FN Thomson Reuters Web of Science™ VR 1.0 PT J AU ROOTBERNSTEIN, RS WESTALL, FC AF ROOTBERNSTEIN, RS WESTALL, FC TI SEROTONIN BINDING-SITES .2. MURAMYL DIPEPTIDE BINDS TO SEROTONIN BINDING-SITES ON MYELIN BASIC-PROTEIN, LHRH, AND MSH-ACTH 4-10 SO BRAIN RESEARCH BULLETIN LA English DT Article DE ADJUVANT; AUTOIMMUNITY; SLEEP FACTORS; NEUROIMMUNOLOGY; AUTISM ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; HORMONE-RELEASING HORMONE; HUMAN-BLOOD PLATELETS; BACTERIAL-CELL WALLS; SLOW-WAVE SLEEP; GUINEA-PIGS; STRUCTURAL REQUIREMENTS; COMPLETE ADJUVANT; BUTANOL EXTRACTS AB Previously, we reported the existence of structurally similar serotonin binding sites on myelin basic protein, LHRH, and MSH-ACTH 4-10. We now report that the adjuvant peptide, muramyl dipeptide (N-acetyl-muramyl-L-Ala-D-isoGln) also binds to these sites. This observation may help to explain previous observations of serotonin-like activity by muramyl peptides, including the promotion of slow-wave sleep and fever induction. The observation may also provide an important link between the immune system and the nervous system that may explain the role of muramyl dipeptide adjuvants in causing autoimmune diseases to serotonin-regulated proteins and their receptors, as well as the alterations in serotonin levels that are often observed in autoimmune diseases. The observation provides concrete evidence for a dual-antigen hypothesis for the induction of autoimmune diseases by an adjuvant-peptide complex. Application of such a mechanism for induction of autoimmunity may be of importance in understanding a number of postinfectious and postvaccinal neuropathies, and suggests a possible etiology for autism, in which many patients have high blood serotonin levels, autoimmune reactions to myelin basic protein, and antibodies to serotonin binding sites. Finally, the observation suggests that glycopeptides may ct as neurotransmitters. C1 CALIF STATE POLYTECH UNIV POMONA,DEPT CHEM,POMONA,CA 91768. RP ROOTBERNSTEIN, RS (reprint author), MICHIGAN STATE UNIV,DEPT PHYSIOL,E LANSING,MI 48824, USA. 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PD DEC PY 1990 VL 13 IS 4 BP 512 EP 514 PG 3 WC Psychology, Developmental SC Psychology GA EK549 UT WOS:A1990EK54900010 ER PT J AU MCCLANNAHAN, LE MCGEE, GG MACDUFF, GS KRANTZ, PJ AF MCCLANNAHAN, LE MCGEE, GG MACDUFF, GS KRANTZ, PJ TI ASSESSING AND IMPROVING CHILD-CARE - A PERSONAL APPEARANCE INDEX FOR CHILDREN WITH AUTISM SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE ASSESSMENT; AUTISTIC CHILDREN; EVALUATION; FEEDBACK; SOCIAL VALIDATION ID NURSING-HOME RESIDENTS; PHYSICAL ATTRACTIVENESS; LIVING ENVIRONMENTS; PROGRAM; DESIGN; STAFF; ORGANIZATION; PERFORMANCE C1 UNIV MASSACHUSETTS,AMHERST,MA 01003. RP MCCLANNAHAN, LE (reprint author), PRINCETON CHILD DEV INST,300 COLD SOIL RD,PRINCETON,NJ 08540, USA. 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Retard. PD DEC PY 1990 VL 28 IS 6 BP 382 EP 383 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA EP809 UT WOS:A1990EP80900010 ER PT J AU SINGH, VK WARREN, RP SINGH, EA AF SINGH, VK WARREN, RP SINGH, EA TI BINDING OF [H-3] SEROTONIN TO LYMPHOCYTES IN PATIENTS WITH NEUROPSYCHIATRIC DISORDERS SO MOLECULAR AND CHEMICAL NEUROPATHOLOGY LA English DT Article ID ALZHEIMERS-DISEASE; SEROTONIN; DEMENTIA; CELLS AB Based on recent studies of neuroimmune networks, the lymphocyte binding of serotonin neurotransmitter was studied in patients with Alzheimer's disease, idiopathic mental retardation, and autism. The specific binding to lymphocytes of [H-3]serotonin, at a single concentration of 