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Rapid and slow effects of corticosterone on glutamatergic transmission in NTS

Rapid, non‐genomic and slower effects of CS on AMPA‐receptor– mediated transmission in NTS neurons were examined in rats using whole‐cell recordings of second‐order NTS neurons receiving arterial chemoreceptor afferent inputs in a brain slice. Measured at least 1 h after 20 min superfusion of the slice with 100 nM CS, CS increased miniature postsynaptic excitatory current (mEPSC) amplitude (control 15.6±1.1pA, n=12, CS 21.2±1.7pA, n=10, p<0.01) but not interval (control 0.77±0.13s, n=12, CS 0.99±0.08s, n=10, p>;0.05). During the 20min superfusion of the slice with 100nM CS, mEPSC amplitude measured during the control period prior to application of CS (15.6±1.1pA, n=5) was not different from that measured during the 4min to 9min following the onset of the CS superfusion (16.4±1.3pA, n=5) or 14min to 19min after the onset of the CS superfusion (16.48±0.83pA, n=5). There were no differences in mEPSC frequency during these time periods. PKC inhibitors chelerythrine choride 1uM or calphostin C 100nM applied 10 min before and during 20 min superfusion with 100 nM CS did not alter delayed CS‐induced increases in mEPSC amplitude. CS does not appear to have a rapid (<20 min) effect on glutamatergic transmission in NTS neurons receiving arterial chemoreceptor afferent inputs; however a 20 min application of CS increased mEPSC amplitude measured at least 1 hr later apparently not mediated by PKC systems. Supported by HL‐088052