Important Interaction Between Urethral Taste Bud-Like Structures and Onuf's
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I the NATURE of SCHIZOTYPY AMONG
THE NATURE OF SCHIZOTYPY AMONG MULTIGENERATIONAL MULTIPLEX SCHIZOPHRENIA FAMILIES by Sarah Irene Tarbox, PhD B.A. Psychology, Brandeis University, 1997 M.S. Psychology, University of Pittsburgh, 2005 Submitted to the Graduate Faculty of Arts and Sciences in partial fulfillment of the requirements for the degree of Doctor of Philosophy University of Pittsburgh 2010 i UNIVERSITY OF PITTSBURGH Faculty of Arts and Sciences This dissertation was presented by Sarah I. Tarbox It was defended on September 8, 2009 and approved by JeeWon Cheong, PhD, Department of Psychology, University of Pittsburgh Daniel Shaw, PhD, Department of Psychology, University of Pittsburgh Vishwajit Nimgaonkar, M.D., PhD, Department of Psychiatry, University of Pittsburgh Laura Almasy, PhD, Department of Genetics, Southwest Foundation for Biomedical Research Dissertation Advisor and Chair: Michael Pogue-Geile, PhD, Department of Psychology, University of Pittsburgh ii Copyright © by Sarah I. Tarbox 2010 iii Michael F. Pogue-Geile, Ph.D. THE NATURE OF SCHIZOTYPY AMONG MULTIGENERATIONAL MULTIPLEX SCHIZOPHRENIA FAMILIES Sarah I. Tarbox, PhD University of Pittsburgh, 2010 Identification of endophenotypes (I. I. Gottesman & Gould, 2003; I. I. Gottesman & Shields, 1972) that correlate with familial liability to schizophrenia and are maximally sensitive to a homogeneous subset of risk genes is an important strategy for detecting genes that affect schizophrenia risk. Symptoms of schizotypy may correlate with familial liability to schizophrenia; however, there are critical limitations of the current literature concerning this association. The present study examined the genetic architecture and genetic association between schizotypy and genetic liability to schizophrenia among multigenerational, multiplex schizophrenia families. Genetic schizotypy factors were identified that significantly correlated with genetic liability to schizophrenia, although some relations were unexpected in direction. -
The Social Defeat Animal Model of Depression Shows
Neuroscience 218 (2012) 138–153 THE SOCIAL DEFEAT ANIMAL MODEL OF DEPRESSION SHOWS DIMINISHED LEVELS OF OREXIN IN MESOCORTICAL REGIONS OF THE DOPAMINE SYSTEM, AND OF DYNORPHIN AND OREXIN IN THE HYPOTHALAMUS C. NOCJAR, a,b* J. ZHANG, c P. FENG a,c AND INTRODUCTION J. PANKSEPP d A reduced ability to experience pleasure, termed anhedo- a Department of Psychiatry, Louis Stokes Cleveland VA Medical Center, Cleveland, OH, USA nia, is a hallmark symptom of depression and is expressed in rodent models of the illness. Various studies suggest that b Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA a dynorphin and orexin interactive dysfunction between the hypothalamus and the dopamine reward system might c Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Case Western Reserve University, exist in depression; and perhaps cause anhedonia symp- Cleveland, OH, USA toms. Dynorphin and orexin modulate each other’s function d Department of Veterinary and Comparative Anatomy, (Eriksson et al., 2004; Li and van den Pol, 2006) as well as Pharmacology and Physiology, College of Veterinary brain reward mechanisms; though dynorphin typically Medicine, Washington State University, Pullman, WA, USA inhibits and orexin stimulates neural activity (Shippenberg, 2009; Aston-Jones et al., 2010). Dynorphin is also co-expressed in nearly all orexin neurons, which are exclu- Abstract—Anhedonia is a core symptom of clinical depres- sively located in dorsomedial and lateral regions of the sion. Two brain neuropeptides that have been implicated in anhedonia symptomology in preclinical depression mod- hypothalamus (Chou et al., 2001). Importantly, hedonic els are dynorphin and orexin; which are concentrated along behaviors that are commonly diminished in depressed lateral hypothalamic dopamine reward pathways. -
Neural Mechanisms of Salt Avoidance in a Freshwater Fish
