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In a muscle fibre, regulation of synthesis of motor endplate macromolecules changes during ontogenetic development. Immature early postnatal muscles of rat can synthesize the asymmetric forms of acetylcholinesterase (AChE) and the molecules of acetylcholine receptor (AChR) also in the endplate free regions. Synthesis of AChR in the endplate free regions is suppressed by the end of the first week, and synthesis of the asymmetric forms of AChE by the fourth week of postnatal development. After denervation of a mature muscle, synthesis of AChR, but not of the asymmetric forms of AChE, is restored in its endplate free regions. Therefore, we assumed that the muscle must be reinner­vated. Molecular forms of AChE were separat­ed by velocity sedimentation in linear sucrose gra­dients. Temporary denervation was achieved by crush lesion to the sciatic nerve. Disuse of the muscle was produced by immobilisation of hind leg joints, while transitory paralysis was induced by α-bungarotoxin administrating. Activity of the asymmetric AChE forms in the endplate free regions was transiently greatly increased by reinnervation of the slow soleus muscle – the muscle reverted to immature postnatal-like state. Transient paralysis of solens muscle due to AChR blockade, followed by reactivation of the muscle, did not trigger that event. The maintenance of immature state requires permanent innervation. Tonic pattern of motor nerve firing is not crucial for this phenomenon to occur. The fast extensor digitorum longus muscle did not return to imma­ture state after reinnervation. The observed dif­ference between fast and slow muscles is prob­ably based on the intrinsic, i.e. genetic, difference between the two types of muscles.