100 nM, was significantly reduced in Alzheimer's disease patients as compared to aged controls (group mean of 3.667 +/- 2.301 v 7.506 +/- 1.717 picomoles; p = 0.001), and in children with idiopathic mental retardation as compared to healthy children (group mean of 3.694 +/- 1.627 v 5.792 +/- 1.902 picomoles; p = 0.003). However, autistic children did not differ significantly from the healthy children (group mean of 5.287 +/- 1.987 v 5.792 +/- 1.902 picomoles; p = 0.475). Reduced lymphocyte binding of serotonin may be an indication of breakdown of an unknown neuroimmune pathway relevant to the pathophysiology of Alzheimer's disease and idiopathic mental retardation. C1 UTAH STATE UNIV,DEV CTR HANDICAPPED PERSONS,DIV BIOMED,LOGAN,UT 84322. RP SINGH, VK (reprint author), UTAH STATE UNIV,DEV CTR HANDICAPPED PERSONS,DEPT BIOL,LOGAN,UT 84322, USA. 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Chem. Neuropathol. PD DEC PY 1990 VL 13 IS 3 BP 167 EP 173 PG 7 WC Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FH664 UT WOS:A1990FH66400001 PM 2099781 ER PT J AU SCHECHTER, MD AF SCHECHTER, MD TI FUNCTIONAL CONSEQUENCES OF FENFLURAMINE NEUROTOXICITY SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE FENFLURAMINE; SEROTONIN; STIMULUS PROPERTIES OF DRUGS; DRUG DISCRIMINATION; SUPERSENSITIVITY; RATS ID DISCRIMINATIVE STIMULUS PROPERTIES; BRAIN-SEROTONIN; ANORECTIC DRUG; MECHANISMS; RELEASE; AUTISM AB Male Sprague-Dawley rats were trained to discriminate the anorectic drug d,l-fenfluramine (2.0 mg/kg intraperitoneally administered) from its vehicle using a food-motivated (fixed-ratio 10 schedule) two-lever operant task. Once trained, doses of 0.5, 1.0 and 1.5 mg/kg fenfluramine tested 20 min after IP administration produced dose-responsive discrimination performance. Subsequently, noncontingent twice-a-day administrations of 1 ml/kg saline were made for 4 days and the dose-effect relationship redetermined on the 13th to 15th day after initiation of the chronic saline regimen. Results of these dose-response experiments indicated that there was no significant effect upon fenfluramine discrimination after multiple saline injections or after 10 days without training. Following four days of retraining, 6.25 mg/kg fenfluramine twice-a-day for four days was followed 10 days later by another dose-response determination. This purportedly neurotoxic regimen of fenfluramine significantly increased the rats' ability to discriminate fenfluramine. These results suggest the possibility that chronic release of serotonin or selective damage to serotonin-containing neurons produced by fenfluramine may lead to postsynaptic supersensitivity as manifested by the functionally increased discriminative performance observed. 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PD JAN PY 1990 VL 19 IS 1 BP 52 EP & PG 0 WC Pediatrics SC Pediatrics GA CL740 UT WOS:A1990CL74000006 PM 1689020 ER PT J AU HERMAN, BH AF HERMAN, BH TI A POSSIBLE ROLE OF PROOPIOMELANOCORTIN PEPTIDES IN SELF-INJURIOUS-BEHAVIOR SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE ADRENOCORTICOTROPIN HORMONE; B-ENDORPHIN; CORTISOL; NALTREXONE; OPIOID PEPTIDES; PROOPIOMELANOCORTIN; SELF-INJURIOUS BEHAVIOR ID LESCH-NYHAN SYNDROME; DORSAL ROOT-GANGLIA; BETA-ENDORPHIN; AUTISTIC-CHILDREN; SPINAL-CORD; BLOOD SEROTONIN; IMMUNOREACTIVE DYNORPHIN; CEREBROSPINAL-FLUID; NALOXONE REVERSAL; INFANTILE-AUTISM AB 1. The hypothesis that opioids may be involved in self-injurious behavior is supported by fifteen years of basic animal research suggesting that opioid peptides of the brain and spinal cord participate in the modulation of antinociception in animals, and research of animal models for self-injurious behavior utilizing exogenously administered opiate agonists. 