Neural Mechanisms of Salt Avoidance in a Freshwater Fish The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Herrera, Kristian J. 2019. Neural Mechanisms of Salt Avoidance in a Freshwater Fish. Doctoral dissertation, Harvard University, Graduate School of Arts & Sciences. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:42029741 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Neural mechanisms of salt avoidance in a freshwater fish A dissertation presented by Kristian Joseph Herrera to The Department of Molecular and Cellular Biology in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the subject of Biology Harvard University Cambridge, Massachusetts April 2019 © 2019 – Kristian Joseph Herrera All rights reserved. Dissertation advisor: Prof. Florian Engert Author: Kristian Joseph Herrera Neural mechanisms of salt avoidance in a freshwater fish Abstract Salts are crucial for life, and many animals will expend significant energy to ensure their proper internal balance. Two features necessary for this endeavor are the ability to sense salts in the external world, and neural circuits ready to execute appropriate behaviors. Most land animals encounter external salt through food, and, in turn, have taste systems that are sensitive to the salt content of ingested material. Fish, on the other hand, extract ions directly from their surrounding environment. As such, they have evolved physiologies that enable them to live in stable ionic equilibrium with their environment. -
Taste and Smell Disorders in Clinical Neurology
TASTE AND SMELL DISORDERS IN CLINICAL NEUROLOGY OUTLINE A. Anatomy and Physiology of the Taste and Smell System B. Quantifying Chemosensory Disturbances C. Common Neurological and Medical Disorders causing Primary Smell Impairment with Secondary Loss of Food Flavors a. Post Traumatic Anosmia b. Medications (prescribed & over the counter) c. Alcohol Abuse d. Neurodegenerative Disorders e. Multiple Sclerosis f. Migraine g. Chronic Medical Disorders (liver and kidney disease, thyroid deficiency, Diabetes). D. Common Neurological and Medical Disorders Causing a Primary Taste disorder with usually Normal Olfactory Function. a. Medications (prescribed and over the counter), b. Toxins (smoking and Radiation Treatments) c. Chronic medical Disorders ( Liver and Kidney Disease, Hypothyroidism, GERD, Diabetes,) d. Neurological Disorders( Bell’s Palsy, Stroke, MS,) e. Intubation during an emergency or for general anesthesia. E. Abnormal Smells and Tastes (Dysosmia and Dysgeusia): Diagnosis and Treatment F. Morbidity of Smell and Taste Impairment. G. Treatment of Smell and Taste Impairment (Education, Counseling ,Changes in Food Preparation) H. Role of Smell Testing in the Diagnosis of Neurodegenerative Disorders 1 BACKGROUND Disorders of taste and smell play a very important role in many neurological conditions such as; head trauma, facial and trigeminal nerve impairment, and many neurodegenerative disorders such as Alzheimer’s, Parkinson Disorders, Lewy Body Disease and Frontal Temporal Dementia. Impaired smell and taste impairs quality of life such as loss of food enjoyment, weight loss or weight gain, decreased appetite and safety concerns such as inability to smell smoke, gas, spoiled food and one’s body odor. Dysosmia and Dysgeusia are very unpleasant disorders that often accompany smell and taste impairments. -
Chapter 05- Mental, Behavioral and Neurodevelopmental Disorders
Chapter 5 Mental, Behavioral and Neurodevelopmental disorders (F01-F99) Includes: disorders of psychological development Excludes2: symptoms, signs and abnormal clinical laboratory findings, not elsewhere classified (R00-R99) This chapter contains the following blocks: F01-F09 Mental disorders due to known physiological conditions F10-F19 Mental and behavioral disorders due to psychoactive substance use F20-F29 Schizophrenia, schizotypal, delusional, and other non-mood psychotic disorders F30-F39 Mood [affective] disorders F40-F48 Anxiety, dissociative, stress-related, somatoform and other nonpsychotic mental disorders F50-F59 Behavioral syndromes associated with physiological disturbances and physical factors F60-F69 Disorders of adult personality and behavior F70-F79 Intellectual disabilities F80-F89 Pervasive and specific developmental disorders F90-F98 Behavioral and emotional disorders with onset usually occurring in childhood and adolescence F99 Unspecified mental disorder Mental disorders due to known physiological conditions (F01-F09) Note: This block comprises a range of mental disorders grouped together on the basis of their having in common a demonstrable etiology in cerebral disease, brain injury, or other insult leading to cerebral dysfunction. The dysfunction may be primary, as in diseases, injuries, and insults that affect the brain directly and selectively; or secondary, as in systemic diseases and disorders that attack the brain only as one of the multiple organs or systems of the body that are involved. F01 Vascular dementia -
