In situations of arterial pO2 decrease, the peripheral chemoreceptors are stimulated, triggering autonomic, respiratory and behavioral responses in order to regain a normal arterial blood pO2. It is known that the respiratory response to hypoxia represents the integration between the stimulation of the peripheral chemoreceptors and the excitatory effects of hypoxia on sympathetic premotor neurons in the RVLM. Therefore, it is important to understand the changes in the neural mechanisms involved in the control of the autonomic activity to the cardiovascular system during different protocols of hypoxia. These studies will help us understand the effects that exposure to chronic intermittent hypoxia (CIH) has on the activity of these neurons when exposed to a new situation of acute tissue hypoxia, and if the origin of these changes are dependent of the synaptic and/or intrinsic properties of the RVLM neurons. Prior exposure to intermittent hypoxia has been regarded as a pre-conditioning stimulus and allows us to relate possible changes in the neurotransmission characteristics and patterns of neurons in the RVLM as a possible neurophysiological substrate for the sympathetic hyperactivity and respiratory chemoreflex potentiation observed in this model. For this study, we will use the patch-clamp techique associated with the previous identification of pre-sympathic neurons with fluorescent retrograde tracers.
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