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202 Theme 1 > Lecture 6 Physiology of Neurons > Flashcards

Lecture 6 Physiology of Neurons Flashcards

1
Q

what are electrical synapses like compared to chemical synapses

A 
faster 
bidirectional 
much smaller gap -3.5nm
no plasticity (no learning)
no amplification
coupled via gap junctions
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2
Q

why is there no amplification in an electrical synapse

A

signal always weakened as transmitted from presynaptic to postsynaptic cell
(signal won’t transmit if postsynaptic cell is too much bigger than presynaptic)

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3
Q

what can’t excitatory presynaptic signal do in post synaptic cells

A

inhibit

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4
Q

what is spatial summation (of signals)

A

a neuron determines whether to fire based on amount of signals received from synapsing neurons
can then reach threshold

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5
Q

what is temporal summation of signals

A

input neuron is firing fast enough so that receiving neuron can add together signals (as can’t recover from small depolarisations fast enough) and reach threshold

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6
Q

what are the steps of an action potential

A 
threshold reached by stimulation
depolarisation
overshoot
repolarisation
after-hyperpolarisation with refractory period 
resting state
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7
Q

what are the important voltages in an action potential

A

rest -70mV (near Ek)
threshold ~-50mV
Vm>0 overshoot (reaches ~+30mV)
inward rectifiers open -60mV (delayed rectifiers already open- repolarisation)

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8
Q

what does action potentials being ‘all-or-none’ mean?

A

carry no info about size of stimulus that stimulated them

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9
Q

how do neurons code the intensity of their synaptic input

A

firing frequency

different neurons for different strength stimuli

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10
Q

how does firing frequency represent the intensity of the activity

A

increasing threshold lowers firing freq and increasing excitatory synaptic activity increases it

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11
Q

how do lengthy synaptic currents affect firing frequency

A

when lengthy synaptic currents are small they create higher threshold potential due to accommodation than larger currents

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12
Q

what is accommodation

A

of Na+
inactivates duding the slower subthreshold depolarisation
first response stronger than later responses

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13
Q

how do different neurons code intensity

A

light touch receptors vs pain receptors - specific neuron for each stimuli

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14
Q

what is excitability

A

how easy it is to start nervous signalling
aka sensitivity in sensory cells, irritability in muscle or effector cells
risk of seizure or spasms if too much

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15
Q

how does increased threshold effect excitability

A

lowers it

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16
Q

what are excitability changes the basis of

A

psychotropic pharmacology - changes in threshold have profound health and behavioural effects

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17
Q

what are channels made up of

A

proteins
sometimes they conduct ions, sometimes they don’t
have different conformational states

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18
Q

what controls voltage-gated channels

A

change states based on transmembrane voltage

open when membrane +ve so can conduct and increase permeability, closing when membrane depolarises

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19
Q

how are inward rectifiers affected by transmembrane voltages

A

inward rectifiers are the opposite of other channels

close when inside positive and open when negative

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20
Q

why is inactivated not the same as closed

A

both non conducting, inactivated is when channel stops conducting (after a delay) when membrane positive inside (closed is when negative)

21
Q

what happens to the membrane when Na+ channels open

A

positive inside as Na+ high on outside than inside

22
Q

what is the potential of the extracellular space

A

electrically joined in all cells so same voltage everywhere

extracellular fluid considered electrical ground

23
Q

what happens to the membrane when K+ channels open

A

negative inside as K+ higher on inside than outside

24
Q

what happens to the membrane when Ca2+ channels open

A

positive inside as Ca2+ higher on outside than inside

passively goes inward

25
Q

how do ionic permeabilities affect voltage

A

increased permeability to K+ makes membrane negative, Na+ opposite

26
Q

how is the voltage of the cell membrane determined

A

inter-related feedback loops
at rest Vm=~Ek
as conductance of K+ is greater than that of Na+ or Ca2+

27
Q

what is lidocaine

A

local anaesthetic, applied topically

28
Q

how does lidocaine work

A

raises the threshold so lowers excitability stopping local action potentials by blocking Na+ channels in pain neurons

29
Q

what is Carbamazepine

A

anticonvulsant

30
Q

how does carbamazepine work

A

inactivates sodium channels to raise AP threshold and lower excitability

31
Q

what are examples of other Na+ channel blockers

A 
antiarrythmic drugs (class 1 eg quinidine) work by lowering conduction velocity to extend refractory period 
fugu fish poison (tetrotoxin (TTX))
32
Q

how does Glibenclamide work

A

sulfonylurea to manage type 1 diabetes

increases excitability of pancreatic beta cells leading to increased insulin secretion (inhibit K+ channels)

33
Q

what is chemical force

A

force on an ion
aka diffusional force
based on difference in concentration across a membrane

34
Q

what is electrical force

A

force on an ion

based on membrane potential (Vm) which varies over time

35
Q

what is the equilibrium potential

A

Ek aka reversal potential of K+
voltage when K+ in(electrical)=out(chemical) as electrochemical forces are in equilibrium
same for other ions

36
Q

what is used to calculate equilibrium potential

A

Nernst Equation

37
Q

how do equilibrium potentials differ

A

the more permeable the cell membrane is to K+ the more the membrane potential approaches the value of Ek

38
Q

what are the equilibrium potentials of Ena, Ek, Eca, Ecl?

A 
ENa = +60  mV
EK  = -90  mV
ECa = +123 mV
ECl = -40  mV (in neurons –65 mV)
39
Q

how do ion channels control voltage

A

open channels conducting with little competition - membrane potential to that ion’s equilibrium potential
both open - halfway point between 2 equilibrium potentials

40
Q

what are action potentials (compared to graded potentials)

A

stereotyped electrical signal
short-duration
in most neurons, skeletal and cardiomyocytes
a spike
all or none
require time to start due to conformational changes

41
Q

what are graded potentials (compared to action potentials)

A 
electrically localised - membrane potential
last a long time
much flatter in shape
conducted almost instantly 
in receptor cells eg cones and rods
variable in duration and voltage
42
Q

how is electricity conducted in axons

A

passive
all + = - at start, Na+ moves in, increasing flow and -ve charges
all charges move simultaneously in same direction
depolarisation jumps to NofR’s - saltatory conduction

43
Q

what makes saltatory conduction down an axon faster

A

large diameter as less resistance

myelinated

44
Q

what are graded potentials issues with transmitting signals

A

changes in membrane potential don’t propagate far via passive electrical forces and voltage diminishes further from source - needs help

45
Q

why do voltage signals in graded potentials decrease further from the source

A

axon has a finite resistance

46
Q

how do graded potentials transmit action potentials

A

transmit along length of axon, the AP re-amplifies the signal but slows down transmission at the nodes due to conformational changes

47
Q

what is saltatory conduction

A

when action potential jumps from node to node for faster conduction velocity

48
Q

what are typical conduction velocities

A

100 m/s for alpha motor fibres (myelinated, 15 um diam.)

1 m/s for C nociceptive fibres (unmyelinated, 0.2 - 1.5 um)

49
Q

clinical uses for conduction velocity

A

Nerve conduction studies are used for evaluation of paraesthesias
numbness, tingling, burning
Evaluation of weakness of the arms and legs

202 Theme 1 (6 decks)

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