DOCSLIB.ORG

Developmental and Stress-Related Changes of Neurotrophic Factor Gene Expression in an Animal Model of Schizophrenia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Developmental and Stress-Related Changes of Neurotrophic Factor Gene Expression in an Animal Model of Schizophrenia Molecular Psychiatry (2001) 6, 285–292 2001 Nature Publishing Group All rights reserved 1359-4184/01 $15.00 www.nature.com/mp ORIGINAL RESEARCH ARTICLE Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia R Molteni1, BK Lipska2, DR Weinberger2, G Racagni1,3 and MA Riva1 1Center for Neuropharmacology, Department of Pharmacological Sciences, University of Milan, Milan, Italy; 2Clinical Brain Disorders Branch, IRP, NIMH, NIH, Bethesda MD, USA; 3IRCCS San Giovanni di Dio-Fatebenefratelli, Brescia, Italy The neonatal (PND 7) lesion of the ventral hippocampus (VH) with ibotenic acid represents a well-established experimental paradigm that recapitulates many schizophrenia-like phenom- ena. In order to investigate molecular changes that could contribute to long lasting conse- quences on brain function, we have investigated the effects of the VH lesion on the expression for the trophic factors FGF-2 and BDNF. We used RNase protection assay to measure their mRNA levels in cortical regions of prepubertal (PND 35) and young adult (PND 56) animals, both under basal condition as well as in response to an acute restraint stress. The expression of BDNF was not altered by the VH lesion in prefrontal (PFC) and frontal cortex (FC) of PND 35 or PND 56 rats. An acute restraint stress at PND 35 produced a significant increase of the neurotrophin expression in PFC of sham as well as lesioned animals. However in young adult animals a significant elevation of BDNF expression was observed only in sham rats. We also found that the VH lesion produced a significant reduction of basal BDNF mRNA levels in the cingulate cortex of young adult, but not prepubertal rats. This effect was not accompanied by changes in the acute modulation of the neurotrophin, which was up-regulated by stress in both experimental groups. Conversely the expression of FGF-2 at PND 35 and PND 56 was not altered by early postnatal VH lesion, and there were no major differences between sham and lesioned animals in response to the acute stress. The changes in trophic factor expression may be relevant for the long-term effects of VH lesion on synaptic plasticity and may determine an increased vulnerability of the brain under challenging situations. Molecular Psychiatry (2001) 6, 285–292. Keywords: brain derived neurotrophic factor; fibroblast growth factor-2; brain plasticity; ibotenic acid; hippocampus; stress Introduction during early stages of gestation, that will affect the function of prefrontal-intracortical connectivity.6–9 Schizophrenia is a complex disorder characterized by Although several factors can contribute to cortical hallucinations, delusions, cognitive deficits and dra- maldevelopment, one possibility is the involvement of matic functional impairment. The neurodevelopmental neurotrophic factors.10 These proteins are important hypothesis of schizophrenia provides a starting point regulators of brain development and neuronal shaping to understand structural and functional abnormalities and play a role in synaptic plasticity as well as in the which have been observed in the brain of schizo- maintenance of cellular homeostasis.11–15 There is a phrenic patients, particularly at the level of prefrontal characteristic temporal and spatial pattern of cortex and hippocampal formation.1–3 expression for these molecules during brain develop- In vivo imaging and postmortem studies on schizo- ment.16,17 Abnormalities in their expression profiles phrenic subjects have demonstrated the presence of during development may affect the functional con- neuropathological abnormalities in the hippocampus nectivity of specific neuronal phenotypes that become that may correlate with the deficits in episodic mem- evident after the brain has reached full maturation. For ory, a form of explicit memory linked to hippocampal example the lack of FGF-2 signaling in FGF-2-deficient function.4,5 Such abnormalities may be the result of mice affects migration of a fraction of neuronal precur- alterations in brain development, probably occurring