1. Ligand-gated channels and Voltage-gated channels (Brand 2021).

2. Voltage-gated channels respond to membrane potential-changes of cells to open the channel(s). But a ligand-gated channel opens directly by the binding of the neurotransmitter to the ionotropic receptor (Katzung, 2018:369). An all-or-nothing fast action potential is initiated for the voltage-gated channel to elicit an effect (Katzung, 2018:369). But the binding of a neurotransmitter gives an effect at a ligand-gated channel and does not need to have a certain number of receptors activated to elicit an effect. Some voltage-sensitive potassium and calcium channels act slower, thus altering the discharge-rate of the neuron. Although the ligand-gated synaptic transmission happens fast (Katzung, 2018:369-370).

Comparison
Ionotropic receptors	Metabotropic receptors
The binding of a neurotransmitter to a ionotropic receptor causes an action by directly opening the ion channel (Katzung, 2018:370).	A metabotropic receptor is a transmembrane G protein-coupled receptor which stimulates the production of second messengers that then mediate intracellular signaling cascades (Katzung, 2018:370).
The effect of the neurotransmitter binding to a receptor is a fast opening of the ion channel. Thus this is a quick action taking place (Katzung, 2018:370).	Effect lasts longer than the effect of an ionotropic receptor activation. Because the stimulation of the Metabotropic-receptor and thus the action caused by the activation, is slow because the end effect does not directly take place (Brand, 2021).
Effect: Ion channels are opened (Brand, 2021).	Effect: Metabolic changes take place (Brand, 2021).

Ionotropic receptors		Metabotropic receptors
Nicotinic receptor	Sodium channels are opened due to depolarization thus EPSP (Excitatory Postsynaptic Potential).	Β1	Adenylyl cyclase system (Receptor is positive-coupled)
5-HT3 receptor	Sodium channels are opened due to depolarization thus EPSP.	Β2	Adenylyl cyclase system (Receptor is positive-coupled)
GABAA receptor	Chloride channels are opened due to hyperpolarization thus IPSP (Inhibitory Postsynaptic Potential).	D1	Adenylyl cyclase system (Receptor is positive-coupled)
"Eksitatoriese" Amino Acid receptor	Sodium and calcium channels are opened due to depolarization thus EPSP.	D2	Adenylyl cyclase system (Receptor is negative-coupled)
		5-HT1A and 5-HT1B	Adenylyl cyclase system (Receptor is negative-coupled)
		5-HT2	Phospholipase C system
		Alfa1	Phospholipase C system
		Alfa2	Adenylyl cyclase system (Receptor is negative-coupled)
		M1	Phospholipase C system
		M2	Adenylyl cyclase system (Receptor is negative-coupled)
		H1	Phospholipase C system (Brand, 2021)

5. EPSP (Excitatory postsynaptic potential): The product of an excitatory pathway, which is also a small depolarization. This results from the binding of an excitatory transmitter to an ionotropic receptor, which then increase the permeability of the channel to cations (Katzung, 2018:371). For example: Acetyl choline binding to a Nicotinic receptor causes depolarization and hence increases the permeability of the channel to sodium (Brand, 2021).

Versus:

IPSP (Inhibitory postsynaptic potential): A selective opening of chloride-channels due to hyperpolarization in response to a stimulation in the inhibitory pathway (Katzung, 2018:371). For example:  Binding of y-amino butyric acid to the GABA_A receptor opens a chloride channel due to hyperpolarization (Brand, 2021).

6. Calcium release is due to the propagation of an action potential down the axon of a presynaptic neuron which then activates voltage sensitive calcium channels in the synaptic terminal. Calcium thus flows into the synaptic terminal which are now responsible for the fusion of synaptic vesicles with the post-synaptic membrane due to an increase in intra-terminal calcium concentration. Ultimately this results in the release of the neurotransmitter out of the vesicle and into the synaptic cleft. Channels on the post-synaptic membrane can now be opened by the binding of neurotransmitters to post-synaptic receptors.  The opening of the post-synaptic ion channels causes a brief membrane permeability change to the ions. Thus a synaptic potential is formed. This means that calcium is responsible for the fusion of vesicles with the pre-synaptic membrane and thus the release of neurotransmitters in the synaptic cleft (Katzung, 2018:371).

Reference list

Brand, L. 2021. Introduction. Study unit 1 [pdf]. Unpublished lecture notes on eFundi, FKLG 312. Potchefstroom: NWU.

Katzung, B.G. 2018. Basic & Clinical Pharmacology. 14th ed. International: McGraw-Hill Education. p. 369-371.