Central release of nitric oxide mediates antinociception induced by aerobic exercise
Nitric oxide (NO) is a soluble gas that participates in important functions of the central nervous system, such as cognitive function, maintenance of synaptic plasticity for the control of sleep, appetite, body temperature, neurosecretion, and antinociception. Furthermore, during exercise large amounts of NO are released that contribute to maintaining body homeostasis. Besides NO production, physical exercise has been shown to induce antinociception. Thus, the present study aimed to investigate the central involvement of NO in exercise-induced antinociception. In both mechanical and thermal nociceptive tests, central [intrathecal (it) and intracerebroventricular (icv)] pretreatment with inhibitors of the NO/cGMP/KATP pathway (L-NOArg, ODQ, and glybenclamide) prevented the antinociceptive effect induced by aerobic exercise (AE). Furthermore, pretreatment (it, icv) with specific NO synthase inhibitors (L-NIO, aminoguanidine, and L-NPA) also prevented this effect. Supporting the hypothesis of the central involvement of NO in exercise-induced antinociception, nitrite levels in the cerebrospinal fluid increased immediately after AE. Therefore, the present study suggests that, during exercise, the NO released centrally induced antinociception.
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Associação Brasileira de Divulgação Científica
2015
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oai:scielo:S0100-879X20150009007902019-03-18Central release of nitric oxide mediates antinociception induced by aerobic exerciseGaldino,G.S.Duarte,I.D.Perez,A.C. Nitric oxide Exercise Pain Antinociception Nitric oxide (NO) is a soluble gas that participates in important functions of the central nervous system, such as cognitive function, maintenance of synaptic plasticity for the control of sleep, appetite, body temperature, neurosecretion, and antinociception. Furthermore, during exercise large amounts of NO are released that contribute to maintaining body homeostasis. Besides NO production, physical exercise has been shown to induce antinociception. Thus, the present study aimed to investigate the central involvement of NO in exercise-induced antinociception. In both mechanical and thermal nociceptive tests, central [intrathecal (it) and intracerebroventricular (icv)] pretreatment with inhibitors of the NO/cGMP/KATP pathway (L-NOArg, ODQ, and glybenclamide) prevented the antinociceptive effect induced by aerobic exercise (AE). Furthermore, pretreatment (it, icv) with specific NO synthase inhibitors (L-NIO, aminoguanidine, and L-NPA) also prevented this effect. Supporting the hypothesis of the central involvement of NO in exercise-induced antinociception, nitrite levels in the cerebrospinal fluid increased immediately after AE. Therefore, the present study suggests that, during exercise, the NO released centrally induced antinociception.info:eu-repo/semantics/openAccessAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research v.48 n.9 20152015-09-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000900790en10.1590/1414-431x20144160 |
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BR |
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English |
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| author |
Galdino,G.S. Duarte,I.D. Perez,A.C. |
| spellingShingle |
Galdino,G.S. Duarte,I.D. Perez,A.C. Central release of nitric oxide mediates antinociception induced by aerobic exercise |
| author_facet |
Galdino,G.S. Duarte,I.D. Perez,A.C. |
| author_sort |
Galdino,G.S. |
| title |
Central release of nitric oxide mediates antinociception induced by aerobic exercise |
| title_short |
Central release of nitric oxide mediates antinociception induced by aerobic exercise |
| title_full |
Central release of nitric oxide mediates antinociception induced by aerobic exercise |
| title_fullStr |
Central release of nitric oxide mediates antinociception induced by aerobic exercise |
| title_full_unstemmed |
Central release of nitric oxide mediates antinociception induced by aerobic exercise |
| title_sort |
central release of nitric oxide mediates antinociception induced by aerobic exercise |
| description |
Nitric oxide (NO) is a soluble gas that participates in important functions of the central nervous system, such as cognitive function, maintenance of synaptic plasticity for the control of sleep, appetite, body temperature, neurosecretion, and antinociception. Furthermore, during exercise large amounts of NO are released that contribute to maintaining body homeostasis. Besides NO production, physical exercise has been shown to induce antinociception. Thus, the present study aimed to investigate the central involvement of NO in exercise-induced antinociception. In both mechanical and thermal nociceptive tests, central [intrathecal (it) and intracerebroventricular (icv)] pretreatment with inhibitors of the NO/cGMP/KATP pathway (L-NOArg, ODQ, and glybenclamide) prevented the antinociceptive effect induced by aerobic exercise (AE). Furthermore, pretreatment (it, icv) with specific NO synthase inhibitors (L-NIO, aminoguanidine, and L-NPA) also prevented this effect. Supporting the hypothesis of the central involvement of NO in exercise-induced antinociception, nitrite levels in the cerebrospinal fluid increased immediately after AE. Therefore, the present study suggests that, during exercise, the NO released centrally induced antinociception. |
| publisher |
Associação Brasileira de Divulgação Científica |
| publishDate |
2015 |
| url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2015000900790 |
| work_keys_str_mv |
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