AbstractChanges in the normal synaptogenetic pattern of the interpeduncular nucleus (IPN) were induced by destruction of one or both habenular nuclei in neonatal rats. The S synapses, the principal habenulointerpeduncular (H‐IPN) afferents, were reduced in number and delayed in time of appearance by unilateral lesions. They were eliminated by bilateral lesions. The crest synapses, also of habenular origin, appeared at ten days of age and were apparently normal in structure after unilateral lesions. However, this actually represented a change in connectivity, since normal crest synapses are of bilateral origin. Following bilateral habenular lesions abnormal crest synapses appeared at 28 days of age. These had normal postsynaptic structure, but presynaptically were formed by non‐habenular axons, usually of two different types at each crest synapse. Lesions induced an early appearance of F synapses, at three days, instead of the normal time after six days of age. Apparently similar processes containing flattened vesicles formed somatic contacts only in lesioned animals beginning at 21 days of age. The axosomatic synapses which were only occasional appeared in the adult appeared at the normal time in lesioned animals. At 28 days of age in both unilaterally and bilaterally lesioned animals these was an increase in number of somatic synapses. This increase was due to an increase of the normal somatic endings plus the appearance of somatic synapses containing flattened vesicles. Both types of somatic contacts were found in similar numbers at subsequent ages up to three months.The changes in S synapses represent Wallerian degeneration. The formation of unilaterally derived crest synapses in unilaterally lesioned animals is interpreted as evidence for a specific recognition mechanism. A postsynaptic control mechanism is proposed to explain the formation of heterologous crest synapses, with the usual distinctive geometry but involving abnormal, non‐habenular presynaptic elements four weeks following neonatal bilateral lesions. The increase in axosomatic synapses is unusual since the dendrites of IPN neurons were deafferented, not their somata. The factors leading to the changes in somatic synapses are discussed. The findings reveal new examples of the complexity of neuronal adaptation to CNS lesions in early life.