Synaptic Transmission


Neurons receive information from sensory organs, send information to motor organs, or share information with other neurons. The process of communicating information is very similar, whether it is to another neuron or to a muscle or gland cell. However, by far the largest number of neuronal connections is with other neurons. The rest of this tutorial therefore focuses on inter-neuronal communication. The transmission of information is accomplished in two ways:

With very few exceptions, mammalian organisms use chemical means to transmit information.

Synapse Structure


Electrical transmission occurs by virtue of the fact that the cells are in direct contact with each other: depolarization of the presynaptic cell membrane causes a depolarization of the postsynaptic cell membrane, and the action potential is propagated further. Here transmission of information is always excitatory: the conduction of information always causes a depolarization of the adjacent cell's membrane.

Chemical transmission, albeit more complex allows for far more control, including the ability to excite or inhibit the postsynaptic cell. Here the conduction of information can cause either depolarization or hyperpolarization, depending on the nature of the chemical substance.

The sequence of events that lead to postsynaptic changes is as follows:

  1. The action potential signal arrives at the axon terminal (the bouton).
  2. The local depolarization causes Ca2+ channels to open. (Is this channel voltage, chemically, or mechanically gated? Answer.)
  3. Ca2+ enters the presynaptic cell because its concentration is greater outside the cell than inside.
  4. The Ca2+, by binding with calmodulin, causes vesicles filled with neurotransmitter to migrate towards the presynaptic membrane.
  5. The vesicle merges with the presynaptic membrane.
  6. The presynaptic membrane and vesicle now forms a continuous membrane, so that the neurotransmitter is released into the synaptic cleft. This process is called exocytosis.
  7. The neurotransmitter diffuses through the synaptic cleft and binds with receptor channel membranes that are located in both presynaptic and postsynaptic membranes. (Are these channels voltage, chemically, or mechanically gated? Answer.)
  8. The time period from neurotransmitter release to receptor channel binding is less than a millionth of a second.

The process is depicted in the diagram below:

Direct and Indirect Binding to Postsynaptic Receptor

There are two kinds of receptor channels: direct and indirect

  1. Direct: the receptor channel allows ions to pass through the membrane. The neurotransmitter acts like a key which opens the ion channel. This is the fastest kind of channel (about 0.5 ms). This is called an ionotropic receptor.
  2. Indirect: the binding of neurotransmitter to the receptor channel causes the release of a molecule, called a secondary messenger, that indirectly activates nearby ion channels. This is called a metabotropic receptor.

Postsynaptic Stimulation

Once the postsynaptic ion channel is opened, whether directly or indirectly, the effect can be either excitatory (depolarizing) or inhibitory (hyperpolarizing).


Neurotransmitter Deactivation

If neurotransmitters were continually in the synaptic cleft, the postsynaptic channels would be continually stimulated and the membrane potential would not be able to become stable. There are three ways in which neurotransmitter is deactivated:

  1. Degradation: Enzymes located in the synaptic cleft break down the neurotransmitter into a substance which has no effect on the receptor channel
  2. Reuptake: The neurotransmitter can reenter the presynaptic cell through channels in the membrane.
  3. Autoreceptors: Receptors for a particular neurotransmitter are located on the presynaptic membrane that act like a thermostat. When there is too much neurotransmitter released in the synapse, it decreases the release of further neurotransmitter when the action potential arrives at the presynaptic membrane. It may accomplish this by decreasing the number of Ca2+ channels that open when the next action potential arrives at the presynaptic terminal


A molecule is considered a neurotransmitter if it meets the following criteria:

There are two classes of neurotransmitters:

Most neurons contain both types of vesicles, but in different concentrations.

Small Molecules

Acetylcholine (ACh)


a. Synthesized from tyrosine

1. Dopamine

2. Norepinepherine

3. Epinepherine

b. Synthesized from tryptophan

1. Serotonin (5-HT)

c. Synthesized from histidine


Amino Acids

Glutamate (Glu)

g-Aminobutyric Acid (GABA)

Large Molecules



As neurotransmitters, each one of these molecules undergo a similar life cycle:

  1. Synthesis: Neurotransmitters are synthesized by the enzymatic transformation of precursors. The biosythetic pathway can be immediate (as in GABA from glutamate) or in multiple steps (as in epinepherine from norepinepherine from dopamine, etc.). The synthesis occurs either at the terminal boutons of the axon, or in the soma. In the latter case, it is transported to the axon terminals probably by way of microtubular tracks.
  2. Storage: They are packaged inside synaptic vesicles. These vesicles vary in size, depending on the size of the neurotransmitter.
  3. Release: The neurotransmitters are released from the presynaptic terminal by exocytosis and diffuse across the synaptic cleft to the postsynaptic membrane
  4. Binding: The neurotransmitters bind to receptor proteins imbedded in the postsynaptic cell's membrane. There are two kinds of receptors: ionotropic (direct) and metabotropic (indirect).
  5. Inactivation: The neurotransmitter is degraded either by being broken down enzymatically, or reused by active reuptake in which case the cycle begins again


Drugs can affect any of the stages in the "life-cycle" of a neurotransmitter.

Drugs that bind with receptors on the post-synaptic (and sometimes pre-synaptic) membrane fall into two groups:

The table below lists some common drugs, they action in the brain and their observable behavior:


Action (Brain)



Acetylcholine receptor agonist

Smokers: relaxation, alertness, reduced desire for food.
Non-smokers: Nausea, vomiting, cramps, and diarrhea.


1. Reduces flow of Ca2+ into cells
2. GABA agonist
3. Increases number of binding sites for glutamate
4. Interferes with some secondary messenger systems

Low doses effect is excitatory.
Moderate to high doses effect is inhibitory.

Cocaine and crack

Blocks reuptake of dopamine and norepinepherine

Feelings of well-being and confidence.
Reduced desire for sleep and food.

Opiates (heroin, morphine, codeine)

Endorphin agonist

Pain suppression and euphoria.
Suppresses cough and diarrhea


Serotonin receptor agonist

Visual hallucinations