Figure 1.

Astrocytes in the nucleus tractus solitarii (nTS) modulate synaptic and neuronal activity. A: the tripartite synapse is composed of afferent terminals (1), nTS neurons (2+3), and astrocytes (4). Afferent terminals release glutamate, which is buffered by astrocyte excitatory amino acid transporters (EAATs), to activate postsynaptic and presynaptic iGluRs and metabotropic glutamate receptors (mGluRs). B: chronic intermittent hypoxia (CIH, blue) and sustained hypoxia (SH, red) differentially alter astrocytic function. CIH decreases EAAT function to result in reduced presynaptic Ca²⁺ entry, Glu release and tractus solitarii-excitatory postsynaptic current (TS-EPSC) amplitude (1), somal depolarization (2), and elevated spontaneous EPSC (sEPSC) frequency (3). SH increases EAAT expression and function to induce time-dependent changes in TS-EPSC amplitude between 1 and 7 days (1), somal depolarization (2), and increases in sEPSC frequency after 3 days of SH (3). Physiological consequences of CIH and SH shown (inset).