Long-term potentiation (LTP) of synaptic strength is a long-lasting form of synaptic plasticity that has been linked to information storage. Although the molecular and cellular events underlying LTP are not yet fully understood, it is generally accepted that changes in dendritic spine calcium levels as well as local protein synthesis play a central role. These two processes may be influenced by the presence of a spine apparatus, a distinct neuronal organelle found in a subpopulation of telencephalic spines. Mice lacking spine apparatuses (synaptopodin-deficient mice) show deficits in LTP and impaired spatial learning supporting the involvement of the spine apparatus in synaptic plasticity. In our review, we consider the possible roles of the spine apparatus in LTP1 (protein synthesis-independent), LTP2 (translation-dependent and transcription-independent) and LTP3 (translation- and transcription-dependent) and discuss the effects of the spine apparatus on learning and memory.