sor during cerebral cortex development18 and reduces the number of cortical neurons and glial cells at maturity.19 Correspondence: MA Riva, Center for Neuropharmacology, Via Because of the importance of growth factors for the Balzaretti 9, 20133 Milan, Italy. E-mail: marivaȰmailserver. unimi.it cortical abnormalities implicated in schizophrenia, we Received 21 September 2000; revised and accepted 27 Nov- studied the expression profile of brain-derived neuro- ember 2000 trophic factor (BDNF) and fibroblast growth factor-2 Neonatal VH lesion alters cortical trophic factor expression R Molteni et al 286 (FGF-2) in a developmental animal model of schizo- Surgery phrenia. Rat pups were lesioned as described previously.48 BDNF, a member of the neurotrophin family, has a Briefly, pregnant Sprague–Dawley rats obtained at 12– wide distribution in the CNS, where it is synthesized 14 days of gestation (Harlan, Indianapolis, IN, USA) predominantly by neurons and is highly expressed in were housed individually in breeding cages with a 12- hippocampus, cerebral cortex, limbic areas and cere- h light/dark cycle and fed ad libitum. Litters of four to bellum.20,21 This neurotrophin plays an important role eight male pups were formed. On the 7th day of age in regulating the survival and differentiation of selec- (PND 7) pups (weight 15–18 g), within each litter were tive populations of neurons during development22,23 randomized to Sham or Lesion status and anaesthet- and is an important mediator of neuronal adaptive ized by hypothermia (placed on ice for 15–20 min). An responses.12–14 The expression of BDNF is regulated by incision was made in the skin overlying the skull and neuronal activity, shows marked and transient changes 0.3 ␮lof10␮g ␮l−1 of ibotenic acid solution (in the in response to a number of neuronal insults, including lesioned rats) or artificial cerebrospinal fluid (in sham- ischemia, hypoglycemia, epileptic activity, immobiliz- operated rats) was infused bilaterally, through a Hamil- 17,24–28 ation stress and trauma and its modulation ton needle, using an infusion pump into the ventral involves a complex interplay between different neuro- hippocampal formation (AP −3.0 mm, ML ± 3.5 mm, 29,30 transmitter systems. VD −5.0 mm, relative to Bregma) at the rate of 0.15 ␮l FGF-2 is a trophic molecule that has a critical role min−1. The pups were warmed and then returned to in the maturation and survival of a variety of neuronal their mothers. On the 25th day of age rats were weaned, phenotypes.15,31 Its expression is regulated by neuronal 32,33 34–36 separated according to the lesion status and grouped activity, neurotransmitters and hormones as two to a cage. well as by learning and physical exercise.37,38 It is well established that FGF-2 has neuroprotective activity over a wide range of neurons39–41 and it may render the 42,43 Experimental procedure cells more resistant to potential lethal damage. The effect of the neonatal VH ibotenic acid lesion on The animal model employed in our study is obtained neurotrophic gene expression as well as the effect of by bilateral infusion of the excitotoxin ibotenic acid in acute stress in sham and lesion animals was assessed the ventral hippocampus (VH) of rats on the 7th day at PND 35 (before puberty) and PND 56 (after puberty). of age44 and reproduces some fundamental features of Rats were randomly assigned to four groups (Sham/No schizophrenia, including dopaminergic overactivity Stress; Sham/Stress; Lesion/No Stress; Lesion/Stress). and emergence of behavioral abnormalities in early The animals undergoing restraint stress were placed for adulthood. Adult rats with the neonatal VH lesion 2 h in transparent plexiglas containers whereas those express exaggerated locomotor response to ampheta- in the control group were left undisturbed in their mine and to acute stress,44 augmented apomorphine- induced stereotypy,45 and altered prepulse inhibition home cages. Rats were killed by decapitation 1 h after of the acoustic startle response.46 Moreover, the the end of immobilization, their brains rapidly expression of behavioral phenotypes is strain-depen- removed and the following cortical regions were dis- dent.47 Neonatal damage of the hippocampus also dis- sected from 2-mm thick slices: prefrontal cortex PFC rupts complex behaviors