“…It is shown that depressor post-stimulus manifestations in the form TD and PTD mediate GABA or glycine monoamines. Us shows the protective purpose of GABA in studies of nonspecific neurodegeneration, especially in the Deiters' nucleus (following unilateral labyrinthectomy) [51], in the spinal cord after lateral hemisection [53][54][55][56] on peripheral nerve injury [57][58][59][60][61], on amyloid model of AD [50,62,63] and also on the rotenone model of PD [64,65]; in neurons mainly the GABAergic nature, in which early involving depressor reactions are accompanied by the recovery process until its completion. Confirmation the assumption of the universal protective assignment of GABA-ergic inhibition is the fact that in some systems during development of the nervous system GABA promotes proliferation, migration, differentiation and maturation of the synapse, expression of the GABA(A) receptor [66].…”