’88) pituitaries. Injections of CRH or CRH-like peptides and metamorphosed axolotls (induced by injections (i.e., sauvagine) elevated whole body thyroid hor- of thyroxine; Jacobs and Kuhn,’87), suggesting a de- mone (Gancedo et al.,’92; Denver,’93,’97a) and cor- velopmental switch in the neuroendocrine control ticosterone (Denver, ’97a) content and accelerated of the thyroid system in amphibia (see Denver,’96). metamorphosis of tadpoles of four frog species Current evidence supports a role for corticotropin- (Rana catesbeiana and Spea hammondii, Denver,’93; releasing hormone (CRH) in the positive regulation of pituitary TSH secretion in tadpoles (Denver,’96, Grant sponsor: NSF; Grant number: IBN-9974672. ’99). CRH is the primary neurohormone regulating *Correspondence to: Robert J. Denver, Department of Molecular, Cel- pituitary adrenocorticotropin (ACTH) secretion in lular and Developmental Biology, 3065C Natural Science Bldg.,The Uni- versity of Michigan, Ann Arbor, MI 48109-1048. E-mail: rdenver@ mammals (see Vale et al., ’97). In amphibians and umich.edu other nonmammalian vertebrates, CRH may play a Received 1 November 2001; Accepted 28 February 2002 Published online in Wiley InterScience (www.interscience.wiley. dual role by regulating both the thyroid and the in- com). DOI: 10.1002/jez.10115 r 2002 WILEY-LISS, INC. CRH ACCELERATES SALAMANDER METAMORPHOSIS 95 Rana perezi, Gancedo et al.,’92; and Bufo arenarum, cage. Digitized images were analyzed for body Miranda et al., 2000). These four species represent lengths using NIH image software. three anuran genera; however, more information from diverse amphibian taxa, especially urodeles, CRH injections is needed to evaluate how generalizable this action Based on the above experiment, CRH injections of CRH is in amphibians. were initiated in 13-week-old A. tigrinum larvae CRH has been shown to activate the thyroid and (mean body length=12.121cm, SE ¼ 0:157; range interrenal axes and to accelerate metamorphosis in 10.69^13.27 cm). Larvae were separated into three anuran larvae; however, there is currently no infor- treatment groups (n ¼ 6/treatment), which in- mation on the actions of CRH in urodeles (salaman- cluded uninjected controls, saline-injected controls ders and newts). In the present study, we tested the (daily i.p. injections of 50 ml phosphate buffered hypothesis that injection of CRH can accelerate saline [PBS]: 0.02 M sodium phosphate, 0.6% so- metamorphosis of larvae of the tiger salamander, dium chloride), and ovine CRH-injected experimen- Ambystoma tigrinum. We injected ovine CRH (i.p.) tals (daily i.p. injections of 1 mg oCRH dissolved in over a period of two weeks and monitored meta- 50 mlPBS). morphic progression by measuring gill length. Metamorphic progression was monitored by mea- suring gill length. Digital images were captured every two days starting at time zero and the length MATERIALS AND METHODS of the right middle gill rachis was measured. The Animals and animal husbandry time in days for each larva to achieve 50% gill re- sorption (GR50) was calculated. This method pro- A. tigrinum egg masses were collected from vides an accurate means to compare rates of ponds located near Pinckney,MI (Michigan scienti- metamorphosis in A. tigrinum (Norris et al., ’73; ¢c collecting permit # CO577). Egg masses were Norris and Platt,’74). placed in polystyrene cages (24 cm  45 cm  20 cm) containing ten liters of dechlorinated water. Upon Statistical analysis hatching, larvae were reared individually in poly- GR50 values were analyzed using Student’s un- styrene cages (20.5 cm  34 cm  11cm) in two liters paired t-test to make pairwise comparisons be- of water and fed brine shrimp, followed by tubifex tween uninjected and saline-injected or between worms, and then beef liver as they grew.Water was saline-injected and CRH-injected groups. Changes changed every two to three days and larvae were in gill length were analyzed over time (each time maintained on a constant 12L:12D light/dark cycle point was analyzed separately) by unpaired t-test 1 and a temperature range of 21^23 C. to compare uninjected or CRH-injected to saline- injected. Determination of body size at RESULTS AND DISCUSSION metamorphosis Growth rates of control and methimazole-treated Previous studies with A. tigrinum larvae in our larvae were similar; however, methimazole-treated laboratory (R. J. Denver, unpublished data) led us larvae never initiated metamorphosis (Fig. 1). Con- to hypothesize that a larva must reach a