such as working memory and (defined as Cg1, Cg3 and IL subregions corresponding social interaction.48 Some of these behavioral abnor- to the plates 6–9 according to the atlas of Paxinos and 51 malities are reversed by treatment with typical and Watson, frontal cortex FC (comprising regions Fr1–3, atypical antipsychotics.49 Using this paradigm, we Par1 and AI from the same slice as PFC) and cingulate have analyzed the expression profile of BDNF and FGF- cortex CC (comprising Cg1 and Cg3 areas from the slice 2 in prefrontal, frontal and cingulate cortex in prepub- corresponding to plates 10–13 in the atlas of Paxinos 51 ertal and mature animals. Since an impairment in and Watson. We have investigated PFC and CC, as coping with specific challenging situations may rep- compared to FC, because they are connected with the resent a long-lasting effect observed after the lesion as hippocampal formation (that is lesioned in our well as other developmental perturbations,50 we have paradigm) and because functional1 and anatomical52 also investigated whether the stress-dependent regulat- changes have been detected at this level in schizo- ory mechanism of neurotrophic
Load more

Recommended publications
  • Signalings and Roles in Central Nervous System
    Volume 9, Number 3; 537-552, June 2018 http://dx.doi.org/10.14336/AD.2017.0702 Review Mammalian Sterile20-like Kinases: Signalings and Roles in Central Nervous System Sheng Chen1, #, *, Yuanjian Fang1, #, Shenbin Xu1, Cesar Reis2, 3, Jianmin Zhang1, 4, * 1Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. 2Department of Physiology and Pharmacology, Loma Linda University, Loma Linda, California, USA. 3Brain Research Institute, Zhejiang University, Hangzhou, Zhejiang, China. 4Collaborative Innovation Center for Brain Science, Zhejiang University, Hangzhou, Zhejiang, China. [Received May 30, 2017; Revised June 16, 2017; Accepted July 2, 2017] ABSTRACT: Mammalian Sterile20-like (MST) kinases are located upstream in the mitogen-activated protein kinase pathway, and play an important role in cell proliferation, differentiation, renewal, polarization and migration. Generally, five MST kinases exist in mammalian signal transduction pathways, including MST1, MST2, MST3, MST4 and YSK1. The central nervous system (CNS) is a sophisticated entity that takes charge of information reception, integration and response. Recently, accumulating evidence proposes that MST kinases are critical in the development of disease in different systems involving the CNS. In this review, we summarized the signal transduction pathways and interacting proteins of MST kinases. The potential biological function of each MST kinase and the commonly reported MST-related diseases in the neural system
    [Show full text]
  • Both Systemic and Local Application of Granulocyte-Colony Stimulating
    BMC Neuroscience BioMed Central Research article Open Access Both systemic and local application of Granulocyte-colony stimulating factor (G-CSF) is neuroprotective after retinal ganglion cell axotomy Tobias Frank†1, Johannes CM Schlachetzki†1, Bettina Göricke1,2, Katrin Meuer1, Gundula Rohde1,2, Gunnar PH Dietz1,2,3, Mathias Bähr1,2, Armin Schneider4 and Jochen H Weishaupt*1,2 Address: 1Department of Neurology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany, 2DFG-Research Center for Molecular Physiology of the Brain (CMPB), Humboldtallee 23, Göttingen, Germany, 3H Lundbeck A/S, 2500 Valby, Denmark and 4Sygnis Bioscience, Im Neuenheimer Feld 515, 69120 Heidelberg, Germany Email: Tobias Frank - [email protected]; Johannes CM Schlachetzki - [email protected]; Bettina Göricke - [email protected]; Katrin Meuer - [email protected]; Gundula Rohde - [email protected]; Gunnar PH Dietz - [email protected]; Mathias Bähr - [email protected]; Armin Schneider - [email protected]; Jochen H Weishaupt* - [email protected] * Corresponding author †Equal contributors Published: 14 May 2009 Received: 10 November 2008 Accepted: 14 May 2009 BMC Neuroscience 2009, 10:49 doi:10.1186/1471-2202-10-49 This article is available from: http://www.biomedcentral.com/1471-2202/10/49 © 2009 Frank et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: The hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) plays a crucial role in controlling the number of neutrophil progenitor cells.
