| Term 
 
        | Compare the distance between pre and post-synaptic cell membranes in electrical and chemical synapses |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Does cytoplasmic continuity exist between post and pre synaptic cell membranes  in electrical and chemical synapses |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Compare the cytoplasmic components  in electrical and chemical synapses |  | Definition 
 
        | e: gap junction channels c: presynaptic active zones and vesicles, postsynaptic receptors
 |  | 
        |  | 
        
        | Term 
 
        | Give the transmission agents in electrical and chemical synapses |  | Definition 
 
        | e: ionic current c: chemical transmitter
 |  | 
        |  | 
        
        | Term 
 
        | Describe the synaptic delay in electrical and chemical synapses |  | Definition 
 
        | e: virtually absent c: at least 0.3ms, 1-5ms
 |  | 
        |  | 
        
        | Term 
 
        | Describe the direction of transmission in electrical and chemical synapses |  | Definition 
 
        | e: bidirectional c: unidirectional
 |  | 
        |  | 
        
        | Term 
 
        | Describe the flexibility in electrical and chemical synapses |  | Definition 
 
        | e: none c: great flexibility due to transmitter and post-synaptic response
 |  | 
        |  | 
        
        | Term 
 
        | Describe the events at an electrical synapse |  | Definition 
 
        | 1. AP arrives in the presynaptic terminal causing depolarisation 2. voltage gated ca2+ channels are opened by depolarsaiton
 3. ca2+ rushed into the terminal at active zones
 4. ca2+ trigger NT release
 5. ca2+ influx can also influence the shape of the AP
 |  | 
        |  | 
        
        | Term 
 
        | What is the neurotransmitter criteria? |  | Definition 
 
        | 1. must be synthesised within the synapse 2. must be present in the presynaptic terminal and be released in amounts sufficient to exert its supposed effects of the post-synaptic neurone/effector organ
 3. when applied exogenously it must mimic exactly the actions of the endogenously released transmitter
 4. must be a specific removal mechanism from its site of action
 |  | 
        |  | 
        
        | Term 
 
        | How are peptide NT synthesised? |  | Definition 
 
        | in the cell body using protein  manufacturing components (i.e. rER, Golgi apparatus) |  | 
        |  | 
        
        | Term 
 
        | How are amine/amino acids NT synthesised? |  | Definition 
 
        | in the synaptic terminal using synthesising enzymes that are transported from the cell body |  | 
        |  | 
        
        | Term 
 
        | Why are NT synthesised this way? |  | Definition 
 
        | so cells can be self-sufficient |  | 
        |  | 
        
        | Term 
 
        | Describe small clear vesicles |  | Definition 
 
        | 40-60nm e.g. GABA, glutamte, dopamine |  | 
        |  | 
        
        | Term 
 
        | Describe large dense core vesicles |  | Definition 
 
        | 90-250nm e.g. neuropeptides |  | 
        |  | 
        
        | Term 
 
        | Define co-existance/co-transmission |  | Definition 
 
        | a single neurone may synthesis and release more tax one transmitter substance |  | 
        |  | 
        
        | Term 
 
        | Describe synaptic vesicles cycling |  | Definition 
 
        | 1. free vesicles are targeting in active zone 2. vesicles dock in active zone
 3. the docked vesicle is primed for exocytosis
 4. vesicles undergo fusion and release their contents in response to a rise in [Ca2+]
 5. fused vesicle membrane is taken up into the cell by endocytosis
 |  | 
        |  | 
        
        | Term 
 
        | What conc can the micro domain around the active zone can ca2+ reach? |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | Synaptobrevin Synaptotagmin
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | vesicle bound protein which binds with SNAP-25 on plasma membrane (vesicle priming/docking) |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | when bound to ca2+ the two c2 domains insert into the membrane and causes the two membranes to fuse by inducing membrane buckling |  | 
        |  | 
        
        | Term 
 
        | Describe the vesicle stages |  | Definition 
 
        | 1. Docking: vesicles move toward and interact with membrane of presynaptic terminal. The distance of these vesicles from a Ca2+ channel cluster ranges from 30-300μm (mean is around 100μm). 2. Priming: vesicles become competent for fusion-pore opening ;all the molecular rearrangements that take place after initial docking of a synaptic vesicle but before exocytosis have occurred.
 3. Fusion-pore opening: Ca2+ induced; once Ca2+ has entered the presynaptic cell, the neurotransmitter will be released. This is related to fast transmitter release.
 |  | 
        |  | 
        
