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Corticosterone (CS) modulation of miniature excitatory postsynaptic currents is altered following exposure to CIH

CS is released after stress and can bind to intracellular receptors in the brain, which in activated form function as transcription factors. We tested the effect of CS on AMPA‐receptor–mediated transmission in NTS neurons from normoxic rats and in rats exposed to CIH ( 9% oxygen for 3min every 10 min, 8 h per day for 7 days). Whole‐cell recordings of second‐order NTS neurons receiving arterial chemoreceptor afferent inputs, labeled with DiA on the carotid body, were obtained in a brain slice. To focus on delayed, gene‐mediated effects of the hormone miniature postsynaptic excitatory currents (mEPSCs) were measured at least 1 h after 20min superfusion of the slice with 100 nM CS. In normoxic rats, CS increased the amplitude (control 16.8±1.0pA, n=10, CS 22.1±1.3pA, n=12, p<0.01) but not the interval (control 0.92±0.15s, n=11, CS 0.77±0.09s, n=11, p>0.05) of mEPSCs. CS had a much different effect in rats exposed to CIH. CS did not increase the amplitude of mEPSCs in the CIH exposed rats from 19.1±1.9pA to 20.1±1.7pA (n=10, p>0.05). Following exposure to CIH, CS reduced mEPSC interval from 1.6±0.4s to 0.75±0.1s (n=10, p<0.05). The present results show that in normoxic rats CS induces a delayed post‐synaptic enhancement of AMPA‐receptor–mediated responses. In rats exposed to CIH, CS does not induce any further post‐synaptic increase in AMPA current but rather increases the probability of glutamate release.