Synaptic Transmission Flashcards
1
Q
What is synaptic transmission?
A
- When info from a presynaptic neuron reaches a cell (post synaptic target)
2
Q
What are the 4 types of synapses?
A
- Gap Junctions: 6 connexion channel, cells act as couples and allow ion flow in between cytoplasm
- CNS Synapses (6 types): axodends, axosoms, axoaxo, dendroden, Gray TI (assymetrical + excited) + Gray TII (symmetrical + inhibitory- if nt perfectly fits it will block)
- NMJ: biggest synapse
- Chemical synapse (most mature synapse): nt (neurotransmitter) goes to synaptic cleft, binds to post synaptic receptors -> response (then nt reuptaken)
3
Q
What are the 3 types of neurotransmitters?
A
- GGG HAD ED
- Amino Acids (GGG): Glutamate, glycine, GABA
- Amines (HAD): Histamine, Ach, DA
- Pepties (ED): Dynorphin, Enkephalin
4
Q
What is Dale’s theory on neurotransmitters?
A
- A neuron will make only one type of neurotransmitter. Exceptions: GABAergic neurons can make both glutamate and it’s derivative GABA
5
Q
What are co transmitters?
A
- 2 neurotransmitters which are released from one nerve terminal
6
Q
What are the 2 types of receptor classification?
A
- Ionotropic= fast, voltage/ chemical
- Metabotropic= slow, long, diverse post synaptic targets
7
Q
What’s the difference between an EPSP + IPSP?
A
- EPSP: depol @ postsynaptic membrane (PS2).
- Nt from PS1 (presynaptic site) activates gated ion channel (Ach / Glutamate) -> EPSP
- IPSP: hyperpol bc increased Cl ( glycine + GABA gated ion channels activated)
8
Q
How are neurotransmitters released?
A
- Ca2+ tells vesicle to release out neurotransmitters (exocytosis)
- Vesicle + presynaptic Membrane fuses
- Endocytosis (pick up nt again)
9
Q
How are neurotransmitter types synthesized?
A
- Peptides (Dynorphin + CCK): made @ RER -> activated @ golgi -> stored @ Bouton in axon terminal
- AA (GABA) + Amimes (Ach + 5HT)= made @ cytosol from enzymes -> vesicle transport -> axon terminal (Storage)
10
Q
What are the ways in which neurotransmitters are recovered/ broken down
A
- Reuptake: Go back to P1 axon, monoamines (Ad, NAd, DA get broken down by enzymes) -> vesicle -> transporters @ glial membrane takes nt away from cleft
- Enzyme Breakdown: @ terminal cytosol/ synaptic cleft
- Diffusion: away from synapse
- Desensitise to neurotransmitter
11
Q
What does synaptic integration dependent of?
A
- Activation of certain amount receptor depends on how much neurotransmitter there is
12
Q
How can synaptic integration of an EPSP be affected?
A
- EPSP summation = depends on nature and location of AP (integration= 1 axon, spatial = different space, temporal = same space in fast succession)
- Dendrites affect nature of synaptic integration
- Longer = less depol/ AP on membrane
- Amplifiers= voltage gated Na/Ca2+/K channels
- Dendritic Na channel can carry AP
13
Q
How can synaptic integration of IPSPs be affected?
A
- By shunt inhibition (blocking of AP from soma to hillock of axon)
- Less than 65mV = hyperpol.
14
Q
What is the difference between Excitatory and inhibitory synapses?
A
- Excite = Gray T1= asymmetrical (e.g. glu can act on as a nt)
- Inhibit= Gray TII = symmetrical (use GABA/ glycine as nt)
15
Q
What is synaptic modulation?
A
- When an excitatory AP transmission is changed by
- another synapse (nt ion gated channel)
- lowering K+ conductance = increase AP of weak/ distance EPSP
- Lowering AP by changes via:
- Phosphorylation to decrease membrane conductance
- Learning & memory= involves secondary messengers, phosphorylation, protein kinase activity
16
Q
What is quantal analysis and what can it tell us about synapse?
A
- QA = count of number of vesicles in relation to an AP
- Shows us that NMJ synapses are far bigger than a CNS synapse
- NMJ = 200 vesicles, EPSP 40 mV
- CNS synapse= 1 vesicle, >1 mV