minimum trol larvae initiated metamorphosis 13 weeks after size or developmental threshold in order to become hatching and all had completed metamorphosis by competent to respond to environmental or neuroen- week 16 (Fig. 1). docrine stimuli. Thus, we ¢rst conducted a study Larvae receiving injections of oCRH metamor- aimed at determining the range of body size at phosed earlier than saline-injected larvae. Signi¢- which spontaneous metamorphosis is initiated in cant di¡erences in gill length were apparent two A. tigrinum larvae reared in the laboratory under days after beginning injections (Fig. 2; T ¼ constant environmental conditions. Two weeks À2:701; P ¼ 0:0223). No signi¢cant di¡erences were after hatching, larvae (n ¼ 10/treatment) were se- detected in gill length between saline-injected and parated into two groups and treated with or with- uninjected larvae (Fig. 2). GR50 values were signi¢- out the goitrogen methimazole dissolved in water cantly lower for oCRH injected animals compared to a concentration of 1mM (Denver et al.,’97). Digi- to saline-injected larvae (Table 1; T ¼ 2:629; tal images of individual larvae were captured P ¼ 0:0340). oCRH injection also resulted in a lar- weekly using an Olympus D-500L digital camera ger number of animals undergoing complete trans- mounted on a tripod at a ¢xed height above the formation than either uninjected or saline-injected 96 G.C. BOORSE AND R.J. DENVER TABLE 1. E¡ects of oCRH on time to 50% gill resorption (GR50) in A. tigrinum larvae1 Number of larvae completing metamorphosis Group GR50 (Days 7 SE) at end of experiment Untreated 14.1 70.7 2 Saline 11.9 7 1.4 3 oCRH2 6.9 7 2.0* 6 1 GR50, mean number of days to reach 50% gill resorption. 2 Larvae were given injections of oCRH (1 mg) every day for 15 days (n ¼ 6/ group). Asterisk designates signi¢cantly di¡erent from saline-treated larvae by unpaired t-test (Po0:05). Fig. 1. Analysis of growth and development of Ambystoma experiment metamorphosed over the subsequent tigrinum larvae for 18 weeks following hatching. Larvae were one to four weeks in the laboratory. reared in the absence (open circles) or presence (closed circles) of the goitrogen methimazole (1mM). Points on the graph repre- This is the ¢rst demonstration of a stimulatory sent means 7 SEM (n ¼ 10/treatment). Arrows indicate the fol- e¡ect of CRH on metamorphosis in a urodele. Pre- lowing progression of metamorphosis in control animals: A) vious studies of four anuran species showed that initial signs of metamorphosis; B) 50% of control animals com- CRH injections cause tadpoles to metamorphose pleting metamorphosis; C) 100% of control animals completing earlier than saline-injected controls (Gancedo metamorphosis.
Recommended publications
  • Hormonal Regulation of Oligodendrogenesis I: Effects Across the Lifespan
    biomolecules Review Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan Kimberly L. P. Long 1,*,†,‡ , Jocelyn M. Breton 1,‡,§ , Matthew K. Barraza 2 , Olga S. Perloff 3 and Daniela Kaufer 1,4,5 1 Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA; [email protected] (J.M.B.); [email protected] (D.K.) 2 Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA; [email protected] 3 Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA 94143, USA; [email protected] 4 Department of Integrative Biology, University of California, Berkeley, CA 94720, USA 5 Canadian Institute for Advanced Research, Toronto, ON M5G 1M1, Canada * Correspondence: [email protected] † Current address: Department of Psychiatry and Behavioral Sciences, University of California, San Francisco, CA 94143, USA. ‡ These authors contributed equally to this work. § Current address: Department of Psychiatry, Columbia University, New York, NY 10027, USA. Abstract: The brain’s capacity to respond to changing environments via hormonal signaling is critical to fine-tuned function. An emerging body of literature highlights a role for myelin plasticity as a prominent type of experience-dependent plasticity in the adult brain. Myelin plasticity is driven by oligodendrocytes (OLs) and their precursor cells (OPCs). OPC differentiation regulates the trajectory of myelin production throughout development, and importantly, OPCs maintain the ability to proliferate and generate new OLs throughout adulthood. The process of oligodendrogenesis, Citation: Long, K.L.P.; Breton, J.M.; the‘creation of new OLs, can be dramatically influenced during early development and in adulthood Barraza, M.K.; Perloff, O.S.; Kaufer, D.
