PHYS: Action Potentials + Synapses Flashcards
1
Q
what is resting membrane potential (RMP)
A
- difference in electrical charge inside vs outside cell (-70mV) @ rest - polarised (charged)
- inside is 70mV more negative than the outside due to -vely charged proteins in the cell
2
Q
3 factors which influence RMP
A
- concentration gradient b/n ECF (Na+, Cl-, Ca2+) and ICF (K+ and -ve proteins)
- electrical gradient (all ions)
- permeability of membrane
3
Q
2 types of membrane ion channels (with conc grad)
A
- leaky channels: open and close randomly = unregulated ion leakage (main contributor to RMP)
- gated channels: open in response to a stimulus e.g. voltage, mechanical or chemical (ligand)
4
Q
2 types of ion transporters (against conc grad)
A
- ATPase pumps e.g. Na+/K+ pump or Ca2+ pump
- ion exchangers e.g. Na+/Ca2+ exchanger
5
Q
permeability of plasma membrane at rest
A
- most permeable to K+
- still permeable to Cl- and Na+
- impermeable to -vely charged intracellular proteins
6
Q
what is equilibrium potential
A
- measure of membrane potential that counterbalances conc grad for one or more ion/s
7
Q
how to calculate equilibrium potential with one ion
A
- Nernst equation
- E(ion) = electrical potential for ion (mV = millivolts)
- Z = CHARGE of ion (1 for Na+ and K+, -1 for Cl-)
- Co = conc of ion outside cell (mmol/L)
- Ci = conc of ion inside cell (mmol/L)
- outside and inside are reversed for anions
8
Q
how do we know that the cell membrane is more permeable to K+ than Na+?
A
- net movement down conc grad (Na+ in and K+ out) via leaky channels
- E(K+) is larger than E(Na+) which means there are more leaky channels for K+
- leak counterbalanced by active Na/K pump
9
Q
sodium potassium pump
A
- maintains RMP: actively counterbalances rate of Na+ and K+ leakage therefore no net movement of ions
- 3 Na+ out and 2 K+ in
- generates -1mV of potential (no role in generating AP)
10
Q
how to calculate equilibrium potential w/ multiple ions
A
- Goldman-Hodgkin-Katz equation (expanded version of Nernst)
- each concentration is multiplied by its relative permeability
- inside and outside for Cl- are reversed b/c anion
11
Q
what is an action potential and how is it initiated?
A
- rapid series of changes in RMP
- may possibly take many sub-threshold stimuli to reach threshold
- once threshold (-50 to -55 mV) is reached by a supra-threshold stimulus, action potential fires
12
Q
polarisation
A
when there is a difference of charge in ECF and ICF (+ve or -ve)
13
Q
resting state
A
- neuron not transmitting action potential
- RMP: -70 mV
- Na+ and K+ channels closed
14
Q
what is the threshold for an action potential and what does this mean in terms of ion flow?
- also what are 2 ways to reach the threshold?
A
- -50 to -55 mV
- point where enough voltage-gated Na+ channels have opened to balance the leakage of K+ ions out
- 2 ways to reach threshold (summation): temporal (same neuron successively firing) or spatial (several neurons firing)
- all or nothing response
15
Q
depolarisation
A
- Na+ ions come in due to opening of Na+ channels
- ICF becomes more positively charged
- K+ channels closed
16
Q
repolarisation
A
- charge returns to RMP after depolarisation
- Na+ channels inactivated and K+ ions start to move
17
Q
hyperpolarisation
A
- K+ goes out due to opening of K+ channels
- Na+ channels begin to reset and close
- cell becomes more negative and then slowly returns to RMP
18
Q
action potential stages
A
- resting > threshold > depolarisation > depolarisation > hyperpolarisation > rest > refractory
19
Q
what is a graded potential?
A
- smaller, localised changes in RMP
- caused by opening of gated ion channels (voltage, ligand, mechanical)
- ‘graded’ = have varying magnitudes based on size of stimulus whereas AP = all or nothing
- spread bidirectionally unlike action potentials
- slower and die out with distance b/c leakage of ions causes loss in current
- can trigger APs in surrounding membranes
- occur @ diff sites than APs
20
Q
equilibrium potential of Na+ and K+
A
- Na+ = +60mV
- K+ = -90mV
21
Q
states of Na+ voltage-gated channels
A
- closed (resting phase): can open if there’s a big enough stimulus
- opened by activation gate (depolarisation): Na+ can enter
- inactivated (cannot open regardless of stimulus) - blocked by inactivation gate (repolarisation)
22
Q
states of K+ voltage-gated channels
A
- closed (resting phase)
- opened (depolarisation): K+ can exit
23
Q
absolute vs relative refractory period
A
- absolute: when another AP cannot be elicited no matter the stimulus (usually during repolarisation b/c Na+ channels are inactivated and haven’t reset yet - unable to open)
- relative: when AP can be elicited but with a stronger stimulus (usually when K+ channels are open during hyperpolarisation and start of rest)
24
Q
where is an AP generated and why?
