membrane and action potential

Describe an action potential. 

1. when the excitable cell depolarisises the NaV channels open making it increase is depolariastion. 

2. the NaV chanels close fast 

3. KV channels start to open this is delayed and it repolarises the membrane 

4. KV doesnt close fast enough so its hyperpolarised 

5. NaV and KV close so it goes back to resting potential 

How do inhibitory postsynaptic potentials work? 

They use negative ions to hyperpolarise the membrane.

What area of a postsynaptic neurone generates an action potential? 

The axon hillock (aka the spike initiation zone)

What are the three fates of a neurotransmitter once released into a synaptic cleft? 

Bind to receptor

Diffuse away

Broken down and recycled by cell

How does an action potential lead to Ca2+ release in muscles? 

action causes a protein-protein interaction between the sarcoplasmic reticulum and a ryanodine receptor ( RyR)   making Ca2+ leave SR

Give two diseases affecting the lower motor neurone. 

Multiple sclerosis (MS)

Motor neurone disease (MND)

what is the resting membrane potential and how is this maintained

• -70mv

• inside has high K+ concentration 

• outside has high concentration of Na+ and Cl- making inside more negative

what are each of the labels

1. dendrites - input region where info is recpted
2. cell body - where the info id inttegrated
3. axon - infomation sent to synpase
4. synpases

what is hyperpolarrisation

membrane potential moves below -70mv

through K+ efflux

what type of cells have voltage gated chanels in their plasma membrane and for what ions

excitable cell

Na+ 
Ca2+ 
K+

how do the NaV CaV KV channels repsond to depolirasation

open

during restign potential what is happenign to the NaV and KV

both closed

what is depolarisation

membrane potential is becoming more positive towrads 0 or above 

happens through Na+ influx

during repolarisation what happens the NaV and Kv

Kv open- K+ move out inside is more negative rapid moveemnt - 1msec
NaV close

durign depolarisation what happens to the NaV and KV 

NaV open - Na+ move in, inside more positiev rapid movemnt- 1msec
KV closed

what does the all or none response mean 

an action potential will only occur if the membrane depolarises to the threshold if not theres no action potential

explain what happens to NaV and KV at each letter

how does the strength of a stimulus affect action potentials

there will be more frequent action potentials

what is an absolute refractory period, why does it happen and hwat does it cause

• where no new action potential can be made no matter how strong the stimulus 

• because the voltage gated Na+ channel are inactiev 

• makes sure each action potential is sperate and unidirectional 

what is a reflective refractory period

• Another action potential can occue but the stimulus has to be very strong

• happens because the K+ channels are still open so the membrane is hyperpolaries

where does absoulte and relative refractory period happen

red- absoulte
green- relative 

do all excitable tissues have the same action potential  

no

how comes action potentioanl move in one direction

the depolarisation moves down the neurone
then there is repolarisation after it so there cant be another action potential making it move in one direction 

how is an EPSP ( excitatory postsynaptic potential) formed

when the neurotransmiter is an inhibitory neurotrasnmiter it causes an action potetial on the next neurone

e.g glutamate

how is an (IPSP) inhibihibitory post synpatic potential formed

when the neurotransmiter from the presynaptic neurone is an inhibirtory neurotransmitter it inhibits the action potential on the post synaptic neurone

e.gGABA

explain this image

• both EPSP and IPSP are passive propagation ( it doesnt use energy to send an action potential down the axon of a neurone)

•  this means theres a rapid decline as the distance from the cell body increases

where are the EPSP and IPSP integrated and what deos this mean

• at the axon hillok 

• where the EPSP and IPSP are converted inyo an action potential if thethreshold is reached

how are the EPSP and IPSP integrated at the axon hillock

- axon hillock- where the axon starts 

- there is summation of all the post synpatic potentials - add up all the post synaptic potentials and if its higher than the threshold an action potential can start   
  

what are the 4 things that affect the conduction velocity  (CV)

1. temperature: higher the faster

2. size: larger diameter the faster 

3. myelination: the more myelination the faster

4. disease - multiple sclerosis (MS) - you dont have myelantion as th eimmuen system destroys it, so decrease speed

what is conduction velocity (CV)

how fast an action potential travels down a nerve

for each fibre fill in the blank 

how does myelination increase conduction velocity

- without myelination the action potential has to constantly propagate the whole nerve 
- with, there is saltatory conduction so the AP can jump so dont have to travel the full distance

how many neuromuscular junctions does each msucle fibre have 

neuromuscula rjunction is the synpase between motor neurone and muscle fibre 

 what is a motor unit

one motor neurone thats axon branches to many axon terminals, and the set of muscle fibres that are innervated(controlled) by these axons. 

