Electrical and Chemical Signalling: Propagation of the AP and the synaptic transmission Flashcards
how does resting state -> propogation of an action potention occur of an unmyelinated axon occur?
where is the trigger zone?
continous propogation:
trigger zone: axon hillock / aka axon initial segment
resting state: high conc of Na+ outside cell, extracellular env: +ve. -70mV inside cell
initiation: voltage gated Na+ channel opens: Na+ go to site A. creates a local zone in both extraceullar and intracellular fluid with a sudden change in charge.THEN go to Site B (which is an area of high conc negative charge) and sodium Na+ ions open here
propogation: Na+ at Site B attracted to -ve chrge –> go to site C. Also attracted to site A, but cant go back bc thats an absolute refractory period: only goes in one direction
propogation continues: Na+ go along site D etc. Site A is now region of repolarisation (new AP can occur)
what does myelin do?
what are gaps of myelin called?
what is concentrated at ^?
myelin: provides high resistance to ion flow across the membrane
gaps of myelin: Node of Ranvier: concentration of voltage gate sodium and potassium channels
how can we think of AP occuring as in myelinated axons? name for this?
(what is size of internode? node?)
AP jumps from one to node to the next: aka saltatory conduction
internode: 1.5mm
node: 1 um
why / how do action potentials jump down axon (myelinated?)
schwann cell insulates axon: no ions leak out of axon
at node of Ranvier: high conc of voltage gated sodium and k channels
when depolarisation occurs: Na+ in at Node of Ran. charge cell moves along unimpeded to next unmyelinated area: Node of Ranvier. electrical signals jump down much faster
repolarisation and hyperpol: open at delayed time at previous node of Ran
would you be able to have one long myelin sheath?
no - would get some charge dissapation. need nodes of Ranvier to top up the depolarisation effect
why do action potentials travel in one direction only?
what is the absolute refractory period of the AP?
- the membrane immediately behind (in direction of cell soma) is in the absolute refractory period
- this is the time in which a 2nd AP cannot be generated
what is relationship between current, voltage and resistance?
how does this relate to axons?
(dont fret about knowing too much i think)
V = IR
- current flowing along axon can leak across the cell membrane or travel through the cytoplams depening on path of least resisitance
- resistance decreases with increased diameter
- larger axons conduct faster
- Membrane resistance is increased with insulation (myelinated fibres have greater membrane resistance due to insulation). for the same fibre diameter as unmyelinated, myelinated have greater conduction velocity.
what myelinates axons in a) PNS b) CNS?
a) Schwann cell: PNS
b) Oligodendrocytes: CNS
why do we have different conduction velocities and how do they achieve this?
fastest conduction velocities have widest axon diameter and myelination:
(size goes down in order - see photo)
Aα fibres are the fastest: motor neurons, muscle spindles, golgi tendon organs
Aβ fibres: touch / mechanical pressure:
Aδ fibres: pain (fast), temp
C fibres: pain (slow), temp and itch. unmyelinated
how does schwann cell form myelin sheath around axon ?
for awareness probs
wraps around around around
what are the two different types of synapse?
- electrical
- chemical: (could be thought of as electrochemical) converts electric signal into chemical singal.
how does chemical synapse work?
- AP passes down axon: depolarisation of presynaptic terminal.
- Ca2+ voltage gated channels open
- increase in cellular Ca2+ is the trigger to release synaptic vesicles
- Synaptic vesicle bind to membrane and release neurotransmitter across synaptic cleft
- NT binds to ionotropic or metabotropic receptors (change from closed to open channels)
- change in membrane potental (hyper or dep) of post synatpic terminal
ONLY ONE DIRECTION
how does electrical synpase work?
- AP in presynaptic terminal goes through gap junction channel
- coupling potential
BOTH DIRECTIONS
what else is present in presynaptic cleft of chemical synapses?
mitochondria ! energy required
what makes it easier for Ca2+ to diffuse across into presynaptic cleft?
calcium concentration outside of cell is 10 000x time higher than inside - large inward concentration and electrical gradient allows free calcium to pass into cell
what is the process called when NT bind to presynaptic cleft?
what is ^ mediated by?
- = docking
- docking is mediated by SNARE complex - ensures membrane fusion of vesicle
what is the process of that NT move across synaptic cleft?
endocytosis
what is the change in signal like at presynaptic cleft?
what does this mean for what happens on post synaptic cleft?
- at presynaptic terminal: AP is converted into an analogue signal (chemical NT)
- at post synaptic cleft: different NT cause excitation or inhibition (depending on the receptor on post synaptic neuron)
how do different excitatory or inhibitory NT work together / agaisnt each other on post-synaptic cleft.
what is the name for this?
- analogue (aka graded) potentials can arrive at trigger zone together and their sum create a suprathreshold signal to cause an AP
OR
- could get one inhibitory and two excitatory -> summed potentials are below threshold so no AP !
addition of excitatory and inhibtory signals = summation
name 4 important NT that are collectively called monoamines
where each expressed?
adrenaline: fight or flight. PNS
noradrenaline: concentration and arousal. PNS. undersupply can depress mood
dopamine: pleasure, learning attention and momevent. CNS. XS: schizophrenia. depleted: Parkinsons
serotonin: mood, hunger and arousal. CNS and gut. depression
= collectively known as monoamines
what is acetylcholine involved with? with NS?
CNS: memory and learning
PNS: neuromuscular junctions (muscle action)
involved in the preganglionic
deteriote in AD
name three amino acid NTs?
name a peptide NT
amino acids:
gaba: calming. major inhib NT. CNS. undersupply: seizures, tremors
glutamate: memory. major excitatory NT. XS: oversupply: overstimlate brain - migraines
glycine: major inhibitory NT in spinal cord
peptides:
endorphins: euphoria
which of gaba and glutamate are excitatory / inhibitory?
gaba: inhibtory
gluatamate: excitatory
Excitatory post synapatic potential (EPSP) and Inhibitory PSP (IPSP).
EPSP:
- depolarisation at post synaptic neuron: increases liklihood of AP
- (e.g. glutamate channels cause an net influx of Na+ & depol)
IPSP:
- hyperpolarisation decreases ability of the membrane to reach threshold: decreases liklihood of AP
- (e.g. gaba and glycine cause net influx of Cl-)
summation of IPSP and EPSP gives probabilty of firing an AP
what is temporal summation?
what is spatial summation?
temporal summation
- post synaptic potentials at same syanpse (A&A) occur in rapid succession
- first potential doesnt have time to dissipate: next potentials add to previous once
spatial summation
- multiple postsynaptic potentials from different synapses (A+B) occur same time and add
- alone, EPSP not strong enough to cause AP. reinforce each other = AP.
which type of summation is this?>
spatial summation: different synapses occur at same time (A+B)
what type of summation is this?
temporal summation: same synapse!!
what does summation allow?
summation allows neurones to integrate large amounts of information
what can excess firing of AP lead to?
seizures
which NT is most common in brain?
glutamate !!