A
- initial origin site (axon hillock)
- highest proportion of sodium channels so lowest threshold needed to produce an AP
25
Q
two modes of conduction of an AP
A
- contiguous conduction (unmyelinated): spread along every patch of membrane down the length of the axon
- saltatory conduction (myelinated): AP jumps over nodes of Ranvier
26
Q
is myelin part of the neuron?
A
- no - separate schwann cells / oligodendrocytes wrap around the axon
27
Q
2 factors which influence speed of AP propagation
A
- diameter of axon: larger axons are faster but take up more space
- degree of myelination: ions can’t penetrate lipids so acts as insulation to speed up transmission
28
Q
demyelinating diseases of CNS and PNS
A
- CNS: MS
- PNS: Guillain-barre syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP)
29
Q
2 types of synapses
A
electrical and chemical
30
Q
electrical synapse
A
- ions flow passively via gap junctions
- bidirectional transmission (very small delay)
- only between neurons
- useful for quick, coordinated movements - shorter distance
- e.g. burst of hormone secretion, CNS and heart
31
Q
chemical synapse
A
- neurotransmitters released from presynaptic neuron via exocytosis (chemical messengers)
- main mechanism of synaptic transmission
- slower, unidirectional transmission
- can be to other neurons or to effector cells (e.g. muscles) - CNS and PNS
- longer distance
32
Q
process of chemical synaptic transmission
A
- action potential arrives @ axon terminal > depolarisation
- voltage-gated Ca2+ channels open > influx of Ca2+ ions
- vesicles release NTs into synaptic cleft via exocytosis
- Ca2+ is removed from axon terminal - either taken up by mitochondria OR ejected from neuron via active Ca2+ pump
- NT diffuses across synaptic cleft and binds to specific receptor on postsynaptic neuron, opening ion channels which causes a GP
- postsynaptic neuron is either excited or inhibited based on which receptor the neurotransmitter binds to
33
Q
why is there a chemical synaptic delay?
A
- takes time for neurotransmitter to be released, diffuse across synaptic cleft and bind to receptors on PSN
34
Q
CNS neurotransmitters
A
- excitatory: glutamate
- inhibitory: GABA, glycine
- all amino acid NTs
35
Q
PNS neurotransmitters
A
- excitatory: Ach, adrenaline, NA
- inhibitory: NA
- all amine NTs
36
Q
difference between amino acid/amine NTs and peptide NTs
A
- amino acid/amine: made in cytosol of axon terminal and bundled into vesicles + faster transmission
- peptides: made in cell body and transported to axon terminals in secretory granules + slower transmission
37
Q
EPSP vs IPSP
A
- excitatory post synaptic potential: GP that causes depolarisation (closer to threshold)
- inhibitory: GP that causes hyperpolarisation (further from threshold)
- note: post synaptic neurons can receive input from both EPSPs and IPSPs and then the cell body decides whether the threshold has been reached or not > AP
38
Q
2 types of neurotransmitter receptors
A
- ionotropic and metabotropic
39
Q
ionotropic receptor
A
- receptor combined w/ ion channel
- ion channel opens when ion (ligand) binds
- rapid but short lived transmission
40
Q
metabotropic receptor
A
- ion channel + separate receptor
- NT binding to the receptor triggers a cascade of events (G-proteins) which leads to opening of ion channel
- slower response but amplifies response of initial neurotransmitter
41
Q
3 ways the action of a NT is terminated
A
- taken back up into pre-synaptic neuron
- degraded by enzymes
- diffuse away from synapse
42
Q
KDR (potassium delayed rectifier) channel
A
- activated by depolarisation
- increases rate of decay of the AP
43
Q
what does the GABA ionotropic receptor conduct?
A
- Cl- ions
44
Q
nervous tissue embryology
A
- ectoderm
- neural plate forms CNS
- neural crest forms PNS
