On the other hand, even though uEPSCs and aEPSCs are produced by GSK2118436 glutamates from different release sites, a single and narrow peak in the distribution of their amplitudes indicates that the release patterns from both of them are quantal in nature. Although our studies did not indicate a variable quantal release of glutamates at the unitary synapses, we made a case to test the influence of variable quantal release on neuronal spike encoding. The timing precision of spike encoding is worse when driven by the currents integrated from variable quantal release, compared with those from quantal release. If the time precision of neuronal encoding underlies the fidelity of brain codes for wellorganized behaviors and memory storage, the variable release quanta and subsequent non-precise neuronal encoding may be related to the functional and psychological disorders in the brain. As the release quanta are controlled by the amount of transmitters in synaptic vesicles and the patterns of their release, the uneven glutamates in synaptic vesicles and the conversion of a release pattern into two states will lead to non-precise encodings in neuronal network and functional disorders in the brain. GABAergic neurons receive glutamatergic synapses that release transmitters from vesicles in constant quanta, and influence the activities of their postsynaptic neurons via the feedback and feedforward ways. The constant glutamates released from the synapses onto GABAergic neurons drives their spike encoding precisely. The precise encoding of GABAergic neurons facilitates reliable spike encoding at their postsynaptic pyramidal neurons. Thus, GABAergic neurons located around excitatory neurons maintain the latter to precisely encode action potentials, in addition to inhibiting postsynaptic neurons and elevating their sensitivity to the inputs. Pyramidal neurons while releasing constant glutamates from synaptic vesicles onto their targets have set up the reliable encoding themselves, a self set-point in homeostasis. The precise encoding of action potentials may circulate among circuitry neurons in the brain. If this chain homeostasis is broken, non-precise encodings in brain networks lead to functional disorders. Glutamatergic synapses in constant quanta drive neuronal encoding more precisely and reliably. If precise neuronal encodings are essential to control well-organized behaviors, it is important to maintain synaptic quantal release, i.e., even glutamates are packed in synaptic vesicles and released from vesicles in a fixed pattern. Glutamate quantity in presynaptic vesicles is influenced by the functions of vesicle glutamate transports and the gradient of glutamates between inside and outside of vesicles. Both processes are ATP-dependent, i.e., rely on cellular metabolisms. Therefore, metabolic disorders lead to non-quantal release from synaptic vesicles and subsequent instability in neuronal encoding. On the other hand, the glutamate release patterns may be regulated in a conversion between kiss-and-run and full-fusion. It remains to be tested how the conversion of release patterns is regulated by presynaptic signals. The patterns of synaptic transmission are regulated by quantal sizes, release probability and release sites.