NEUR 414 1st Edition Exam 3 Study Guide Unit 5 6 Presynaptic Terminal Where are synapses two regions hippocampus and neocortex memories stored here Neocortex comes in at 4 goes to 5 6 and then up to 1 3 neocortical neurons typical pyramidal cell has many dendrites with multiple protrusions called spines each spine forms a connection with another neuron s axon via a synapse if memory is stored in neuronal connections it must be tied to the synapse Synapse 2 types Type 1 asymmetrical SV spherical excitatory neurotransmitters in the vesicles excitatory Type 2 symmetrical SV oval or flattened don t all have to be this shaped only need 1 inhibitory classifications are only true for electron microscopy 3 regions of the synapse Presynaptic region how do we get proteins to the synapse bulk of protein synthesis occurs in soma and dendrites need active transport active transport motor proteins two types kinesin anterograde orthograde dynein retrograde transport takes hours to days problem with delayed delivery proteins have short half life solutions prolonged half life vesicle storage vesicle recycling vesicles reside in 2 locations releasable pool reside in active zone are in contact with the membrane reserve pool reside above active zone needed for replacement of old synaptic vesicles high frequency stimulation synapsin many binding sites sticky proteins bind up synaptic vesicles and bind them to actin what mediates them being let to is their phosphorylation when when it is phosphorylated it lets go of whatever it was bound to at site 9 this is what allows them to go form reserve to release pool consists of 10 homologous proteins Syn 1a b Syn 11a b and Syn IIIa f isoforms generated from 3 different genes SYN1 SYN2 SYN3 Synapsin 1 and 2 found at presynaptic terminal expression increases wiht development of synapses expression linked to SV producotin action potential know chart resting potential Na cannot flow in but K channels are open threshold depolarization until hit action potential Na channels open up K channels close repolarization Na channels close K open hyperpolarization Na channels close K open until lower than starting resting potential Action potential is a Ca dependent process have to get depolarization down the presynaptic terminal so we can open voltage gated Ca channels w o them the process of binding and releasing cannot start Synaptic vesicle release Evoked synchronous release fast release of synaptic vesicle occurs with action potential what we typically think of two phases slow fast STEPS slow vesicle comes over and synaptobrevin interacts with syntaxin 1 to form a snare complex puts vesicle into priming stage 1 in priming stage 1 the snare complex isnt completely stable if you had Ca floating around it could interact with it causing it to fuse and the contents would be expelled spont mini event if mini event doesn t happen complexin comes in and interacts stabilizing it and free floating Ca can no longer bind moving it to priming stage 2 waiting in active zone line separating 2 is action potential fast snaptotagmin binds to Ca and causes a confirmation change so that it comes down to complex 2 and is ready to accept Ca but ONLY from synaptotagmin once received fusion pore opens and then you have vesicle releasing into synaptic cleft and vesicle is part of docking zone how can this be faster 2 synaptotagmin bind Ca and synaptic vesicles Synaptotagmin 2 Synaptotagmin 1 synaptotagmin 9 Step down inhibitory on elevated platform if it steps down it is shocked experiment looking at SNAP 25 and mRNA in hippocampus darker staining mRNA on the training side more dark on training than control don t know why we are getting this increase experiment running wheels added confusion SNAP 25 didn t increase if you have an animal under exercise you see a rise in BDNF rise in exercise in BDNF in Hilus CA1 and CA3 also increased in enriched conditioning as well BDNF if learning increased BDNF it should increase the number of docked vesicles in the places in the brain where the increase occurs need to produce more proteins to help with the physical docking SNAP 25 and syntaxin can assume the inhibitory is an increase of SNAP 25 as an increase in vesicles Evoked asynchronous release occurs after action potential is inhibited by synchronous release complexin dominant during high frequency trains inhibitory synapses not in synchronization with an action potential or doesn t have to be STEPS here Ca comes in and interacts with Priming stage 1 when you go from 1 to 2 thats when you need complexin coming in complexin prevents free floating Ca from coming in and complexin blocks asynchronize release independent of synaptotagmin if complexin doesn t bind then fusion pore opening happens multiple action potentials come in and depleat priming stage 2 Ca builds up from priming stage 1 and doesn t wait until priming stage 2 and goes to fusion pore opening complexin doesn t interact goes immediately from priming stage 1 to fusion pore opening spontaneous mini release doesn t rely on voltage gated Ca channels rely on Ca leaking out not mediated by synaptic terminal can be syns or asyns Kindling process of inducing seizures in rodents electric shocks to the brain postsynaptic region synaptic cleft