Although there is a wealth of evidence that synapses in the central nervous system have plasticity, much less is known about its functional role. The observation that the modification of neuronal connection often occurs following brain damage suggests that synaptic plasticity underlies recovery from brain damage.
Studies in invertebrates showed that changes in synaptic transmission is the neuronal mechanism for the behavioral modification in this speceis. The studies using marmmals also indicate that synaptic plasticity is the basis for behavioral modification. In the latter, collateral sprouting may also play an important role.

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A role of inositol phospholipids in the cellular responses for the stimulations by neuromodulators and hormones was found to be very important. Inositol phospholipids are hydrolyzed immediately after the cell stimulation. The hydrolyzed products from phosphatidylinositol 4, 5-bisphosphate (PIP₂), inositoltrisphosphate (IP₃) and diacylglycerol, are thought to be new types of second messengers in the signal transduction systems. In the neurotransmission, however, nerve impulses transmitted synapse very fast (within 1 msec). In such a case a new type of signaling system should be considered.
Gellerally speaking, it is evident that PIP₂ breakdown occurs in preference to other biochemical reactions when cell receptor is stimulated. By the removal of IP₃ from PIP₂, a sort of distortion wave might be produced in the lipid bilayer membrane of nerve cell. Then the level of IP₃ increased gradually (within about 100 msec) accompanying the elevated concentration of intracellular Ca²⁺, which activate various kinds of biochemical reactions successively, including protein phosphorylation, and the metabolic turnover of phosphatidylinositol. Finally, phosphoprotein will be dephosphorylated by phosphatase and the signaling system returned to the initial resting state. These process might occur in the release and reception of neurotransmitter in the synapse.

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