synaptic transmission Flashcards
Opening Na channels
depolarises the cell (excitatory)
Opening K+ channels
hyperpolarises the cell (inhibitory)
Opening Cl- channel
hyperpolarises the cell (inhibitory)
Opening Ca+ channels
depolarises the cell (excitatory)
EPSPs
excitatory post synaptic potentials
- Excitatory PSPs
○ Depolarise the membrane (more +ve)
○ Open some Na+ or Ca+ channels
○ Increases probability of AP
IPSPs
Inhibitory post synaptic potentials
Inhibitory post synaptic potentials
○ Hyperpolarise membrane (more negative)
○ Open some Cl- or K+ channels
○ Decreases probability of AP
post synaptic potentials
- PSPs are not all or nothing
- They are graded
- ESPSs and IPSPs are summed (spatially and temporally) to decided whether the neurone generates an AP
Threshold for AP generation
- If the axon trigger zone exceeds -55mV, all voltage gated Na+ channels open and AP is generated
all voltage gated Na+ channels open and AP is generated when
If the axon trigger zone exceeds -55mV
The sum of all IPSPs and EPSPs cause
either depolarisation of hyperpolarisation
IPSPs cause
hyperpolarisation
EPSPs cause
depolarisation
2 ways neurones generate PSPs
direct electrical transmission
by use of a chemical mediator
○ Direct electrical transmission
§ Rare
§ Cardiac muscle, some types of smooth muscle and some neurons
By use of a chemical mediator
§ Common
§ Neuron and muscle, neuron and neuron, sensory receptor cells and neurons
direct electrical synapses
- APs (ions) travel through gap junctions between presynaptic and postsynaptic neurons
- Synapse has gap junctions - hole in the plasma membrane of both cells where ions can flow through
○ Allows Na to flow into the post synaptic neurone
- Synapse has gap junctions - hole in the plasma membrane of both cells where ions can flow through
Chemical synapses
- Neurotransmitter molecules cross the synapse and signal the post synaptic neuron by binding receptors and inducing change
○ Glutamate decarboxylase
Takes off a carboxyl group and it changes from glutamate to GABA
choline acetyltransferase
puts Acetyl CoA and choline together to make acetyl choline
adrenaline made from
modified tyrosine
how are neurotransmitters stored
in vesicles
where are nuerotransmitter containing vesicles stored
docked at the cell membrane
how are nuerotransmitter containing vesicles released
exocytosis
how is exocytosis of neurotransmitter containing vesicle triggered
action potential
v-snare on neurotransmitter vesicle
synaptobrevin
t-snare on cell membrane
SNAP
why do synaptobrevin and SNAP only partially assemble
blocked by complexin
stops them from binding
how does SNAP and synaptobrevin fuse
- Synaptotagmin is activated by Ca+ and moves complexin out the way
synaptotagmin is activated by
Calcium
how does calcium get to the presynaptic nerve
presynaptic terminus contains voltage gated calcium channels instead of voltage gated sodium channels
AP depolarises and Ca channels open
Ca binds synaptotagmin
2 classes of receptors
ionotropic and metabotropic
ionotropic receptors
open/close an ion channel
○ Ligand gated ion channels
metabotropic receptors
○ Active an enzyme
○ Ligand binding outside cell activates enzyme inside the cell
○ Receptor tyrosine kinases, G-protein coupled receptors
acetyl choline nuerotransmitter can have multiple effects
- Excitatory: Nicotinic - opens Na+ channels
- Inhibitory: Muscarinic - opens K+ channels
two main neurotransmitters of the CNS
glutamate and GABA
two main neurotransmitters of the PNS
acetylcholine and noradrenaline
glutamate is
dominant excitatory neurotransmitter in the CNS
glutamate acts via
iGluRs and mGluRs
inotropic and metabotropic glutamate receptors
iGluRs activated by glutamate
AMPA - Na Channel
NMDA Na and Ca channel
both EPSPs
GABA is
The dominant inhibitory CNS neurotransmitter
GABA binds
GABA alpha receptors (ionotorpic)
GABA beta receptors (metabotropic)
GABA alpha receptors
ionotropic
Cl- channels causing influx of Cl- causing hyper polarisation
IPSP
acetyl choline
○ Excitatory or inhibitory
PNS nuerotransmitter
when is acetyl choline excitatory
§ Nicotinic receptors
□ Ionotropic - ligand gated Na+ channel
□ Always excitatory
when is acetyl choline inhibitory
§ Muscarinic - often inhibitory, can be excitatory
□ Metabotropic - activates enzymes
noradrenaline
PNS nuerotransmitter
excitatory or inhibitory
2 types of receptors triggered by noradrenaline
alpha and beta adrenergic
moth metabotropic, activate enzymes and can be excitatory or inhibitory
heart rate is controlled by
acetyl choline and noradrenaline
noradrenaline and acetyl choline are
- Antogonists - one is excitatory and one is inhibitory
speeding up heart rate
- Noradrenaline -excitatory
○ Bind to beta adrengeric which opens ca;cium channel to excite the cell - heart rate speeds up
slowing heart rate
- Acytyl choline binds to muscarinic receptor to open potassium chanel to hyperpolarise the cell and inhibit it to slow the heart rate
2 ways of stopping neurotransmitters
neurotransmitter reuptake
nuerotransmitter degredation
- Neurotransmitter reuptake
○ Uptake by presynaptic neuron or local glial cells
○ Most NT: serotonin, glutamate, dopamine, noradrenaline, GABA
- Neurotransmitter degradation
○ Enzymes in the synapse chew up neurotransmitter molecules
○ Mostly done with acetyl choline
making acetyl choline
choline acetyltransferase
degrading acetyl choline
acetylcholinesterase
how is the process of clearing nuerotransmitter sped up
glial cells uptake nuerotransmitter