Examples of graded potentials
Generator potentials at sensory receptors
Postsynaptic potentials at synapses
Endplate potentials at neuromuscular junction
Pacemaker potentials in pace maker tissues
How are graded potentials decremental
loose signal therefore can only be used over short distances
How are graded potentials graded
as the intensity of stimuli effects signals amplitude
How can cells be hyperpolorised
Opening of Cl gates, letting Cl in- fast ISPS
Opening K gates letting K out the cell - slow ISPS
How can cells be depolarised
Opening Na gate letting Na into the cell - fast ESPS
closing K gate, so K remains in the cell - slow EPSP
Why is potassium gates slower in producing a response
are G protein coupled - metabotrophic
How are post synaptic potentials produced
by a neurotransmitter opening or closing ion channels
= ligand-gated ion channels
What are the two different ways Graded potentials can summate
Temporal - same signal
spatial - different signals
Name two inhibitory PSP
GABA and Glycine
What must happen for an action potential to be fired
reach threshold potential > -55mV
What depolarises cells in AP quickly
Na channels open and move into cell rapidly then close again
What are the two different threshold stimulus
Sub threshold -sits above threshold but decreases as travels, therefore no AP fired
Suprathreshold - remains above threshold, fired AP
How does the refractory period occur
Threshold is reached and opens Na channels they only stay open for a short time though.
K+ permeability slowly rises as more K+ channels (this time the voltage dependent ones) open and leave the cell this causes repolarisation, and we eventually return to RMP
How do action potentials self propagate
When a voltage gate opens it depolarises the next gate stimulating it to open as well
How can signle only move forward
As the neighbouring gate thats just stimulated the other gate is now in refractory period therefore can not be stimulated to open again so signal can only be passed forward
How is the speed of AP increased
Larger axons - conducts quicker as resistance decreased, passive current spreads quicker
Myelination - increase the membrane resistance, preventing current leaking out, so passive current spreads quicker
What are properties of AP
mediated by voltage-gated channels have a threshold are all-or-none can only encoded stimulus intensity in their firing frequency, not amplitude are self-propagating have a refractory period travel slowly
Why is the frequency of the signals encoded
As AP fired are all the same size due to all or non phenomenon, therefore its how stimulus intensity is measured
What are the gaps in-between myelin sheath called
Nodes of ranvier
What is the movement because the refractory period of cells called
saltatory conduction
What is myelin sheath produced by in the CNS and the PNS
CNS- oligodendrites
PNS- schwann cells
Where are the voltage gated Na channles located
In between myelinated axons = Node of raniver
How does myelin sheath do to our AP conduction
The depolarisation evoked by voltage-gated Na channels at one node of Ranvier by spreads as a local circuit While this is decremental it travels further because less current is wasted leaking out of the membrane or charging up the capacitance, therefore big enough to reach the next node and trigger another AP.
What is the effect of demyelination
Big local current delays quicker, therefore does not depolarise the next node e.g. multiple sclerosis
What is the order of action potential fibres in most sensitivity to pressure and least sensitive to anaesthetics
A alpha (biggest) A beta A gamma A delta B C (smallest)
What size of fibres are most sensitive to anaesthetics
small fibres - C
What type of fibres are most likely to go numb if you lie in them for to long e.g. anoxia
Large fibres
What fibre signal is the fastest and what
A alpha because it has the largest axon
List what happens at NMJ?
Action potential in motor neurone
Opens voltage-gated Ca2+ channels in presynaptic terminal
Triggers fusion of vesicles
Acetylcholine (ACh) released
Diffuses across synaptic cleft
Binds to ACh (nicotinic) receptors
Opens ligand-gated Na+/K+ channels
Evokes graded (local) potential (end plate potential)
Always depolarises adjacent membrane to threshold
Opens voltage-gated Na+ channels - evokes new AP
ACh removed by acetylcholinesterase
How does tetoduoxin work
Blocks Na+ channel
Jaro spider toxin
Blocks Ca2+ channels, therefore no transmitter release
How does Botulinum toxin work
Blocks transmitter release
How does curare work
blocks Ach receptors and so prevents the end plate potential
How does anticholinesterases work
block ACh breakdown and so increase trasnmission at the NMJ
What is the difference between CNS synapse and NMJ
Range of Neurotransmitters
Range of postsynaptic potentials
There is different anatomical arrangements of synapse
Different synaptic connectivity of neurons
What NT is made on demand
Nitric Oxide
How is ACH transmitter differ from other NT
Is inactivated by breakdown where others are inactivated by uptake
What type of potential does NMJ have and what is its features
endplate potential - only excites and is specific
What is the range of post synaptic potentials
Fast EPSPs (ionotropic)
Slow EPSPs (metabotropic)
Fast IPSPs
Slow IPSPs
What are the different anatomical synapse arrangement in the CNS
Axo-somatic - axon on the cell body
Axo-dendritic - axon on dendrite
Axo-axonal - axon on axon
What is the different synaptic connectivity pathways
convergence
divergence
feedback inhibition
monosynaptic vs polysynaptic pathways
How does feedback inhibition work
AP travels down, NT causes feedback inhibition, therefore fires one AP then stops
What synaptic connectivity pathway gives more scope for synaptic integration i.e. add in an inhibitory neurone
Polysynaptic
Where is graded and AP fired from
graded - dendrites/cell body
AP - trigger zone, axon helix
What potential uses both ligand and voltage
graded
What is the resting membrane potential and how is maintained
-70mV
leaky potassium channels