2. Clinical biochemical and pharmacological research conducted over the past five years has also suggested the possibility that opioid peptides may play an important etiological role in the elaboration of self -injurious behavior in some individuals. 3. An opioid overactivity self-injurious hypothesis is supported by results of one study indicating elevated Fraction II opioids (enkephalins) in the lumbar-thecal cerebrospinal fluid of self-injurious children compared to controls, and by the five out of six published studies demonstrating statistically significant decreases in the frequency of self-injurious behavior with the opiate antagonist, naltrexone. 4. A very recent investigation has suggested that some self-injurious individuals show abnormalities in their plasma proopiomelanocortin peptide response to naltrexone, thereby indicating a possible dysfunction in the responsitivity of the proopiomelanocortin system of the hypothalamic - pituitary - adrenal axis of these individuals. 5. These data and results of other investigations have resulted in the elaboration of the original opioid hypothesis to a more comprehensive biochemical model that focuses on this proopiomelanocortin dysregulation. 6. Because of biochemical and functional interrelationships between proopiomelanocortin peptides and certain other neurochemical systems in the brain, it is proposed that pineal melatonin and serotonin may also be involved in this dysregulation. Further basic and clinical research will be needed to test the proposed biochemical model for self-injurious behavior. C1 CHILDRENS HOSP,NATL MED CTR,BRAIN RES CTR,WASHINGTON,DC 20010. CHILDRENS HOSP,NATL MED CTR,DEPT PSYCHIAT & PSYCHOL,WASHINGTON,DC 20010. GEORGE WASHINGTON UNIV,SCH MED,DEPT PSYCHIAT & BEHAV SCI,WASHINGTON,DC 20052. GEORGE WASHINGTON UNIV,SCH MED,DEPT PEDIAT,WASHINGTON,DC 20052. 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PY 1986 VL 31 IS 1-4 BP 111 EP 112 PG 2 WC Neurosciences SC Neurosciences & Neurology GA F5547 UT WOS:A1986F554700193 ER PT J AU MORIHISA, JM FEINSTEIN, C RIES, A GREBB, JA COPOLLA, R WEINBERGER, DR AF MORIHISA, JM FEINSTEIN, C RIES, A GREBB, JA COPOLLA, R WEINBERGER, DR TI A CONTROLLED INVESTIGATION OF THE ELECTROPHYSIOLOGICAL CONCOMITANTS OF CHILDHOOD AUTISM SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 WASHINGTON CHILDRENS NATL MED CTR,NIMH,CLIN NEUROPSYCHIAT & NEUROBEHAV SECT,WASHINGTON,DC. NR 0 TC 0 Z9 0 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0020-7454 J9 INT J NEUROSCI JI Int. J. Neurosci. PY 1986 VL 31 IS 1-4 BP 112 EP 112 PG 1 WC Neurosciences SC Neurosciences & Neurology GA F5547 UT WOS:A1986F554700194 ER PT J AU SANUA, VD AF SANUA, VD TI A TRANS-NATIONAL SURVEY OF MENTAL-HEALTH PROFESSIONALS ON THE ETIOLOGY OF INFANTILE-AUTISM AND CHILDHOOD SCHIZOPHRENIA SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 ST JOHNS UNIV,QUEENS,NY. NR 0 TC 0 Z9 0 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0020-7454 J9 INT J NEUROSCI JI Int. J. Neurosci. PY 1986 VL 31 IS 1-4 BP 115 EP 115 PG 1 WC Neurosciences SC Neurosciences & Neurology GA F5547 UT WOS:A1986F554700198 ER PT J AU SANUA, VD AF SANUA, VD TI THE ORGANIC ETIOLOGY OF INFANTILE-AUTISM - A CRITICAL-REVIEW OF THE LITERATURE SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Review RP SANUA, VD (reprint author), ST JOHNS UNIV,JAMAICA,NY 11439, USA. 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