Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia
The interaction between pulmonary ventilation (V E) and body temperature (Tb) is essential for O2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interac...
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| Format: | Article |
| Language: | English |
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Associação Brasileira de Divulgação Científica
2004-01-01
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| Series: | Brazilian Journal of Medical and Biological Research |
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| Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000019 |
| _version_ | 1819153545246539776 |
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| author | Paula P.M. de Branco L.G.S. |
| author_facet | Paula P.M. de Branco L.G.S. |
| author_sort | Paula P.M. de |
| collection | DOAJ |
| description | The interaction between pulmonary ventilation (V E) and body temperature (Tb) is essential for O2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interaction are not well known. Since L-glutamate is released centrally in response to peripheral chemoreceptor stimulation and glutamatergic receptors are spread in the central nervous system we tested the hypothesis that central L-glutamate mediates the ventilatory and thermal responses to hypoxia. We measured V E and Tb in 40 adult male Wistar rats (270 to 300 g) before and after intracerebroventricular injection of kynurenic acid (KYN, an ionotropic glutamatergic receptor antagonist), alpha-methyl-4-carboxyphenylglycine (MCPG, a metabotropic glutamatergic receptor antagonist) or vehicle (saline), followed by a 1-h period of hypoxia (7% inspired O2) or normoxia (humidified room air). Under normoxia, KYN (N = 5) or MCPG (N = 8) treatment did not affect V E or Tb compared to saline (N = 6). KYN and MCPG injection caused a decrease in hypoxia-induced hyperventilation (595 ± 49 for KYN, N = 7 and 525 ± 84 ml kg-1 min-1 for MCPG, N = 6; P < 0.05) but did not affect anapyrexia (35.3 ± 0.2 for KYN and 34.7 ± 0.4ºC for MCPG) compared to saline (912 ± 110 ml kg-1 min-1 and 34.8 ± 0.2ºC, N = 8). We conclude that glutamatergic receptors are involved in hypoxic hyperventilation but do not affect anapyrexia, indicating that L-glutamate is not a common mediator of this interaction. |
| first_indexed | 2024-12-22T15:06:53Z |
| format | Article |
| id | doaj.art-2b665c5d262c4fb28a9cf7d1f023f6af |
| institution | Directory Open Access Journal |
| issn | 0100-879X 0034-7310 |
| language | English |
| last_indexed | 2024-12-22T15:06:53Z |
| publishDate | 2004-01-01 |
| publisher | Associação Brasileira de Divulgação Científica |
| record_format | Article |
| series | Brazilian Journal of Medical and Biological Research |
| spelling | doaj.art-2b665c5d262c4fb28a9cf7d1f023f6af2022-12-21T18:21:57ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X0034-73102004-01-01371015811589Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexiaPaula P.M. deBranco L.G.S.The interaction between pulmonary ventilation (V E) and body temperature (Tb) is essential for O2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interaction are not well known. Since L-glutamate is released centrally in response to peripheral chemoreceptor stimulation and glutamatergic receptors are spread in the central nervous system we tested the hypothesis that central L-glutamate mediates the ventilatory and thermal responses to hypoxia. We measured V E and Tb in 40 adult male Wistar rats (270 to 300 g) before and after intracerebroventricular injection of kynurenic acid (KYN, an ionotropic glutamatergic receptor antagonist), alpha-methyl-4-carboxyphenylglycine (MCPG, a metabotropic glutamatergic receptor antagonist) or vehicle (saline), followed by a 1-h period of hypoxia (7% inspired O2) or normoxia (humidified room air). Under normoxia, KYN (N = 5) or MCPG (N = 8) treatment did not affect V E or Tb compared to saline (N = 6). KYN and MCPG injection caused a decrease in hypoxia-induced hyperventilation (595 ± 49 for KYN, N = 7 and 525 ± 84 ml kg-1 min-1 for MCPG, N = 6; P < 0.05) but did not affect anapyrexia (35.3 ± 0.2 for KYN and 34.7 ± 0.4ºC for MCPG) compared to saline (912 ± 110 ml kg-1 min-1 and 34.8 ± 0.2ºC, N = 8). We conclude that glutamatergic receptors are involved in hypoxic hyperventilation but do not affect anapyrexia, indicating that L-glutamate is not a common mediator of this interaction.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000019Kynurenic acid-->alpha-Methyl-4-carboxyphenyl-glycine (MCPG)HypoxiaVentilationBody temperature |
| spellingShingle | Paula P.M. de Branco L.G.S. Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia Brazilian Journal of Medical and Biological Research Kynurenic acid -->alpha-Methyl-4-carboxyphenyl-glycine (MCPG) Hypoxia Ventilation Body temperature |
| title | Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia |
| title_full | Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia |
| title_fullStr | Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia |
| title_full_unstemmed | Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia |
| title_short | Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia |
| title_sort | glutamatergic neurotransmission modulates hypoxia induced hyperventilation but not anapyrexia |
| topic | Kynurenic acid -->alpha-Methyl-4-carboxyphenyl-glycine (MCPG) Hypoxia Ventilation Body temperature |
| url | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2004001000019 |
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