    [Show full text]
  • Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease
    cells Review Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease Chongxu Zhang 1, Tengjiao Cui 1, Renzhi Cai 1, Medhi Wangpaichitr 1, Mehdi Mirsaeidi 1,2 , Andrew V. Schally 1,2,3 and Robert M. Jackson 1,2,* 1 Research Service, Miami VAHS, Miami, FL 33125, USA; [email protected] (C.Z.); [email protected] (T.C.); [email protected] (R.C.); [email protected] (M.W.); [email protected] (M.M.); [email protected] (A.V.S.) 2 Department of Medicine, University of Miami Miller School of Medicine, Miami, FL 33101, USA 3 Department of Pathology and Sylvester Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33101, USA * Correspondence: [email protected]; Tel.: +305-575-3548 or +305-632-2687 Received: 25 August 2020; Accepted: 17 October 2020; Published: 21 October 2020 Abstract: Growth hormone-releasing hormone (GHRH) is secreted primarily from the hypothalamus, but other tissues, including the lungs, produce it locally. GHRH stimulates the release and secretion of growth hormone (GH) by the pituitary and regulates the production of GH and hepatic insulin-like growth factor-1 (IGF-1). Pituitary-type GHRH-receptors (GHRH-R) are expressed in human lungs, indicating that GHRH or GH could participate in lung development, growth, and repair. GHRH-R antagonists (i.e., synthetic peptides), which we have tested in various models, exert growth-inhibitory effects in lung cancer cells in vitro and in vivo in addition to having anti-inflammatory, anti-oxidative, and pro-apoptotic effects. One antagonist of the GHRH-R used in recent studies reviewed here, MIA-602, lessens both inflammation and fibrosis in a mouse model of bleomycin lung injury.
    [Show full text]
  • Somatostatin, an Inhibitor of ACTH Secretion, Decreases Cytosolic Free Calcium and Voltage-Dependent Calcium Current in a Pituitary Cell Line
    The Journal of Neuroscience November 1986, &Ii): 3128-3132 Somatostatin, an Inhibitor of ACTH Secretion, Decreases Cytosolic Free Calcium and Voltage-Dependent Calcium Current in a Pituitary Cell Line Albert0 Luini,* Deborah Lewis,t Simon Guild,* Geoffrey Schofield,t and Forrest Weight? *Laboratory of Cell Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892, j-Laboratory of Preclinical Studies, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852, and *Experimental Therapeutics Branch, National Institute on Neurological, Communicative Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892 Somatostatin is a neurohormone peptide that inhibits a variety (corticotropin releasing factor, vasointestinal peptide, isopro- of secretory responses in different cell types. We have investi- terenol, and forskolin) and to secretagogues independent of CAMP gated the effects of somatostatin on calcium current and intra- formation, such as potassium, 8-bromocyclic AMP, calcium cellular free calcium in AtT-20 cells, a pituitary tumor line in ionophores (Axelrod and Reisine, 1984) and phorbol esters which the inhibitory actions of this peptide have been well char- (Heisler, 1984). Somatostatin blocks the stimulation of secretion acterized. At concentrations similar to those that inhibit adre- by all of these agents (Axelrod and Reisine, 1984; Richardson, nocorticotropic hormone (ACTH) release, somatostatin and its 1983). A previously described mechanism of action of somato- analogs reduced the levels of intracellular free calcium (as mea- statin is the blockade of the secretagogue-evoked stimulation sured by the Quin-2 technique). Nifedipine and other blockers of CAMP synthesis (Heisler et al., 1982). We now report a novel of voltage-dependent calcium channels also reduced cytosolic effect of somatostatin; namely, the inhibition of voltage-depen- calcium levels.
