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      Nitric oxide contributes to learning and memory deficits observed in hypothyroid rats during neonatal and juvenile growth

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          Abstract

          INTRODUCTION:

          Severe cognitive impairment follows thyroid hormone deficiency during the neonatal period. The role of nitric oxide (NO) in learning and memory has been widely investigated.

          METHODS:

          This study aimed to investigate the effect of hypothyroidism during neonatal and juvenile periods on NO metabolites in the hippocampi of rats and on learning and memory. Animals were divided into two groups and treated for 60 days from the first day of lactation. The control group received regular water, whereas animals in a separate group were given water supplemented with 0.03% methimazole to induce hypothyroidism. Male offspring were selected and tested in the Morris water maze. Samples of blood were collected to measure the metabolites of NO, NO 2, NO 3 and thyroxine. The animals were then sacrificed, and their hippocampi were removed to measure the tissue concentrations of NO 2 and NO 3.

          DISCUSSION:

          Compared to the control group's offspring, serum thyroxine levels in the methimazole group's offspring were significantly lower ( P<0.01). In addition, the swim distance and time latency were significantly higher in the methimazole group ( P<0.001), and the time spent by this group in the target quadrant (Q1) during the probe trial was significantly lower ( P<0.001). There was no significant difference in the plasma levels of NO metabolites between the two groups; however, significantly higher NO metabolite levels in the hippocampi of the methimazole group were observed compared to controls ( P<0.05).

          CONCLUSION:

          These results suggest that the increased NO level in the hippocampus may play a role in the learning and memory deficits observed in childhood hypothyroidism; however, the precise underlying mechanism(s) remains to be elucidated.

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          Oxidative damage in the central nervous system: protection by melatonin.

          Russel Reiter (1998)
          Melatonin was recently reported to be an effective free radical scavenger and antioxidant. Melatonin is believed to scavenge the highly toxic hydroxyl radical, the peroxynitrite anion, and possibly the peroxyl radical. Also, secondarily, it reportedly scavenges the superoxide anion radical and it quenches singlet oxygen. Additionally, it stimulates mRNA levels for superoxide dismutase and the activities of glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase (all of which are antioxidative enzymes), thereby increasing its antioxidative capacity. Also, melatonin, at least at some sites, inhibits nitric oxide synthase, a pro-oxidative enzyme. In both in vivo and in vitro experiments melatonin has been shown to reduce lipid peroxidation and oxidative damage to nuclear DNA. While these effects have been observed primarily using pharmacological doses of melatonin, in a small number of experiments melatonin has been found to be physiologically relevant as an antioxidant as well. The efficacy of melatonin in inhibiting oxidative damage has been tested in a variety of neurological disease models where free radicals have been implicated as being in part causative of the condition. Thus, melatonin has been shown prophylactically to reduce amyloid beta protein toxicity of Alzheimer's disease, to reduce oxidative damage in several models of Parkinson's disease (dopamine auto-oxidation, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine), to protect against glutamate excitotoxicity, to reduce ischemia-reperfusion injury, to lower neural damage due to gamma-aminolevulinic acid (phorphyria), hyperbaric hyperoxia and a variety of neural toxins. Since endogenous melatonin levels fal 1 markedly in advanced age, the implication of these findings is that the loss of this antioxidant may contribute to the incidence or severity of some age-associated neurodegenerative diseases.
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            Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures.