    [Show full text]
  • 8667.Full-Text.Pdf
    The Journal of Neuroscience, November 15, 1997, 17(22):8667–8675 Brain-Derived Neurotrophic Factor, Neurotrophin-3, and Neurotrophin-4 Complement and Cooperate with Each Other Sequentially during Visceral Neuron Development Wael M. ElShamy and Patrik Ernfors Department of Medical Biochemistry and Biophysics, Laboratory of Molecular Neurobiology, Doktorsringen 12A, Karolinska Institute, 171 77 Stockholm, Sweden The neurotrophins nerve growth factor (NGF), brain-derived they are essential in preventing the death of N/P ganglion neurotrophic factor (BDNF), neurotrophin-3 (NT3), and neurons during different periods of embryogenesis. Both NT3 neurotrophin-4 (NT4) are crucial target-derived factors control- and NT4 are crucial during the period of ganglion formation, ling the survival of peripheral sensory neurons during the em- whereas BDNF acts later in development. Many, but not all, of bryonic period of programmed cell death. Recently, NT3 has the NT3- and NT4-dependent neurons switch to BDNF at later also been found to act in a local manner on somatic sensory stages. We conclude that most of the N/P ganglion neurons precursor cells during early development in vivo. Culture stud- depend on more than one neurotrophin and that they act in a ies suggest that these cells switch dependency to NGF at later complementary as well as a collaborative manner in a devel- stages. The neurotrophins acting on the developing placode- opmental sequence for the establishment of a full complement derived visceral nodose/petrosal (N/P) ganglion neurons are
    [Show full text]
  • Journal of Neuroinflammation Biomed Central
    Journal of Neuroinflammation BioMed Central Research Open Access Immune modulation and increased neurotrophic factor production in multiple sclerosis patients treated with testosterone Stefan M Gold1,2, Sara Chalifoux1, Barbara S Giesser1 and Rhonda R Voskuhl*1 Address: 1Department of Neurology, Neuroscience Research Building 1, 635 Charles E. Young Drive South, University of California Los Angeles, CA, 90095, USA and 2Cousins Center, 300 Medical Plaza, University of California Los Angeles, CA, 90095, USA Email: Stefan M Gold - [email protected]; Sara Chalifoux - [email protected]; Barbara S Giesser - [email protected]; Rhonda R Voskuhl* - [email protected] * Corresponding author Published: 31 July 2008 Received: 29 May 2008 Accepted: 31 July 2008 Journal of Neuroinflammation 2008, 5:32 doi:10.1186/1742-2094-5-32 This article is available from: http://www.jneuroinflammation.com/content/5/1/32 © 2008 Gold et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Multiple sclerosis is a chronic inflammatory disease of the central nervous system with a pronounced neurodegenerative component. It has been suggested that novel treatment options are needed that target both aspects of the disease. Evidence from basic and clinical studies suggests that testosterone has an immunomodulatory as well as a potential neuroprotective effect that could be beneficial in MS. Methods: Ten male MS patients were treated with 10 g of gel containing 100 mg of testosterone in a cross-over design (6 month observation period followed by 12 months of treatment).
    [Show full text]
  • Deficiency in Androgen Receptor Aggravates the Depressive-Like
    cells Article Deficiency in Androgen Receptor Aggravates the Depressive-Like Behaviors in Chronic Mild Stress Model of Depression Yi-Yung Hung 1,2, Ya-Ling Huang 1, Chawnshang Chang 3,* and Hong-Yo Kang 2,4,* 1 Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital, and Chang Gung University College of Medicine, Kaohsiung 833, Taiwan 2 Graduate Institute of Clinical Medical Sciences, College of Medicine, Chang Gung University, Kaohsiung 833, Taiwan 3 George Whipple Lab for Cancer Research, Departments of Pathology, Urology and Radiation Oncology, and The Wilmot Cancer Center, University of Rochester Medical Center, Rochester, NY 14646, USA 4 Department of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan * Correspondence: [email protected] (C.C.); [email protected] (H.-Y.K.); Tel.: +886-7-731-7123 (ext. 8898) (H.-Y.K.) Received: 11 July 2019; Accepted: 28 August 2019; Published: 2 September 2019 Abstract: While androgen receptor (AR) and stress may influence the development of the major depressive disorder (MDD), the detailed relationship, however, remains unclear. Here we found loss of AR accelerated development of depressive-like behaviors in mice under chronic mild stress (CMS). Mechanism dissection indicated that AR might function via altering the expression of miR-204-5p to modulate the brain-derived neurotrophic factor (BDNF) expression to influence the depressive-like behaviors in the mice under the CMS. Adding the antiandrogen flutamide with the stress hormone corticosterone can additively decrease BDNF mRNA in mouse hippocampus mHippoE-14 cells, which can then be reversed via down-regulating the miR-204-5p expression.
