Figure 5. Mechanisms leading to disruption of inhibitory synapse strength and kinetics.
(A) Reduced strength may result from a shift in the inhibitory reversal potential (EIPSC). Distribution and regression analysis of EIPSC of control (circles) and SNHL (squares) neurons recorded in the inferior colliculus. Note that SNHL leads to a 24 mV depolarization in the mean E IPSC (p = 0.0001) [132]. (B) Altered kinetics may result from a disruption of GABAA-receptor subunit composition. SNHL sIPSCs are significantly prolonged as compared with controls (compare before zolpidem traces between control and SNHL; *p < 0.05). An α1 subunit-specific agonist (zolpidem) prolongs sIPSC durations in control, but not in SNHL neurons, suggesting that the kinetic difference is due to failed α1 function following SNHL. Bar graphs show that zolpidem is only effective at prolonging durations for control neurons (mean ± SEM; *p < 0.05) [138]. The number of recorded neurons is shown within each bar.
sIPSC: Spontaneous inhibitory postsynaptic current; SNHL: Sensorineural hearing loss.