抄録
The vestibulo-ocular reflex (VOR) and optokinetic response (OKR) work cooperatively to compensate for the eye position during head movement. The floccular region of the cerebellar cortex regulates the amplitude and timing of these reflexes through the inhibitory synaptic outputs of Purkinje neurons. Both the VOR and OKR undergo adaptive changes, when the retinal slip causing the blur of visual image occurs continuously. Long-term depression (LTD), a type of plasticity at the synapses between parallel fibers and a Purkinje cell, in the flocculus, has been proposed to contribute to the adaptation of VOR and OKR. The progress in the study on cerebellar LTD has revealed numbers of molecules involved in LTD. Glutamate receptor-like molecule δ2 (GluD2) and delphilin are proteins specifically expressed at the postsynaptic membrane of Purkinje neurons and involved in LTD. GluD2 knockout mice show failure of LTD induction and impaired adaptation of VOR and OKR. On the other hand, delphilin knockout mice show facilitation of the LTD induction and the enhanced adaptation of OKR. These results suggest that the cerebellar LTD is involved in the adaptation of reflex eye movements. In addition, a delayed OKR is observed in the GluD2 knockout mice, which seems to be caused by the abnormal Purkinje neuron activities.