    [Show full text]
  • Neurohormone Secretion Persists After Post-Afterdischarge Membrane Depolarization and Cytosolic Calcium Elevation in Peptidergic Neurons in Intact Nervous Tissue
    The Journal of Neuroscience, October 15, 2002, 22(20):9063–9069 Neurohormone Secretion Persists after Post-Afterdischarge Membrane Depolarization and Cytosolic Calcium Elevation in Peptidergic Neurons in Intact Nervous Tissue Stephan Michel and Nancy L. Wayne Department of Physiology, David Geffin School of Medicine at University of California at Los Angeles, Los Angeles, California 90095 The purpose of this work was to test the hypothesis that an secretion or on the post-AD membrane potential (Vm ) and electrical afterdischarge (AD) causes prolonged elevation in post-AD Ca 2ϩ signal, ruling out a role for extracellular calcium 2ϩ 2ϩ cytosolic calcium levels that is associated with prolonged se- in the post-AD elevation of [Ca ]i. Both Vm and [Ca ]i re- cretion of egg-laying hormone (ELH) from peptidergic neurons turned to baseline well before ELH secretion, such that neither in intact nervous tissue of Aplysia. Using a combination of prolonged membrane depolarization nor prolonged Ca 2ϩ sig- radioimmunoassay measurement of ELH secretion, electro- naling can fully account for the extent of the persistent secre- physiological measurement of membrane potential, and optical tion of ELH. These findings suggest a unique relationship be- imaging of the concentration of intracellular free calcium ions tween membrane excitability, Ca 2ϩ signaling, and prolonged 2ϩ ([Ca ]i ), we verified that there was persistent secretion of ELH neuropeptide secretion. after the end of the AD; this was accompanied by prolonged post-AD membrane depolarization and prolonged post-AD el- Key words: action potential; Aplysia; bag cell neurons; cal- 2ϩ evation in [Ca ]i. Extracellular treatment with the calcium che- cium imaging; calcium signaling; egg-laying hormone; exocyto- lator EGTA had no effect on the pattern or magnitude of ELH sis; membrane potential; neuroendocrine; neurosecretion ϩ Dependence of exocytosis on Ca 2 influx from extracellular fluid in living tissue.
    [Show full text]
  • NIH Public Access Author Manuscript Neuroscience
    NIH Public Access Author Manuscript Neuroscience. Author manuscript; available in PMC 2010 August 18. NIH-PA Author ManuscriptPublished NIH-PA Author Manuscript in final edited NIH-PA Author Manuscript form as: Neuroscience. 2004 ; 126(3): 533±540. doi:10.1016/j.neuroscience.2004.03.036. HIPPOCAMPAL CORTICOTROPIN RELEASING HORMONE: PRE- AND POSTSYNAPTIC LOCATION AND RELEASE BY STRESS Y. Chena, K. L. Brunsona, G. Adelmannb, R. A. Bendera, M. Frotscherb, and T. Z. Barama,* aDepartments of Anatomy/Neurobiology and Pediatrics, ZOT 4475, University of California at Irvine, Irvine, CA 92697-4475, USA bInstitute of Anatomy, University of Freiburg, Albertstrasse 17, D-79104 Freiburg, Germany Abstract Neuropeptides modulate neuronal function in hippocampus, but the organization of hippocampal sites of peptide release and actions is not fully understood. The stress-associated neuropeptide corticotropin releasing hormone (CRH) is expressed in inhibitory interneurons of rodent hippocampus, yet physiological and pharmacological data indicate that it excites pyramidal cells. Here we aimed to delineate the structural elements underlying the actions of CRH, and determine whether stress influenced hippocampal principal cells also via actions of this endogenous peptide. In hippocampal pyramidal cell layers, CRH was located exclusively in a subset of GABAergic somata, axons and boutons, whereas the principal receptor mediating the peptide’s actions, CRH receptor 1 (CRF1), resided mainly on dendritic spines of pyramidal cells. Acute ‘psychological’ stress led to activation of principal neurons that expressed CRH receptors, as measured by rapid phosphorylation of the transcription factor cyclic AMP responsive element binding protein. This neuronal activation was abolished by selectively blocking the CRF1 receptor, suggesting that stress-evoked endogenous CRH release was involved in the activation of hippocampal principal cells.
