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Watch this video to learn about the release of a neurotransmitter. The action potential reaches the end of the axon, called the axon terminal, and a chemical signal is released to tell the target cell to do something—either to initiate a new action potential, or to suppress that activity. In a very short space, the electrical signal of the action potential is changed into the chemical signal of a neurotransmitter and then back to electrical changes in the target cell membrane. What is the importance of voltage-gated calcium channels in the release of neurotransmitters?
| Characteristics of Neurotransmitter Systems | ||||
|---|---|---|---|---|
| System | Cholinergic | Amino acids | Biogenic amines | Neuropeptides |
| Neurotransmitters | Acetylcholine | Glutamate, glycine, GABA | Serotonin (5-HT), dopamine, norepinephrine, (epinephrine) | Met-enkephalin, beta-endorphin, VIP, Substance P, etc. |
| Receptors | Nicotinic and muscarinic receptors | Glu receptors, gly receptors, GABA receptors | 5-HT receptors, D1 and D2 receptors, α-adrenergic and β-adrenergic receptors | Receptors are too numerous to list, but are specific to the peptides. |
| Elimination | Degradation by acetylcholinesterase | Reuptake by neurons or glia | Reuptake by neurons | Degradation by enzymes called peptidases |
| Postsynaptic effect | Nicotinic receptor causes depolarization. Muscarinic receptors can cause both depolarization or hyperpolarization depending on the subtype. | Glu receptors cause depolarization. Gly and GABA receptors cause hyperpolarization. | Depolarization or hyperpolarization depends on the specific receptor. For example, D1 receptors cause depolarization and D2 receptors cause hyperpolarization. | Depolarization or hyperpolarization depends on the specific receptor. |
For proteins to function correctly, they are dependent on their three-dimensional shape. The linear sequence of amino acids folds into a three-dimensional shape that is based on the interactions between and among those amino acids. When the folding is disturbed, and proteins take on a different shape, they stop functioning correctly. But the disease is not necessarily the result of functional loss of these proteins; rather, these altered proteins start to accumulate and may become toxic. For example, in Alzheimer’s, the hallmark of the disease is the accumulation of these amyloid plaques in the cerebral cortex. The term coined to describe this sort of disease is “proteopathy” and it includes other diseases. Creutzfeld-Jacob disease, the human variant of the prion disease known as mad cow disease in the bovine, also involves the accumulation of amyloid plaques, similar to Alzheimer’s. Diseases of other organ systems can fall into this group as well, such as cystic fibrosis or type 2 diabetes. Recognizing the relationship between these diseases has suggested new therapeutic possibilities. Interfering with the accumulation of the proteins, and possibly as early as their original production within the cell, may unlock new ways to alleviate these devastating diseases.
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