It has been suggested that bidirectional long-term synaptic plasticity may be induced in the brainstem, at medial vestibular nucleus (MVN) synapses, by high frequency vestibular nerve stimulation (HFS, 100Hz) and its association with postsynaptic membrane hyperpolarization, that simulates the inhibitory cerebellum input. However, induction of opposite synaptic changes has been also evidenced by stimulation of vestibular afferents alone, delivered at the same high frequency but with different patterns. In fact, long-term potentiation (LTP) is induced by four 2 s HFS bursts (long-burst stimulation, LBS) with inter-burst interval (IBI) of 5 s, while long-term depression (LTD) by thirty 0.55 s HFS bursts (short-burst stimulation, SBS) with 10 s IBI. To find out the stimulus characteristics that guide the shift from LTP to LTD we analyzed, in rat brainstem slices, the induction of synaptic long-term effects at type B MVN neurons, by applying LBS or SBS with diverse burst number (BN) and IBIs. It results that either LBS and SBS can induce both LTP and LTD, through NMDA receptor activation, and the occurrence of LTP or LTD depends on the IBI, while is BN independent. Thus, LTP is induced by shorter IBIs than LTD. These results demonstrate that the shift LTP-LTD is primary guided by the pause between the HFS bursts, which likely regulates the dynamic of postsynaptic Ca2+ elevation, in relation with its enhancement during the bursts and decay during the IBI. In this view, we can speculate that repetitive vestibular activation, with different ratio between excitatory and inactive periods, might result in different postsynaptic Ca2+ level, which finally leads to either LTP or LTD. On the whole, this study demonstrates that glutamatergic vestibular synapse in the MVN can assure “per se” NMDA-dependent bidirectional plasticity and puts forward a new aspect for understanding the adaptive vestibular phenomena.
The repetition timing of high frequency stimulation bursts drives the bidirectional synaptic plasticity at the central vestibular synapses
SCARDUZIO, MARIANGELA;PANICHI, Roberto;PETTOROSSI, Vito Enrico;GRASSI, Silvarosa
2012
Abstract
It has been suggested that bidirectional long-term synaptic plasticity may be induced in the brainstem, at medial vestibular nucleus (MVN) synapses, by high frequency vestibular nerve stimulation (HFS, 100Hz) and its association with postsynaptic membrane hyperpolarization, that simulates the inhibitory cerebellum input. However, induction of opposite synaptic changes has been also evidenced by stimulation of vestibular afferents alone, delivered at the same high frequency but with different patterns. In fact, long-term potentiation (LTP) is induced by four 2 s HFS bursts (long-burst stimulation, LBS) with inter-burst interval (IBI) of 5 s, while long-term depression (LTD) by thirty 0.55 s HFS bursts (short-burst stimulation, SBS) with 10 s IBI. To find out the stimulus characteristics that guide the shift from LTP to LTD we analyzed, in rat brainstem slices, the induction of synaptic long-term effects at type B MVN neurons, by applying LBS or SBS with diverse burst number (BN) and IBIs. It results that either LBS and SBS can induce both LTP and LTD, through NMDA receptor activation, and the occurrence of LTP or LTD depends on the IBI, while is BN independent. Thus, LTP is induced by shorter IBIs than LTD. These results demonstrate that the shift LTP-LTD is primary guided by the pause between the HFS bursts, which likely regulates the dynamic of postsynaptic Ca2+ elevation, in relation with its enhancement during the bursts and decay during the IBI. In this view, we can speculate that repetitive vestibular activation, with different ratio between excitatory and inactive periods, might result in different postsynaptic Ca2+ level, which finally leads to either LTP or LTD. On the whole, this study demonstrates that glutamatergic vestibular synapse in the MVN can assure “per se” NMDA-dependent bidirectional plasticity and puts forward a new aspect for understanding the adaptive vestibular phenomena.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