    [Show full text]
  • 1 General Overview of the Endocrine System Questions to Be Thinking
    General Overview of the Endocrine System Questions to be thinking about to help organize your learning of the components of the Endocrine System: Anatomy 1) Where are the different hormone producing cells located? 2) What hormone does a particular type of endocrine cell or neuron produce? General Overview of the Endocrine System Questions to be thinking about to help organize your learning of the components of the Endocrine System: Hormones 1) What is their general chemical structure? 2) How does their structure affect their function? 3) Where are they produced? 4) What environmental or physiological stimuli regulate their production and secretion? 5) Is their production and secretion under direct neural or hormonal control? 6) What are their targets? 7) What effects do they produce on their targets? 8) How do they produce their effects on their targets (how is the signal transduced? i.e. receptor mechanisms) 1 Often endocrine cells are clumped together into a well defined gland (e.g. pituitary, thyroid, adrenal, testes, ovaries), but not always (e.g. gut, liver, lung). Often endocrine cells are clumped together into a well defined gland (e.g. pituitary, thyroid, adrenal, testes, ovaries), but not always (e.g. gut, liver, lung). Remember, it's cells that produce hormones, not glands. Although many glands secrete more than one type of hormone, most neurons or endocrine cells only produce one type of hormone (there are a few exceptions). 2 Some Terminology Neurohormone: a hormone that is produced by a neuron Some Terminology All of the hormones we discuss can be classified as belonging to one of 2 general functional categories: 1] Releasing hormone (or factors) — hormone that acts on endocrine cells to regulate the release of other hormones.
    [Show full text]
  • The Cryptic Gonadotropin-Releasing Hormone Neuronal System Of
    RESEARCH ARTICLE The cryptic gonadotropin-releasing hormone neuronal system of human basal ganglia Katalin Skrapits1*, Miklo´ s Sa´ rva´ ri1, Imre Farkas1, Bala´ zs Go¨ cz1, Szabolcs Taka´ cs1, E´ va Rumpler1, Vikto´ ria Va´ czi1, Csaba Vastagh2, Gergely Ra´ cz3, Andra´ s Matolcsy3, Norbert Solymosi4, Szila´ rd Po´ liska5, Blanka To´ th6, Ferenc Erde´ lyi7, Ga´ bor Szabo´ 7, Michael D Culler8, Cecile Allet9, Ludovica Cotellessa9, Vincent Pre´ vot9, Paolo Giacobini9, Erik Hrabovszky1* 1Laboratory of Reproductive Neurobiology, Institute of Experimental Medicine, Budapest, Hungary; 2Laboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Budapest, Hungary; 31st Department of Pathology and Experimental Cancer Research, Semmelweis University, Budapest, Hungary; 4Centre for Bioinformatics, University of Veterinary Medicine, Budapest, Hungary; 5Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary; 6Department of Inorganic and Analytical Chemistry, Budapest University of Technology and Economics, Budapest, Hungary; 7Department of Gene Technology and Developmental Biology, Institute of Experimental Medicine, Budapest, Hungary; 8Amolyt Pharma, Newton, France; 9Univ. Lille, Inserm, CHU Lille, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Lille Neuroscience & Cognition, Lille, France Abstract Human reproduction is controlled by ~2000 hypothalamic gonadotropin-releasing *For correspondence: [email protected] (KS); hormone (GnRH) neurons. Here, we report the discovery and characterization of additional [email protected] (EH) ~150,000–200,000 GnRH-synthesizing cells in the human basal ganglia and basal forebrain. Nearly all extrahypothalamic GnRH neurons expressed the cholinergic marker enzyme choline Competing interests: The acetyltransferase. Similarly, hypothalamic GnRH neurons were also cholinergic both in embryonic authors declare that no and adult human brains.
