Adaptive depression in synaptic transmission in the nucleus of the solitary tract after in vivo chronic intermittent hypoxia: evidence for homeostatic plasticity.

The respiratory system is highly pliable in its adaptation to low-oxygen (hypoxic) environments. After chronic intermittent hypoxia (CIH), alterations in the regulation of cardiorespiratory system become persistent because of changes in the peripheral chemoreceptor reflex. We present evidence for the induction of a novel form of homeostatic plasticity in this reflex pathway in the nucleus tractus solitarius (NTS), the site of termination of the chemosensory afferent fibers. CIH induces an increase in NTS postsynaptic cell activity initiated by spontaneous presynaptic transmitter release that is counterbalanced by a reduction in evoked synaptic transmission between sensory afferents and NTS second-order cells. This is accomplished via presynaptic mechanisms involving changes in neurotransmitter release and calcium/calmodulin-dependent kinase II activation.