Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluated the effect of microinjection of the non-N-methyl-D-aspartate (NMDA) receptor antagonist, cyano, 3-dihydro-7-nitrogluinoxaline-2, 3-dione (CNQX), into the arcuate nucleus of the hypothalamus on ventilation in male and female rats. Conscious rats received saline or 50, 100, or 200 pmol concentrations of CNQX on separate days. Significant interactions between dose and gender were observed on frequency, inspiratory (TI) and expiratory (TE) time, and tidal volume. CNQX depressed frequency, but increased tidal volume in female rats. Effects of CNQX in males on these ventilatory parameters were considerably less. In CNQX-treated females the decrease in frequency of breathing was primarily due to an increase in TI. Exposure of CNQX-treated female rats to hypercapnia, but not to hypoxia transiently decreased TI. No effect of CNQX was noted on oxygen consumption or body temperature. Thus, non-NMDA receptors in the arcuate nucleus are involved in modulating ventilatory patterns in a gender-specific manner independent of its effects on oxygen consumption or body temperature.
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PMID:Gender-specific effects of CNQX administered into the arcuate nucleus on ventilatory patterns in rats. 1048 99

Cardioinhibitory cardiac vagal neurons (CVNs) do not receive inspiratory-related excitatory inputs under normal conditions. However, excitatory purinergic and serotonergic pathways are recruited during inspiratory activity after episodes of hypoxia and hypercapnia (H/H). Prenatal nicotine (PNN) exposure is known to dramatically change cardiorespiratory responses and decrease the ability to resuscitate from H/H. This study tested whether PNN exposure alters excitatory neurotransmission to CVNs in the nucleus ambiguus during and after H/H. Spontaneous and inspiratory evoked excitatory postsynaptic currents were recorded in CVNs from rats that were exposed to nicotine (6 mg x kg(-1) x d(-1)) throughout the prenatal period. In contrast to unexposed animals, in PNN animals H/H recruited excitatory neurotransmission to CVNs during inspiratory-related activity that was blocked by the alpha3beta4 nicotinic acetylcholine receptor (nAChR) blocker alpha-conotoxin AuIB (alpha-CTX AuIB, 100 microM) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 50 microM) and d(-)-2-amino-5-phosphonopentanoic acid (AP5, 50 microM), selective AMPA/kainate and N-methyl-d-aspartate receptor blockers, respectively. Following H/H, there was a significant increase in inspiratory-related excitatory postsynaptic currents that were unaltered by alpha-CTX AuIB or ondansetron, a 5-HT3 receptor blocker, but were subsequently inhibited by pyridoxalphosphate-6-azophenyl-2', 4'-disulphonic acid (100 microM), a purinergic receptor blocker and CNQX and AP5. The results from this study demonstrate that with PNN exposure, an excitatory neurotransmission to CVNs is recruited during H/H that is glutamatergic and dependent on activation of alpha3beta4-containing nAChRs. Furthermore, exposure to PNN abolishes a serotonergic long-lasting inspiratory-related excitation of CVNs that is replaced by recruitment of a glutamatergic pathway to CVNs post H/H.
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PMID:Abolishment of serotonergic neurotransmission to cardiac vagal neurons during and after hypoxia and hypercapnia with prenatal nicotine exposure. 1909 27