    [Show full text]
  • Osmoregulation of Vasopressin Secretion Via Activation of Neurohypophysial Nerve Terminals Glycine Receptors by Glial Taurine
    The Journal of Neuroscience, September 15, 2001, 21(18):7110–7116 Osmoregulation of Vasopressin Secretion via Activation of Neurohypophysial Nerve Terminals Glycine Receptors by Glial Taurine Nicolas Hussy, Vanessa Bre` s, Marjorie Rochette, Anne Duvoid, Ge´ rard Alonso, Govindan Dayanithi, and Franc¸ oise C. Moos Laboratoire de Biologie des Neurones Endocrines, Centre National de la Recherche Scientifique (CNRS) Unite´ Mixte de Recherche 5101, Centre CNRS–Institut National de la Sante´ et de la Recherche Me´ dicale de Pharmacologie et d’Endocrinologie, 34094 Montpellier Cedex 5, France Osmotic regulation of supraoptic nucleus (SON) neuron activity minals is confirmed by immunohistochemistry. Their implication depends in part on activation of neuronal glycine receptors in the osmoregulation of neurohormone secretion was as- (GlyRs), most probably by taurine released from adjacent as- sessed on isolated whole neurohypophyses. A 6.6% hypo- trocytes. In the neurohypophysis in which the axons of SON osmotic stimulus reduces by half the depolarization-evoked neurons terminate, taurine is also concentrated in and osmo- vasopressin secretion, an inhibition totally prevented by strych- dependently released by pituicytes, the specialized glial cells nine. Most importantly, depletion of taurine by a taurine trans- ensheathing nerve terminals. We now show that taurine release port inhibitor also abolishes the osmo-dependent inhibition of from isolated neurohypophyses is enhanced by hypo-osmotic vasopressin release. Therefore, in the neurohypophysis, an os- and decreased by hyper-osmotic stimulation. The high osmo- moregulatory system involving pituicytes, taurine, and GlyRs is sensitivity is shown by the significant increase on only 3.3% operating to control Ca 2ϩ influx in and neurohormone release reduction in osmolarity.
    [Show full text]
  • Involvement of Arginine Vasopressin and V1b Receptor in Heroin Withdrawal and Heroin Seeking Precipitated by Stress and by Heroin
    Neuropsychopharmacology (2008) 33, 226–236 & 2008 Nature Publishing Group All rights reserved 0893-133X/08 $30.00 www.neuropsychopharmacology.org Involvement of Arginine Vasopressin and V1b Receptor in Heroin Withdrawal and Heroin Seeking Precipitated by Stress and by Heroin ,1,3 2,3 2 2 1 Yan Zhou* , Francesco Leri , Erin Cummins , Marisa Hoeschele and Mary Jeanne Kreek 1 2 Laboratory of the Biology of Addictive Diseases, The Rockefeller University, New York, NY, USA; Department of Psychology, University of Guelph, Guelph, ON, Canada A previous study has shown that the stress responsive neurohormone arginine vasopressin (AVP) is activated in the amygdala during early withdrawal from cocaine. The present studies were undertaken to determine whether (1) AVP mRNA levels in the amygdala or hypothalamus, as well as hypothalamic–pituitary–adrenal (HPA) activity, would be altered during chronic intermittent escalating heroin administration (10 days; 7.5–60 mg/kg/day) or during early (12 h) and late (10 days) spontaneous withdrawal; (2) foot shock stress would alter AVP mRNA levels in the amygdala or hypothalamus in rats withdrawn from heroin self-administration (7 days, 3 h/day, 0.05 mg/kg/ infusion); and (3) the selective V1b receptor antagonist SSR149415 (1 and 30 mg/kg, intraperitoneal) would alter heroin seeking during tests of reinstatement induced by foot shock stress and by heroin primes (0.25 mg/kg), as well as HPA hormonal responses to foot shock. We found that AVP mRNA levels were increased during early spontaneous withdrawal in the amygdala only. This amygdalar AVP mRNA increase was no longer observed at the later stage of heroin withdrawal.
    [Show full text]
  • Somatostatin Gastrin and C-Peptide in Thyroid Dysfunctions
    Med. J. Cairo Univ., Vol. 62, No. 3, September: 677 - 682, 1994 Somatostatin Gastrin and C-Peptide in Thyroid Dysfunctions MOHAMMAD A. ABDEL HAFEZ, M.D.; NAHED ABDEL GHANY, M.D.; SHERIF M. NAGUIB, M.D.; NAGUA E. SOBHY, M.D. and MOHAMMAD S. MOGAWER, M.D. The Departments of Medical Biochemistry and Internal Medicine, Faculty of of Medicine, Cairo University. Abstract Three groups of subjects were chosen; 20 patients with primary hypothyroidism, 20 patients with primary hyperthyroidism and a third group of 15 euthyroid subjects as a control group. Plasma somatostatin, gastrin and C-peptide were determined in both fasting and lh postprandial after standard oral glucose load. FT3, FT4, TSH, oral glucose tolerance curve, serum cholesterol and triglycerides were also determined. It was found that both basal and stimulated somatostatin plasma concentrations were el- evated in hypothyroidism and diminished in hyperthyroidism. On the contrary, serum gastrin and C-peptide were decreased. Elevated somatostatin level in hypothyroidism has an inhibitory effect on gastrin and C-peptide. C-peptide was elevated in hyper- thyroidism, however glucose intolerance was noticed in only 20% of these subjects. Elevated gastrin level in hyperthyroidism suggests a role for gastrointestinal distur- bances observed in these patients. Introduction had shown that somatostatin inhibits the hepatic T4 deiodenase, thus promoting its SOMATOSTATIN was first isolated from conversion to rTg rather than T3. the hypothalamus and was subsequently found in large amounts in endocrine cells This study was done to investigate the of the stomach, pancreas and thyroid gland level of somatostatin as well as gastrin and Ill.
