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1997). The other principal finding of our study is that acute intermittent hypoxia produced by 10 episodes of isocapnic hypoxia results in enhanced respiratory and sympathetic neural responses to acute hypoxia, whether pLTF occurs or not. Our data show for the first time that the sympathetic hypoxic chemoreflex is augmented following acute intermittent hypoxia (Fig. 6). These findings agree with previous reports that CIH enhanced sympathetic responses to hypoxia in anaesthetized rats (Greenberg et al. 1999a; Braga et al. 2006), and conscious rats (Huang et al. 2009). Data from human studies strongly supported http://www.selleckchem.com/products/AZD0530.html the idea that short-term intermittent exposure to hypoxia can facilitate the reflex response to hypoxia (Cutler et al. 2004; Leuenberger et al. 2007). The enhancement of phrenic amplitude chemoreflex was also observed. Interestingly, with phrenic LTF, the peak phrenic amplitude during hypoxia increased 129% after AIH (from 168 �� 16 to 217 �� 20% of control baseline, P http://en.wikipedia.org/wiki/Diglyceride that AIH has little effect on the central respiratory generator. Our work agrees with previous reports that the reflex response to hypoxia is sensitized in animals after AIH (Fuller, 2005) and CIH (Ling et al. 2001), and in healthy human after AIH (Lusina et http://www.selleckchem.com/products/GDC-0941.html al. 2006). The mechanism underlying the enhanced peripheral chemoreflex responses following intermittent hypoxia is not clear. Two main possibilities should be considered and are likely to represent neural plasticity. First, intermittent hypoxia may lead to altered activity of neurochemical circuits at the level of the brainstem. The caudal NTS (i.e. commissural NTS, SolC) is the central site of termination of afferent neurones whose peripheral axons are found in the carotid body, providing important homeostatic feedback on the (as well as the CO2/pH) status of the arterial blood (Guyenet, 2000; Lahiri et al. 2006). Plasticity in synaptic transmission in SolC could occur on a short- and/or long-term time scale. Mifflin (1997) demonstrated in intact rats that 2 min of 100�C300 Hz stimulation of the carotid sinus, aortic or vagus nerve augmented monosynaptic and polysynaptic EPSPs and action potential discharge. De Paula et al. (2007) also demonstrated that exposure to CIH for 7 days alters the responses of NTS neurones to exogenous application of the inotropic excitatory amino acid agonists AMPA and NMDA.