The opening and closing of a ligand-gated ion channel depend on the binding of a "ligand", which refers to a small molecule that may bind to ion channels.
If their binding results in the opening of the channel, the ligand is called "agonist". Neurotransmitters are endogenous agonists.
If their binding renders the channel unresponsive to its endogenous agonist, the ligand is called "antagonist" or "blocker". Three commonly observed ligand-gated ion channels
are illustrated below.
Figure 3-4. nAChR. Its endogenous agonist is acetylcholine (ACh), it can also be opened by a component in cigarette, nicotine.
That is how nAChR got its name. The channel is permeable to sodium and potassium ions when it is open, but the sodium influx is greater than the potassium outflux.
Hence the net result is an inward positive ionic current, causing depolarization. [Source: Wikipedia]
Figure 3-5. GABAA receptor. The opening of this channel leads to the influx of chloride ions (Cl-)
resulting in decrease of membrane potential. Thus the opening of GABAA receptor has inhibitory effect on neuronal firing. The commonly used sleeping pill,
benzodiazepine, can enhance the efficacy of its endogenous agonist, GABA. [Source: Möhler, 2002]
Figure 3-6. NMDA receptor. The opening of this channel causes sodium and calcium ions to flow inward, resulting in depolarization.
The NMDA receptor is a unique ligand-gated ion channel. Its intrinsic gate is regulated by the neurotransmitter glutamate.
On the other hand, the channel pore could be blocked by magnesium (Mg2+) ions from the extracellular side. Hence, the NMDA receptor is regulated not only
by glutamate, but also the extracellular Mg2+ concentration and membrane potential. The depolarizing electric field (outward) may repel Mg2+ out of the pore.
This unique property enables the NMDA receptor to play a key role in learning and memory (see this article).
[Source: Longone et al, 2011.]