    [Show full text]
  • THE NEUROHORMONE SEROTONIN MODULATES the PERFORMANCE of a MECHNOSENSORY NEURON DURING TAIL POSITIONING in the CRAYFISH by HSING
    THE NEUROHORMONE SEROTONIN MODULATES THE PERFORMANCE OF A MECHNOSENSORY NEURON DURING TAIL POSITIONING IN THE CRAYFISH by HSING-JU TSAI Submitted in partial fulfillment of the requirements For the degree of Master of Science Thesis Adviser: Dr. Debra Wood Department of Biology CASE WESTERN RESERVE UNIVERSITY August, 2009 CASE WESTERN RESERVE UNIVERSITY SCHOOL OF GRADUATE STUDIES We hereby approve the thesis/dissertation of _____________________________________________________ candidate for the ______________________degree *. (signed)_______________________________________________ (chair of the committee) ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ ________________________________________________ (date) _______________________ *We also certify that written approval has been obtained for any proprietary material contained therein. TABLE OF CONTENTS LIST OF FIGURES ...........................................................................................................2 LIST OF ABBREVIATIONS............................................................................................3 ABSTRACT ......................................................................................................................4 INTRODUCTION .............................................................................................................5 BACKGROUND................................................................................................................8
    [Show full text]
  • Multifactorial Basis and Therapeutic Strategies in Metabolism-Related Diseases
    nutrients Review Multifactorial Basis and Therapeutic Strategies in Metabolism-Related Diseases João V. S. Guerra 1,2,† , Marieli M. G. Dias 1,3,† , Anna J. V. C. Brilhante 3,4, Maiara F. Terra 1,3, Marta García-Arévalo 1,* and Ana Carolina M. Figueira 1,* 1 Brazilian Center for Research in Energy and Materials (CNPEM), Brazilian Biosciences National Laboratory (LNBio), Polo II de Alta Tecnologia—R. Giuseppe Máximo Scolfaro, Campinas 13083-100, Brazil; [email protected] (J.V.S.G.); [email protected] (M.M.G.D.); [email protected] (M.F.T.) 2 Graduate Program in Pharmaceutical Sciences, Faculty Pharmaceutical Sciences, University of Campinas, Campinas 13083-970, Brazil 3 Graduate Program in Functional and Molecular Biology, Institute of Biology, State University of Campinas (Unicamp), Campinas 13083-970, Brazil; [email protected] 4 Brazilian Center for Research in Energy and Materials (CNPEM), Brazilian Biorenewables National Laboratory (LNBR), Polo II de Alta Tecnologia—R. Giuseppe Máximo Scolfaro, Campinas 13083-100, Brazil * Correspondence: [email protected] or [email protected] (M.G.-A.); ana.fi[email protected] (A.C.M.F.) † Both authors contributed equally to this work. Abstract: Throughout the 20th and 21st centuries, the incidence of non-communicable diseases (NCDs), also known as chronic diseases, has been increasing worldwide. Changes in dietary and physical activity patterns, along with genetic conditions, are the main factors that modulate the Citation: Guerra, J.V.S.; Dias, metabolism of individuals, leading to the development of NCDs. Obesity, diabetes, metabolic M.M.G.; Brilhante, A.J.V.C.; Terra, associated fatty liver disease (MAFLD), and cardiovascular diseases (CVDs) are classified in this M.F.; García-Arévalo, M.; Figueira, group of chronic diseases.
    [Show full text]