Axodendritic dark sinuous endings occurred on the day of birth (PO) in the synaptic areas of lamina II. These terminals (TI) turned very electron dense and shrunken after capsaicin administration. From day P2, TI-terminals exhibited fluoride-resistant acid phosphatase (FRAP) reactivity. Such findings revealed their origin from primary afferent fine fibers. Dark scalloped, FRAP-reactive, central terminals of type I glomeruli (CI) were first observed on P5. During the ensuing survival times up to P20 an increasing number of CI-terminals seemed to evolve from the less mature TI-endings that gradually disappeared. A few large clear boutons, similar to the central terminals of type II glomeruli (CII) of the adult which arise from thick afferents, were also present in deep lamina II on the day of birth and became more numerous thereafter. From P5, both CI- and CII-endings developed pre- and postsynaptic contacts with vesicle-containing profiles though it was sometimes difficult to distinguish the axonic (V2) from the dendritic (V1-presynaptic dendritic) profiles. CI-boutons established as many presynaptic as postsynaptic contacts with vesicle-containing profiles. In contrast, CII-terminals were mostly postsynaptic to vesicle-containing profiles. Thus, the boutons generated by thin (CI-boutons) and thick (CII-boutons) primary axons gradually develop synapses with vesicle-containing profiles probably arising from local interneurons. The resulting pre- and/or postsynaptic interactions may contribute to the physiological maturation of somatosensory integration that occurs postnatally.