Musical Anhedonia: a Review
JOURNAL OF PSYCHOPATHOLOGY 2020;26:308-316 Review DOI: 10.36148/2284-0249-389 Musical anhedonia: a review Francesco Bernardini1, Laura Scarponi2, Luigi Attademo3, Philippe Hubain4, Gwenolé Loas4, Orrin Devinsky5 1 SPDC Pordenone, Department of Mental Health, AsFO Friuli Occidentale, Pordenone, Italy; 2 USC Psichiatria 1, Department of Mental Health, ASST Papa Giovanni XXIII, Bergamo, Italy; 3 SPDC Potenza, Department of Mental Health, ASP Basilicata, Potenza, Italy; 4 Erasme Hos- pital, Université Libre de Bruxelles (ULB), Bruxelles, Belgium; 5 NYU Comprehensive Epilepsy Center, Department of Neurology, New York University School of Medicine, New York, USA SUMMARY Objectives Anhedonia, or the inability or the loss of the capacity to experience pleasure, is a core feature of several psychiatric disorders. Different types of anhedonia have been described includ- ing social and physical anhedonia, appetitive or motivational anhedonia, consummatory and anticipatory anhedonia. Musical anhedonia is a rare condition where individuals derive no reward responses from musical experience. Methods We searched the PubMed electronic database for all articles with the search term “musical anhedonia”. Results A final set of 12 articles (six original research articles and six clinical case reports) comprised the set we reviewed. Conclusions Individuals with specific musical anhedonia show normal responses to other types of reward, Received: April 21, 2020 suggesting a specific deficit in musical reward pathways. Those individuals are not necessar- Accepted: June 8, 2020 ily affected by psychiatric conditions, have normal musical perception capacities, and normal recognition of emotions depicted in music. Individual differences in the tendency to derive Correspondence pleasure from music are associated with structural connections from auditory association Francesco Bernardini areas in the superior temporal gyrus to the anterior insula. -
Unit 3 Problems Related to Sex
UNIT 3 PROBLEMS RELATED TO SEX Structure 3.0 Introduction 3.1 Objectives 3.2 Sexuality 3.3 Problems Related to Sex and Sexual Dysfunction 3.3.1 Classification of Sexual Dysfunction 3.3.2 Epidemiology of Sexual Dysfunction 3.3.3 Etiology of Sexual Dysfunction 3.3.4 Common Sexual Problems and Dysfunctions: Clinical Picture 3.3.5 Sexual Dysfunction: Diagnostic Evaluation 3.3.6 Management of Sexual Dysfunction 3.4 Gender Identity Disorders (Gender dysphoria) 3.5 Paraphilias 3.6 Homosexuality 3.7 Let Us Sum Up 3.8 Answers to Self-Assessment Questions 3.9 Unit End Questions 3.10 References 3.11 Suggested Readings 3.0 INTRODUCTION Love and intimacy form the foundation of any relationship. The characteristics of an intimate relationship include an enduring behavioural interdependence, attachment and need fulfillment. Intimate relationships include friendships, dating and marital relationships and spiritual relationships. Intimacy does not necessarily mean sex. Every human interaction offers the possibility of love, “a strong feeling of deep affection”. Love is a total submission of will, the absolute dedication of the entire being to the beloved. Sternberg has described three components of love: intimacy, commitment and passion. Passionate love is marked by a strong sexual longing. ‘Sex’ (as commonly used in English language) refers to male or female based on biological characteristics. However ‘gender’ refers to public lived role as male or female; gender identity refers to the social identity of the individual. Gender identity (usually set before 18 months of age) in a child is irreversibly established before 3 years of age. -
Chapter 16 Lecture Outline A. Gustation
