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Adding a synaptic connection - Neuronbank Help neuronbank.org | Synaptic Proteins & Receptors - R&D Systems rndsystems.com | Synaptic competition during visual system development researchresources.bumc.bu... | 2006 - Neuronal Development, Synaptic Function, and Behavior - WormBaseWik wormbase.org |
Neuron A (transmitting) to neuron B (receiving) 1. Mitochondria 2. synaptic vesicle with neurotransmitters 3. Autoreceptor 4. Synapse with neurotransmitter released (serotonin) 5. Postsynaptic receptors activated by neurotransmitter (induction of a postsynaptic potential) 6. Calcium channel 7. Exocytosis of a vesicle 8. Recaptured neurotransmitter In a neuron, synaptic vesicles (or neurotransmitter vesicles) store various neurotransmitters that are released at the synapse. The release is regulated by a voltage-dependent calcium channel. Vesicles are essential for propagating nerve impulses between neurons and are constantly recreated by the cell. The area in the axon which holds groups of vesicles is an axon terminal or "bouton". Up to 130 vesicles can be released per bouton over a ten minute period of stimulation at 0.2 Hz.[1]
[edit] FormationSynaptic vesicles are made of a lipid bilayer in which transport proteins specific to each type of neurotransmitter are inserted. Neurotransmitters are moved from the cell's cytoplasm into the vesicles by vesicular transporters that rely on active transport mechanisms involving an exchange of protons (H+ ions). The necessary proton gradient is created by V-ATPase, which breaks down ATP for energy. Vesicular glutamate transporters, for example, sequester glutamate into vesicles by this process. The stoichiometry for the movement of different neurotransmitters into a vesicle is given in the following table.
membranes are tethered to SNAP via ATPase. [edit] Effects of neurotoxinsSome neurotoxins, such as batrachotoxin, are known to destroy synaptic vesicles. The tetanus toxin damages vesicle-associated membrane proteins (VAMP), a type of v-SNARE, while botulinum toxins damage t-SNARES and v-SNARES and thus inhibit synaptic transmission.[2] A spider toxin called α-Latrotoxin binds to neurexins, damaging vesicles and causing massive release of neurotransmitters. [edit] Vesicle poolsVesicles in the nerve terminal are grouped into three pools: the readily releasable pool, the recycling pool and the reserve pool.[3] These pools are distinguished by their function and position in the nerve terminal. The readily releasable pool are docked to the cell membrane, making these the first group of vesicles to be released on stimulation. The readily releasable pool is small and is quickly exhausted. The recycling pool is proximate to the cell membrane, and tend to be cycled at moderate stimulation, so that the rate of vesicle release is the same, or lower than, the rate of vesicle formation. This pool is larger than the readily releasable pool, but it takes longer to become mobilised. The reserve pool constitutes the vast majority of vesicles in the nerve terminal, but it is not clear that vesicles in this pool are released under normal conditions. Under experimental conditions, this pool is mobilised by intense stimulation, and might only occur once the other two pools are exhausted.[3] [edit] See also[edit] References
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