    [Show full text]
  • Neuronal Caspase-3 Signaling: Not Only Cell Death
    Cell Death and Differentiation (2010) 17, 1104–1114 & 2010 Macmillan Publishers Limited All rights reserved 1350-9047/10 $32.00 www.nature.com/cdd Review Neuronal caspase-3 signaling: not only cell death M D’Amelio*,1,2, V Cavallucci1,2 and F Cecconi*,1,2 Caspases are a family of cysteinyl aspartate-specific proteases that are highly conserved in multicellular organisms and func- tion as central regulators of apoptosis. A member of this family, caspase-3, has been identified as a key mediator of apoptosis in neuronal cells. Recent studies in snail, fly and rat suggest that caspase-3 also functions as a regulatory molecule in neurogenesis and synaptic activity. In this study, in addition to providing an overview of the mechanism of caspase-3 activation, we review genetic and pharmacological studies of apoptotic and nonapoptotic functions of caspase-3 and discuss the regulatory mechanism of caspase-3 for executing nonapoptotic functions in the central nervous system. Knowledge of biochemical pathway(s) for nonapoptotic activation and modulation of caspase-3 has potential implications for the understanding of synaptic failure in the pathophysiology of neurological disorders. Fine-tuning of caspase-3 lays down a new challenge in identifying pharmacological avenues for treatment of many neurological disorders. Cell Death and Differentiation (2010) 17, 1104–1114; doi:10.1038/cdd.2009.180; published online 4 December 2009 The role of caspases in programmed cell death has been inhibited by Smac/Diablo and Omi/HtrA2, which are released reviewed many times.1–3 It is widely accepted that, in mam- from the intermembrane space when mitochondria are mals, two main pathways (Figure 1) have evolved for damaged.
    [Show full text]
  • Review Article Protective Action of Neurotrophic Factors and Estrogen Against Oxidative Stress-Mediated Neurodegeneration
    Hindawi Publishing Corporation Journal of Toxicology Volume 2011, Article ID 405194, 12 pages doi:10.1155/2011/405194 Review Article Protective Action of Neurotrophic Factors and Estrogen against Oxidative Stress-Mediated Neurodegeneration Tadahiro Numakawa,1, 2 Tomoya Matsumoto,2, 3 Yumiko Numakawa,4 Misty Richards,1, 5 Shigeto Yamawaki,2, 3 and Hiroshi Kunugi1, 2 1 Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan 2 Core Research for Evolutional Science and Technology Program (CREST), Japan Science and Technology Agency (JST), Saitama 332-0012, Japan 3 Department of Psychiatry and Neurosciences, Division of Frontier Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan 4 Peptide-prima Co., Ltd., 1-25-81, Nuyamazu, Kumamoto 861-2102, Japan 5 The Center for Neuropharmacology and Neuroscience, Albany Medical College, Albany, NY 12208, USA Correspondence should be addressed to Tadahiro Numakawa, [email protected] Received 11 January 2011; Revised 28 February 2011; Accepted 29 March 2011 Academic Editor: Laurence D. Fechter Copyright © 2011 Tadahiro Numakawa et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Oxidative stress is involved in the pathogenesis of neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. Low levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) are important for maintenance of neuronal function, though elevated levels lead to neuronal cell death.