Anatomy Lecture Notes Chapter 16 Chapter 16 Lecture Outline A. gustation - gustatory receptor cells are located in organs called taste buds 1. taste buds located in mucosa of mouth and pharynx most are on the sides of fungiform and circumvallate papillae 2. taste buds made of epithelial cells taste pores are openings in the surface of the epithelium gustatory cells - receptor cells supporting cells - separate gustatory cells from each other basal cells - immature cells that replace the other cells 3. gustatory cells have microvilli on apical surface, just inside taste pore membrane covering microvilli contains receptors for sweet, salty, sour, bitter and umami (glutamate) gustatory cells synapse with sensory neurons at base of taste bud Strong/Fall 2008 page 1 Anatomy Lecture Notes Chapter 16 4. gustatory cells activated when molecules dissolved in saliva bind to membrane receptors on microvilli gustatory cell releases neurotransmitter, which initiates action potential in sensory neuron 5. afferent pathways: VII - facial anterior 2/3 of tongue IX - glossopharyngeal posterior 1/3 of tongue X - vagus epiglottis and pharynx sensory neurons terminate in solitary nucleus in medulla oblongata thalamus gustatory cortex B. olfaction - receptors located in olfactory epithelium 1. olfactory epithelium covers superior nasal conchae and superior nasal septum 2. olfactory epithelium contains olfactory cells bipolar neuron receptors supporting cells columnar e. basal cells form new olfactory cells 3. olfactory cells have apical dendrites that project -
Trkb Expression and Dependence Divides Gustatory Neurons Into Three Subpopulations Jennifer Rios-Pilier and Robin F
Rios-Pilier and Krimm Neural Development (2019) 14:3 https://doi.org/10.1186/s13064-019-0127-z RESEARCHARTICLE Open Access TrkB expression and dependence divides gustatory neurons into three subpopulations Jennifer Rios-Pilier and Robin F. Krimm* Abstract Background: During development, gustatory (taste) neurons likely undergo numerous changes in morphology and expression prior to differentiation into maturity, but little is known this process or the factors that regulate it. Neuron differentiation is likely regulated by a combination of transcription and growth factors. Embryonically, most geniculate neuron development is regulated by the growth factor brain derived neurotrophic factor (BDNF). Postnatally, however, BDNF expression becomes restricted to subpopulations of taste receptor cells with specific functions. We hypothesized that during development, the receptor for BDNF, tropomyosin kinase B receptor (TrkB), may also become developmentally restricted to a subset of taste neurons and could be one factor that is differentially expressed across taste neuron subsets. Methods: We used transgenic mouse models to label both geniculate neurons innervating the oral cavity (Phox2b+), which are primarily taste, from those projecting to the outer ear (auricular neurons) to label TrkB expressing neurons (TrkBGFP). We also compared neuron number, taste bud number, and taste receptor cell types in wild-type animals and conditional TrkB knockouts. Results: Between E15.5-E17.5, TrkB receptor expression becomes restricted to half of the Phox2b + neurons. This TrkB downregulation was specific to oral cavity projecting neurons, since TrkB expression remained constant throughout development in the auricular geniculate neurons (Phox2b-). Conditional TrkB removal from oral sensory neurons (Phox2b+) reduced this population to 92% of control levels, indicating that only 8% of these neurons do not depend on TrkB for survival during development. -
Sex Differences in Symptom Presentation of Schizotypal
Philadelphia College of Osteopathic Medicine DigitalCommons@PCOM PCOM Psychology Dissertations Student Dissertations, Theses and Papers 2009 Sex Differences in Symptom Presentation of Schizotypal Personality Disorder in First-Degree Family Members of Individuals with Schizophrenia Alexandra Duncan-Ramos Philadelphia College of Osteopathic Medicine, [email protected] Follow this and additional works at: http://digitalcommons.pcom.edu/psychology_dissertations Part of the Clinical Psychology Commons Recommended Citation Duncan-Ramos, Alexandra, "Sex Differences in Symptom Presentation of Schizotypal Personality Disorder in First-Degree Family Members of Individuals with Schizophrenia" (2009). PCOM Psychology Dissertations. Paper 40. This Dissertation is brought to you for free and open access by the Student Dissertations, Theses and Papers at DigitalCommons@PCOM. It has been accepted for inclusion in PCOM Psychology Dissertations by an authorized administrator of DigitalCommons@PCOM. For more information, please contact [email protected]. Philadelphia College of Osteopathic Medicine Department of Psychology SEX DIFFERENCES IN SYMPTOM PRESENTATION OF SCHIZOTYPAL PERSONALITY DISORDER IN FIRST-DEGREE FAMILY MEMBERS OF INDIVIDUALS WITH SCHIZOPHRENIA By Alexandra Duncan-Ramos, M.S., M.S. Submitted in Partial Fulfillment of the Requirements of the Degree of Doctor of Psychology July 2009 PHILADELPHIA COLLEGE OF OSTEOPATHIC MEDICINE DEPARTMENT OF PSYCHOLOGY Dissertation Approval This is to certify that the thesis presented to us by Alexandra Duncan-Ramos on the 23rd day of July, 2009 in partial fulfillment of the requirements for the degree of Doctor of Psychology, has been examined and is acceptable in both scholarship and literary quality. Committee Members' Signatures: Barbara Golden, Psy.D., ABPP, Chairperson Brad Rosenfield, Psy.D. Monica E. Calkins, Ph.D. -
