Aim: 

17b-Estradiol (E2) can be directly synthesised within the brain where it exerts rapid effects on the neuron excitability and synaptic plasticity, by influencing glutamate NMDA receptors. This study was aimed at investigating the possible influence of E2 on the spontaneous and evoked activity of neurons in the medial vestibular nuclei (MVN).

Methods: 

In rat brainstem slices, we analysed, by extracellular recordings, the effects of E2 (1 nM) on the field potential evoked in the MVN by vestibular afferent stimulation and on the spontaneous neuron firing rate. In addition, by intracellular patch-clamp recordings, we verified the possible influence of E2 on evoked AMPA and NMDA currents and on intrinsic neuron excitability.

Results: 

E2 provoked two opposite long-lasting effects, consisting of potentiation of field potential and depression of neuron firing rate. Both these effects were prevented by the antagonist of estrogen receptors (ERa and ERb), ICI 182,780 (100 nM). In addition, E2 synaptic potentiation was impeded by NMDA receptor block (AP-5). Intracellular recordings under block of AMPA receptors (NBQX) confirmed the E2 enhancement of the evoked NMDA current and showed that the depression of spontaneous firing rate is due to an E2 inhibition of the intrinsic neuron excitability.

Conclusion: 

Our results show that E2 can facilitate the NMDA transmission and inhibit neuron excitability in the MVN, by interacting with ERs. We suggest that E2 may have a role in enhancing the efficacy of vestibular synaptic inputs by increasing the signal/noise ratio.