    [Show full text]
  • Growth Factor Family (Brain-Derived Neurotrophic Factor/Polymerase Chain Reaction/Neurotrophic Factor/Mrna) KEVIN R
    Proc. Nati. Acad. Sci. USA Vol. 87, pp. 8060-8064, October 1990 Neurobiology Molecular cloning of a human gene that is a member of the nerve growth factor family (brain-derived neurotrophic factor/polymerase chain reaction/neurotrophic factor/mRNA) KEVIN R. JONES AND Louis F. REICHARDT Howard Hughes Medical Institute, Room U426, University of California-San Francisco, San Francisco, CA 94143 Communicated by William A. Catterall, June 18, 1990 (received for review May 4, 1990) ABSTRACT Cell death within the developing vertebrate Y is a pyrimidine, and W is A or T) or 2B2 (TAYTTYTW- nervous system is regulated in part by interactions between YGARACNAARTG; where N is any nucleotide) and 4A1' neurons and their innervation targets that are mediated by (DATNCKDATRAANCKCCA; where D is G, A, or T and neurotrophic factors. These factors also appear to have a role K is G or T) were used at 5 ,uM to amplify 500 ng of human in the maintenance of the adult nervous system. Two neuro- genomic DNA in a 50-,ul PCR mixture (7). After 45 cycles of trophic factors, nerve growth factor and brain-derived neuro- amplification (temperature profile: 94TC for 1 min; 45TC for 2 trophic factor, share substantial amino acid sequence identity. min; 55TC for 15 sec; 72TC for 2 min), reaction products were We have used a screen that combines polymerase chain reaction separated on a 3% NuSieve agarose gel (FMC) and a band of amplification of genomic DNA and low-stringency hybridiza- tion with degenerate oligonucleotides to isolate human BDNF the expected molecular size (approximately 165 base pairs) and a human gene, neurotrophin-3, that is closely related to was excised.
    [Show full text]
  • Ciliary Neurotrophic Factor Prevents Degeneration of Adult
    Proc. Natl. Acad. Sci. USA Vol. 90, pp. 6315-6319, July 1993 Neurobiology Ciliary neurotrophic factor prevents degeneration of adult rat substantia nigra dopaminergic neurons in vivo (neuronal death/axotomy/trophic factor/tyrosine hydroxylase/Parkinson disease) THEO HAGG* AND SILVIO VARON Department of Biology, University of California, San Diego, La Joila, CA 92093-0601 Communicated by Dominick P. Purpura, March 29, 1993 (receivedfor review December 10, 1992) ABSTRACT We have investigated the neuroprotective ef- effect was seen for their transmitter enzyme, choline acetyl- fects of recombinant human ciliary neurotrophic factor transferase (ChAT). In the present study, we investigated in (CNTF) for injured dopaminergic neurons of the adult rat adult rats whether CNTF could also have protective effects substantia nigra compacta. Fourteen days after a unilateral for injured and degenerating dopaminergic neurons of the ansetion of the nigrostriatal pathway two-thirds of the substantia nigra compacta. neurons (identiffed by retograde labeling) had degenerated. In sharp contrast, 73% (a few cases, >90%) of this ceil loss was prevented by continuous infusion of CNTF close to the injured METHODS neurons. However, CNTF did not prevent the disappearance of Nigrostriatal Transection. Female Sprague-Dawley rats the transmitter-synthesizing enzyme tyrosine hydroxylase. (200 g; Bantin & Kingman, Fremont, CA; housed and cared Thus, CNTF has potent neurotrophic effects for injured adult for according to National Institutes of Health and U.S. rat dopaminergic
    [Show full text]
  • Nerve Growth Factor and Related Substances: a Brief History and an Introduction to the International NGF Meeting Series
    International Journal of Molecular Sciences Editorial Nerve Growth Factor and Related Substances: A Brief History and an Introduction to the International NGF Meeting Series Ralph A. Bradshaw 1,2, William Mobley 3 and Robert A. Rush 4,* 1 Department of Physiology and Biophysics, University of California, Irvine, CA 92697, USA; [email protected] 2 Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA 3 Department of Neuroscience, University of California, San Diego, La Jolla, CA 92093, USA; [email protected] 4 Department of Human Physiology, Flinders University, Adelaide, SA 5001, Australia * Correspondence: robert.rush@flinders.edu.au; Tel.: +61-4-1419-0126 Academic Editors: Margaret Fahnestock and Keri Martinowich Received: 12 April 2017; Accepted: 10 May 2017; Published: 26 May 2017 Abstract: Nerve growth factor (NGF) is a protein whose importance to research and its elucidation of fundamental mechanisms in cell and neurobiology far outstrips its basic physiological roles. It was the first of a broad class of cell regulators, largely acting through autocrine and paracrine interactions which will be described herein. It was of similar significance in establishing the identity and unique roles of neurotrophic factors in the development and maintenance of the peripheral and central nervous systems. Finally, it contributed to many advances in the elaboration of cell surface receptor mechanisms and intracellular cell signaling. As such, it can be considered to be a “molecular Rosetta Stone”. In this brief review, the highlights of these various studies are summarized, particularly as illustrated by their coverage in the 13 NGF international meetings that have been held since 1986.
