The cell communicates through the action potential (AP). Prerequisite to develop an action potential are ion channels, a lipid bilayer and a potential across the membrane. Action potentials are generated by voltage-gated ion channels embedded in the membrane. These channels are shut when the membrane potential is near the membrane potential of the cell, but they rapidly begin to open if the membrane potential increases to a precisely defined threshold value. The shift in membrane polarity leads aging to inactivity in the ion channels. This is the start of the repolarization phase, ending with the cell again assuming its steady-state condition. The AP propagates along the neuron’s axon toward its ends and thereby connects with other neuronal synapses, motor cells or glands.

As the AP reached the axonal end, the electrical potential is transformed into chemical signals. This happens in the synapse. The AP leads to release of neurotransmitters, which are stored in presynaptic vesicles, into the synaptic cleft. Then the neurotransmitters diffuse to the postsynaptic membrane (on the dendrite), bind to a receptor, and induce a signal that can be excited or inhibited. In other words, synaptic inputs to a neuron cause the membrane to depolarize or hyperpolarize.

A chemical synaptic transmission provides flexibility and provides the opportunity to a wide range of chemical transmitters and receptors in a single synapse.

Formation of the synapses and the plasticity of the synapses changes over time and during the normal aging. Biochemical changes seem to play an important role in the aging brain. Alteration in syntheses and turnover of neurotransmitters has been observed. The reduction of dopamine synthesis and dopamine receptors has been linked to motility disturbance and change in cognitive flexibility. Alterations in calcium regulation, glutamate, and serotonin are also described. Calcium plays an important role in neuronal firing and propagation of AP. Glutamate is an excitatory neurotransmitter, and it is a documented age-related decrease, especially in the parietal gray matter and basal ganglia. Interconnections of neuronal network are involved in human cognition and mental life and are thought to represent a cognitive reserve. The neuronal degeneration is part of the normal aging process.

Through learning we can build, strengthen, or remodel the circuits. This leads to structural and biochemical changes, as a response to increase or decrease in their activity, with the development of new synapses and up- and downregulations of neurotransmitters, receptors, and ion channels.

Synapses are capable of forming memory traces by means of long-lasting increase in signal transmission between two neurons—a change in synaptic strength. One of the most interesting and studied forms of neural memory is the long-term potentiation, which was first described back in 1973, but is still not fully understood. The phenomenon is characterized by the fact that the neurotransmitter glutamate acts on a special type of receptor known as the NMDA receptor. The NMDA receptor has an “associative” property: if the two cells involved in the synapse are both activated at approximately the same time, a channel opens that permits calcium to flow into the target cell. A second messenger induces a cascade that ultimately leads to an increase in the number of glutamate receptors on the target cell, thereby increasing the effective strength of the synapse. This change in strength can last for weeks.