Ligand-gated and Voltage-gated ion channels
CNS Receptor |
Ionotropic/ Metabotropic |
Transduction Mechanism |
GABA |
Ionotropic |
Open Channels |
Nicotinic |
Ionotropic |
Open Channels |
EAA |
Ionotropic |
Open Channels |
5-HT3 |
Ionotropic |
Open Channels |
Adenyl Cyclase System: - B1+B2 - D1 |
Metabotropic |
Stimulate the production of second-messengers (c-AMP) |
Adenyl Cyclase System: - D2 & A2 - 5-HT1a, 5HT1b - M2 - GABAb
|
Metabotropic |
Supress the formation of second-messengers. |
Phospholipase C system: - A1 - 5-HT2 - M1,H1
|
Metabotropic |
Stimulates the formation of second-messengers (IP3,DAG) |
EPSP (Excitatory Postsynaptic Potential) the activation of an additional AP (action potential) due to depolarization. An example would be when acetylcholine binds to a nicotinic receptor. Sodium channels open up which results in depolarization.
IPSP (Inhibitory Postsynaptic Potential) is the suppression of an additional AP (action potential) due to hyperpolarization. An example would be when gamma-butyric amino acid binds to a GABA receptor. Chloride channels open up which results in hyperpolarization.
Depolarization is caused when an AP (action potential) reaches the axon terminal of a presynaptic neuron. Voltage-gated calcium channels allows for an influx of calcium into the presynaptic membrane. A fusion is caused between the synaptic vesicles and the presynaptic membrane. Synaptic vesicles release neurotransmitters into the synaptic cleft. Neurotransmitters diffuse across the synaptic cleft to bind to the receptors on the postsynaptic membrane in order to elicit an effect. Calcium is essential for the release of neurotransmitters, which then elicits an effect.