Brazilian journal of medical and biological research = Revista brasileira de pesquisas médicas e biológicas
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Braz. J. Med. Biol. Res. · Oct 2004
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 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. ⋯ 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 +/- 0.4 masculine C for MCPG) compared to saline (912 +/- 110 ml kg-1 min-1 and 34.8 +/- 0.2 masculine C, 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.