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Gravity alteration is one of the critical environmental factors in the space, causing various abnormal behaviors related with the malfunctioned vestibular system. Due to the high plastic responses in the central vestibular system, the behavioral failures were resolved in a short period of time (in approx. 72 h). However, the plastic neurotransmission underlying the functional recovery is still elusive. To understand the neurotransmitter-induced plasticity under hypergravity, the extracellular single neuronal recording and the immunohistochemistry were conducted in the vestibular nucleus (VN). The animals were grouped as control, 24-h, 72-h, and 15-day exposing to 4G-hypergravity, and each group had two subgroups based on the origins of neuronal responses, such as canal and otolith. The averaged firing rates in VN showed no significant difference in the subgroups (canal-related:  p  > 0.105, otolith-related:  p  > 0.138). Meanwhile, the number of NMDAr was significantly changed by the exposing duration to hypergravity. The NMDAr decreased in 24 h ( p  = 1.048 × 10 –9 ), and it was retrieved in 72 h and 15 days ( p  < 4.245 × 10 –5 ). Apparently, the reduction and the retrieval in the number of NMDAr were synchronized with the generation and recovery of the abnormal behaviors. Thus, the plasticity to resolve the hypergravity-induced malfunctional behaviors was conducted by regulating the number of NMDAr.

Hypergravity-induced malfunction was moderated by the regulation of NMDA receptors in the vestibular nucleus