        | Term 
 
        | What are the functions of vesicle proteins? |  | Definition 
 
        | 1. Restraint of vesicles: interaction with the cytoskeleton to move vesicles over a short distance. 2. Recruitment of neurotransmitter vesicles from the reserve pool to the releasable pool.
 3. Docking of vesicles: attachment to the presynaptic plasma membrane.
 4. Priming of vesicles: preparation for release.
 5. Rapid fusion and exocytosis upon intracellular Ca2+ increase.
 6. Endocytosis: recycling and reuptake into presynaptic cell.
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | synaptobrevin (vesicle) are incorporated into the membranes of transport vesicles during budding.
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | SNAP-25, syntaxin (target) are located in the membranes of target membranes.
 |  | 
        |  | 
        
        | Term 
 
        | How does ca2+ binding allow synaptotagmin to initiate formation of SNARE complex? |  | Definition 
 
        | a) calcium binding allows synaptotagmin to initiate formation of SNARE complex b) SNARE complex forms with snaptotagmin, calcium increase causes membrane juxtaposition and allows fusion
 |  | 
        |  | 
        
        | Term 
 
        | Vesicles in the nerve terminal are grouped into three pools, which are distinguished by their function and position in the nerve terminal - what are they? |  | Definition 
 
        | 1. Readily releasable pool 2. Recycling pool
 3. Reserve pool
 |  | 
        |  | 
        
        | Term 
 
        | Describe the readily releasable pool |  | Definition 
 
        | 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. |  | 
        |  | 
        
        | Term 
 
        | Describe the recycling pool |  | Definition 
 
        | proximate to the cell membrane, and tend to be cycled at moderate stimulation, so that the rate of vesicle release is the same as, or lower than, the rate of vesicle formation. This pool is larger than the readily releasable pool, but it takes longer to become mobilised. |  | 
        |  | 
        
        | Term 
 
        | Describe the reserve pool |  | Definition 
 
        | 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 occur only once the other two pools are exhausted. |  | 
        |  | 
        
        | Term 
 
        | What toxins affect NT release? |  | Definition 
 
        | botulinum and tetanus both produce the enzyme zinc endoprotease. This enzyme catalyses the hydrolysis of peptide bonds, which means it has the ability to cleave the SNARE proteins actively involved in vesicle fusion.
 |  | 
        |  | 
        
        | Term 
 
        | What proteins are affected by toxins? |  | Definition 
 
        | Synaptobrevin: cleaved by both C. botulinum and C. tetani. 
 SNAP-25: cleaved by C. botulinum.
 
 Syntaxin: cleaved by C. botulinum.
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | 1. vesicles cluster at the active zone waiting to be released by the synaptic neurone 2. vesicles fuse with post-synaptic membrane and release NT into cleft
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | 1. reuptake of NT into terminal 2. diffusion of NT
 3. enzymatic breakdown of NT
 4. binding of NT to postsynaptic receptors/presynaptic auto receptors
 |  | 
        |  | 
        
        | Term 
 
        | What do vesicle transporters do? |  | Definition 
 
        | concentrate NT into vesicles several Its may utilise a single type of transporter
 low level specificity
 |  | 
        |  | 
        
        | Term 
 
        | What do membrane transporters do? |  | Definition 
 
        | responsible for reuptake of NT from synaptic cleft high levels of specificity needed
 |  | 
        |  | 
        
        | Term 
 
        | How does a NT enter a vesicle? |  | Definition 
 
        | energy is released demo breakdown of ATP into ADP on veils surface using ATPase proton produced is transported into vesicles
 proton dependent 'antiporters' transport NTs
 |  | 
        |  | 
        
        | Term 
 
        | Describe membrane transporters |  | Definition 
 
        | sequester NTs maintain ion gradients
 provide nutrients
 sodium dependent sympoters
 active trnapsort concentrates NT in cytoplasm
 |  | 
        |  | 
        
        | Term 
 
        | How many sodiums are swapped for choline
 GABA
 Glutamate
 |  | Definition 
 | 
        |  | 
        
        | Term 
 | Definition 
 
        | the arrangement of inhibitory and excitatory cells in a circuit that generates excitation by the transient inhibitor of a tonically active neurone |  | 
        |  | 
        
        | Term 
 
        | Draw and explain disinhibition diagram |  | Definition 
 | 
        |  |