( the group of muscle fibres that are conrolled by the same motor neurone)

explain how a muscle can contract starting from nueromuscular junction

1. an AP comes down to the preynpatic neurone makign ti become depolarised 

2. this makescoltage gated  Ca2+ ion channles open and they move in 

3. this makes the vesicels with the neurotransmitter move and fuse with membrane 

4. excocytosis 

5. then they are detected by receptors on post synpatic neurone 

6. this makes Na+ ion chanels open makign the cell depolarise and an action potential starts 

7. the action potential reaches the t tubules which intereact with the RyR on the smooth endoplamic reticulum making Ca2+ be reelased 

8. Ca2 binds to troponin and contractions start

what are the 3 steps in the presynpatic neurotransmiiter release for AcH (simple)

1. synthesis

2. packaging 

3. release

what happens during syntheis of ACh of the presynaptic neurotransmitter release

ChAT (choline acetyltransferase) joins choline + acetyl Co A = ACh

what happens during packaging of the neurotransmitter release in Ach

ACh is packaged into vesicles by trasporter VAChT

what happens during the neurotransitter stage release of AcH

an AP comes and depolarises the terminal this makes the CaV, so calcium ions enetr this actiavtes the vesicles fusing ti release ACh

what happens in the synpatic cleft during the cholinergic synpase with ACh

1. ACh binds to the receptor after diffusign across the cleft

2. some ACh just diffuses away 

3.  the ACh is degreaded by Acetyl choline esterase making choline and acetic acid 

4. the choline is moved by the choline transpoorter back into the presynpatic neurone 

5.   acetic aid diffuse awaty

what happens at the post synpatic neurone on the cholinergic recptor ( once it reaches the muscle)

1. the ACh has now bound ot the muscle nicotine ACh recptors 

2. this allows the ACh recpetors to open  ( they are ligand gated ion channels)

3. so the ligand gated ion channels open  so sodium ions move in 

4. this creates an excitatory postsynpatic  potential 

5.  if it reaches the threshold it will make an action potential 

how deos multiple sclerosis effect motor neurones

• it demyelinates the CNS and PNS

• its an autoimmune disease 

how does motor neurone disease affect motor neurones

• degeneration of the motor neurone 

 explain negatuive feedback with the motor neurone and skeletal msucle 

• the motor neurone has branches to renshaw cells as well as the skeltal msucle 

• the renshaw cell has receptors for ACh so when the motor neurone releases ACh it makes an action potential on th renshaw cell 

• the renshaw cell releases IPSP such as glycine so it inhibits an acrion potential back onto th emotor neurone

• this stops another action potential so stops it from releasing ACh

how do drugs work ( overview)

• they bind to proteins altering its function

• they excert chemical chnage on components of the cell

what are 4 types of proteins drugs bind to 

1. ion channels 

2. carrier molecules ( transporter)

3. receptors

4. enzymes

where can the proteins that drugs bind to be found

on the cell membrane 
     or
inside the cell

what is an agonist

a drug that enhances the function of a protein if there is a deficit 

what is an antagonist

• the drug binds to the receptor stopping it from being activated 

• it has affinty 

• it has no efficacy

 

what type of cell do drugs usually work o and how 

• act on "normal" cell  healthy cells

• they block, mimic or stimulate the action of endogenous ( naturally produced) molecueles/ processes

what is the type of drug that doesnt act on normal cell (healthy cell)

chemotherapeutic drugs

what happnes to receptors after a molecule bids to its binding site

the receptor changes shape this starts the process which change the function of the cell

how fast do g protein coupled recptors work

seconds

how fast do kinase linked receptors work 

minutes

how fast do nuclear receptors work

hours