            V Dawson, T. Dawson, E London … (1991)
            Nitric oxide (NO) mediates several biological actions, including relaxation of blood vessels, cytotoxicity of activated macrophages, and formation of cGMP by activation of glutamate receptors in cerebellar slices. Nitric oxide synthase (EC 1.14.23.-) immunoreactivity is colocalized with nicotinamide adenine di-nucleotide phosphate diaphorase in neurons that are uniquely resistant to toxic insults. We show that the nitric oxide synthase inhibitors, N omega-nitro-L-arginine (EC50 = 20 microM) and N omega-monomethyl-L-arginine (EC50 = 170 microM), prevent neurotoxicity elicited by N-methyl-D-aspartate and related excitatory amino acids. This effect is competitively reversed by L-arginine. Depletion of the culture medium of arginine by arginase or arginine-free growth medium completely attenuates N-methyl-D-aspartate toxicity. Sodium nitroprusside, which spontaneously releases NO, produces dose-dependent cell death that parallels cGMP formation. Hemoglobin, which complexes NO, prevents neurotoxic effects of both N-methyl-D-aspartate and sodium nitroprusside. These data establish that NO mediates the neurotoxicity of glutamate.
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              Recent advances in our understanding of neurodegeneration.

              Kurt A Jellinger (2009)
              Neurodegenerative diseases are featured by progressive dysfunction and death of cells in selected areas in the nervous system, determining clinical presentation. Neuronal loss is associated with conformational changes in proteins that result in extra- and intra-cellular accumulation of misfolded proteins, representing the hallmarks of many neurodegenerative disorders, summarized as proteinopathies. Intermediate forms such as oligomers and protofibrils are thought to have cytotoxic effects to neurons. Major basic processes, caused by genetic, environmental, and endogenous factors, in addition to abnormal protein dynamics with defective degradation due to deficiency of the ubiquitin-proteosomal-autophagy system, include oxidative stress and free radical formation, impaired bioenergetics and mitochondrial dysfunction, disruption of neuronal Golgi apparatus and transport, molecular chaperones, neurotrophins and "neuroinflammatory" processes. These mechanisms are interrelated in vicious circles finally leading to programmed cell death. A common feature of these conditions is a long run until sufficient protein accumulates, followed by a cascade of symptoms over many years with increasing disability leading to death. This provides a wide therapeutic window, especially in groups at risk identified early and preclinical diagnosis becomes feasible. Neurodegenerative disorders are classified according to known genetic mechanisms or to the major components of protein deposits. Although this has been a productive paradigm for the development of diagnostic consensus criteria, recent molecular biologic and genetic approaches have revealed that there are both overlap and intraindividual diversities between different phenotypes, related to synergistic mechanisms between major pathologic proteins (beta-amyloid, tau, alpha-synuclein, TDP-43), suggesting common pathogenic mechanisms. The nature, time course, and molecular causes of cell degeneration and demise, and the role of various pathogenic factors are a matter of considerable debate, but recent studies have provided insight into the basic processes in neurodegeneration and the roles of cell death programs common to this complex group of disorders, offering new ways for future prevention and treatment strategies.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clinics (Sao Paulo)
                Title: Clinics
                Publisher: Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
                ISSN (Print): 1807-5932
                ISSN (Electronic): 1980-5322
                Publication date (Print): November 2010
                Volume: 65
                Issue: 11
                Pages: 1175-1181
                Affiliations
                [I ]Neuroscience Research Center, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran.
                [II ]Department of Physiology, School of Medicine, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran.
                [III ]Immunology Research Center, Buali Institute, Mashhad University of Medical Sciences (MUMS), Mashhad, Iran.
                [IV ]Department of Parasitology, Pasteur Institute of Iran, Tehran, Iran.
                Author notes
                E-mail: hosseinim@ 123456MUMS.ac.ir Tel.: 0511-8828564-5
                Article
                Publisher ID: cln_65p1175
                DOI: 10.1590/S1807-59322010001100021
                PMC ID: 2999716
                PubMed ID: 21243293
                SO-VID: 2dadc854-c339-458d-b43b-25cfa8e47202
                Copyright © Copyright © 2010 Hospital das Clínicas da FMUSP
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 May 2010
                Date revision received : 30 May 2010
                Date accepted : 23 August 2010
                Page count
                Pages: 7
                Categories
                Subject: Basic Research

                ScienceOpen disciplines: Medicine
                Keywords: learning,hypothyroidism,offspring,nitric oxide,memory
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: learning, hypothyroidism, offspring, nitric oxide, memory

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