A neuron is composed of three parts: cell body (soma), one or more dendrites, and a single axon. The cell body is similar to other types of cells, containing a nucleus and other typical organelles. The dendrites project from the cell body to receive signals from other neurons. The axon extends from the cell body to transmit the signals to other neurons through synapses. A synapse is a junction between an axon terminal and a dendrite, typically at spine (a small membranous protrusion from the dendrite). An axon may have one or more terminals and a dendrite may contain many spines. Thus, a single neuron can receive inputs from many neurons and transmit to many neurons.

Figure 4.1. The mechanism of synaptic transmission. "T" represents the neurotransmitters which are stored in vesicles (represented by circles) at the presynaptic axon terminal. The action potential at the presynaptic terminal causes the entry of Ca²⁺ ions through voltage-activated calcium channels, leading to the release of neurotransmitters.

At the axon terminal, neurotransmitters are stored in vesicles. When the nerve impulse arrives, membrane depolarization will open calcium channels for the entry of Ca²⁺ ions, which then induce the release of neurotransmitters stored in the vesicles. The neurotransmitters then diffuse through the synaptic cleft (about 200 - 500 Å wide) to act on their receptors in the dendrite of a postsynaptic neuron.

Figure 4.2. Chemical structures of major neurotransmitters.

The receptors for neurotransmitters can be classified into two categories: G-protein-coupled receptors and ionotropic receptors. G-protein-coupled receptors are involved in signal transduction. Like other agonists, binding of neurotransmitters on G-protein-coupled receptors may trigger a series of signaling processes (more info). The ionotropic receptors form an ion channel which may be activated upon binding of specific neurotransmitters. Upon activation, some synaptic channels (e.g., acetylcholine and glutamate receptor channels) cause the postsynaptic membrane to depolarize while others (e.g., GABA and glycine receptor channels) cause hyperpolarization.

In the postsynaptic neuron, the membrane potential change at spines will propagate along the membrane to other regions, with possibility of being attenuated. Since a neuron contains many spines and each spine may cause membrane potential change, the membrane potential at any region is determined by the summation of these membrane potential changes when they reach the region. If the membrane is depolarized to a value above the threshold, the action potential will be generated at the region. If an action potential is generated at the "axon hillock" (the region connecting the cell body to the axon), it will be able to travel along the axon to the terminals.

Hyperpolarization has a negative effect on the generation of action potentials. For this reason, the depolarization potential at spines is often called "excitatory postsynaptic potential" (EPSP) and the hyperpolarization potential is called "inhibitory postsynaptic potential" (IPSP).

The glutamate receptor (GluR) channel plays a critical role in the Hebbian type of learning. It may be divided into three subtypes: NMDA, kainate and AMPA. All glutamate receptors bind efficiently to the glutamate molecule, but their binding affinity for other agonists varies. The NMDA subtype has a high binding affinity for the NMDA molecule, but low affinity for the kainate or AMPA molecule. Therefore, a channel formed by NMDA receptors can be activated by NMDA or glutamate, but not by kainate or AMPA. Similarly, the channel formed by AMPA receptors can be activated by AMPA or glutamate, but not by NMDA or kainate.