Increased hippocampal GABAergic inhibition after long-term high-intensity sound exposure

Abstract

Exposure to loud sounds is related to harmful mental and systemic effects. The hippocampal function can be affected to either high-intensity sound exposure or long-term sound deprivation. We previously showed that hippocampal long-term potentiation (LTP) is inhibited after ten days of daily exposure to 2 minutes of high-intensity noise (110 dB), in the hippocampi of Wistar rats. Here we investigated how the glutamatergic and GABAergic neurotransmission mediated by ionotropic receptors is affected by the same protocol of high-intensity sound exposure. We found that while the glutamatergic transmission both by AMPA/kainate and NMDA receptors in the Schaffer-CA1 synapses is unaffected by long-term exposure to high-intensity sound, the amplitude of the inhibitory GABAergic currents is potentiated, but not the frequency of both spontaneous and miniature currents. We conclude that after prolonged exposure to short periods of high-intensity sound, GABAergic transmission is potentiated in the hippocampal CA1 pyramidal neurons. This effect could be an essential factor for the reduced LTP in the hippocampi of these animals after high-intensity sound exposure. We conclude that prolonged exposure to high- intensity sound could affect hippocampal inhibitory transmission and consequently, its function.

Fig 1. Evoked excitatory AMPA/KA post-synaptic currents (EPSCs) in CA1 pyramidal cells.

A. EPSCs recorded in the presence of Picrotoxin (20 μM) at -80 mV from control and stimulated animals. D. Mean AMPA/KA current amplitudes evoked at -80 mV. C. IV relationships for AMPA/KA currents. C. EPSCs in response to a 20 Hz train of stimuli. D. P1/Pn relationships.

Fig 2. Evoked excitatory NMDA post-synaptic currents (EPSCs) in CA1 pyramidal cells.

A. EPSCs recorded in the presence of picrotoxin (20 μM) and DNQX (10 μM) at +50 mV from control and stimulated animals. B. Mean NMDA current amplitudes evoked at +50 mV. C. IV relationships for DNQX-sensitive NMDA currents.

Fig 3. Spontaneous inhibitory post-synaptic currents (sIPSCs) in CA1 pyramidal cells.

A. sIPSCs recorded in the presence of DNQX (10 μM) at -80 mV, from control and stimulated animals. B. Mean frequency of IPSCs from controls and stimulated animals. Ci. Mean current amplitudes and, Cii, Amplitude histograms of spontaneous currents from control and stimulated animals (error bars were omitted for clarity). D. Mean half-widths of recorded IPSCs from control and stimulated animals. *p<0.05.

Fig 4. Spontaneous miniature inhibitory post-synaptic currents (mIPSCs) in CA1 pyramidal cells.

A. Current traces recorded in the presence of DNQX (10 μM) and TTX (1 μM) at -80 mV, from control and stimulated animals. B. Mean frequency of mIPSCs from controls and stimulated animals. Ci. Mean current amplitudes and Cii, amplitude histograms of spontaneous currents from control and stimulated animals (error bars were omitted for clarity). D. Mean half-widths. E. Mean fast decay time constants. F. Mean slow decay time constants. *p<0.05, ***p<0.001.