    [Show full text]
  • BDNF and Cortisol Integrative System – Plasticity Vs. Degeneration
    Frontiers in Neuroendocrinology 55 (2019) 100784 Contents lists available at ScienceDirect Frontiers in Neuroendocrinology journal homepage: www.elsevier.com/locate/yfrne BDNF and Cortisol integrative system – Plasticity vs. degeneration: ☆ Implications of the Val66Met polymorphism T ⁎ Gilmara Gomes de Assisa,b, , Eugene V. Gasanovc a Department of Applied Physiology, Mossakowski Medical Research Centre Polish Academy of Sciences, Warsaw, Poland b Lab. of Behavioral Endocrinology, Brain Institute, Federal University of Rio Grande do Norte, Natal, Brazil c Laboratory of Neurodegeneration, International Institute of Molecular and Cell Biology in Warsaw, Poland ARTICLE INFO ABSTRACT Keywords: BDNF is the neurotrophin mediating pro-neuronal survival and plasticity. Cortisol (COR), in turn, is engaged in Brain-derived neurotrophic factor the coordination of several processes in the brain homeostasis. Stress-responsive, both factors show an in- Cortisol tegrative role through their receptor’s dynamics in neurophysiology. Furthermore, the Val66Met BDNF poly- Val66Met polymorphism morphism may play a role in this mechanism. Aim: to investigate BDNF-COR interaction in the human neu- Depression rophysiology context. Methods: We collected all papers containing BDNF and COR parameters or showing COR Exercise analyses in genotyped individuals in a PubMed search – full description available on PROSPERO – CRD42016050206. Discussion: BDNF and COR perform distinct roles in the physiology of the brain whose systems are integrated by glucocorticoid receptors dynamics. The BDNF polymorphism appears to have an in- fluence on individual COR responsivity to stress. BDNF and COR play complementary roles in the nervous system where COR is a regulator of positive/negative effects. Exercise positively regulates both factors, regardless of BDNF polymorphism. 1.
    [Show full text]
  • Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy Patrick Suezaki University of the Pacific
    University of the Pacific Scholarly Commons Dugoni School of Dentistry Faculty Articles Arthur A. Dugoni School of Dentistry 2-2017 Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy Patrick Suezaki University of the Pacific Nan (Tori) Xiao University of the Pacific, [email protected] Follow this and additional works at: https://scholarlycommons.pacific.edu/dugoni-facarticles Part of the Dentistry Commons Recommended Citation Suezaki, P., & Xiao, N. (2017). Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy. Journal of Dentistry and Oral Biology, 2(3), 1–2. https://scholarlycommons.pacific.edu/dugoni-facarticles/415 This Article is brought to you for free and open access by the Arthur A. Dugoni School of Dentistry at Scholarly Commons. It has been accepted for inclusion in Dugoni School of Dentistry Faculty Articles by an authorized administrator of Scholarly Commons. For more information, please contact [email protected]. Mini Review Journal of Dentistry and Oral Biology Published: 08 Feb, 2017 Potential Ciliary Neurotrophic Factor Application in Dental Stem Cell Therapy Patrick Suezaki1 and Nan Xiao2* 1Doctor of Dental Surgery Program, Arthur A. Dugoni School of Dentistry University of the Pacific, USA 2Department of Biomedical Sciences, Arthur A. Dugoni School of Dentistry University of the Pacific, USA Abstract Neurotrophic factors have long been considered growth factors that promote survival and growth of various neuronal tissues. Recent studies showed that neurotrophic factors are also present in dental pulp and periodontal ligament. This paper reviews the literature about the ciliary neurotrophic factor (CNTF), a member of the neurotrophic factor family, and indicates the potential clinical application of CNTF in dental stem cell therapy.
    [Show full text]