Nomina Histologica Veterinaria, First Edition
NOMINA HISTOLOGICA VETERINARIA Submitted by the International Committee on Veterinary Histological Nomenclature (ICVHN) to the World Association of Veterinary Anatomists Published on the website of the World Association of Veterinary Anatomists www.wava-amav.org 2017 CONTENTS Introduction i Principles of term construction in N.H.V. iii Cytologia – Cytology 1 Textus epithelialis – Epithelial tissue 10 Textus connectivus – Connective tissue 13 Sanguis et Lympha – Blood and Lymph 17 Textus muscularis – Muscle tissue 19 Textus nervosus – Nerve tissue 20 Splanchnologia – Viscera 23 Systema digestorium – Digestive system 24 Systema respiratorium – Respiratory system 32 Systema urinarium – Urinary system 35 Organa genitalia masculina – Male genital system 38 Organa genitalia feminina – Female genital system 42 Systema endocrinum – Endocrine system 45 Systema cardiovasculare et lymphaticum [Angiologia] – Cardiovascular and lymphatic system 47 Systema nervosum – Nervous system 52 Receptores sensorii et Organa sensuum – Sensory receptors and Sense organs 58 Integumentum – Integument 64 INTRODUCTION The preparations leading to the publication of the present first edition of the Nomina Histologica Veterinaria has a long history spanning more than 50 years. Under the auspices of the World Association of Veterinary Anatomists (W.A.V.A.), the International Committee on Veterinary Anatomical Nomenclature (I.C.V.A.N.) appointed in Giessen, 1965, a Subcommittee on Histology and Embryology which started a working relation with the Subcommittee on Histology of the former International Anatomical Nomenclature Committee. In Mexico City, 1971, this Subcommittee presented a document entitled Nomina Histologica Veterinaria: A Working Draft as a basis for the continued work of the newly-appointed Subcommittee on Histological Nomenclature. This resulted in the editing of the Nomina Histologica Veterinaria: A Working Draft II (Toulouse, 1974), followed by preparations for publication of a Nomina Histologica Veterinaria. -
Onset of Taste Bud Cell Renewal Starts at Birth and Coincides with a Shift In
RESEARCH ARTICLE Onset of taste bud cell renewal starts at birth and coincides with a shift in SHH function Erin J Golden1,2, Eric D Larson2,3, Lauren A Shechtman1,2, G Devon Trahan4, Dany Gaillard1,2, Timothy J Fellin1,2, Jennifer K Scott1,2, Kenneth L Jones4, Linda A Barlow1,2* 1Department of Cell & Developmental Biology, University of Colorado Anschutz Medical Campus, Aurora, United States; 2The Rocky Mountain Taste and Smell Center, University of Colorado Anschutz Medical Campus, Aurora, United States; 3Department of Otolaryngology, University of Colorado Anschutz Medical Campus, Aurora, United States; 4Department of Pediatrics, Section of Hematology, Oncology, and Bone Marrow Transplant, University of Colorado Anschutz Medical Campus, Aurora, United States Abstract Embryonic taste bud primordia are specified as taste placodes on the tongue surface and differentiate into the first taste receptor cells (TRCs) at birth. Throughout adult life, TRCs are continually regenerated from epithelial progenitors. Sonic hedgehog (SHH) signaling regulates TRC development and renewal, repressing taste fate embryonically, but promoting TRC differentiation in adults. Here, using mouse models, we show TRC renewal initiates at birth and coincides with onset of SHHs pro-taste function. Using transcriptional profiling to explore molecular regulators of renewal, we identified Foxa1 and Foxa2 as potential SHH target genes in lingual progenitors at birth and show that SHH overexpression in vivo alters FoxA1 and FoxA2 expression relevant to taste buds. We further bioinformatically identify genes relevant to cell adhesion and cell *For correspondence: locomotion likely regulated by FOXA1;FOXA2 and show that expression of these candidates is also LINDA.BARLOW@CUANSCHUTZ. altered by forced SHH expression.