Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Biology 🧬 > nervous system > Flashcards

nervous system Flashcards

1
Q

muscle contraction

A
  • action potential depolarises sarcolemma, spreads down t-tubules to sarcoplasmic reticulum
  • causes Ca2+ to be released into sarcoplasm
  • Ca2+ binds to protein on tropomyosin, causing it to change shape
  • causes tropomyosin to be pulled out of binding site
  • exposes binding site and allows myosin to bind
  • creates an actin-myosin bridge
  • myosin pulls actin (requires energy)
  • ATP attaches to myosin head, causes actinomyosin bridge to break
  • ATP is hydrolysed, energy released to re-cock myosin head, binds to different BS further along actin
  • process repeats (if Ca+ present)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is a receptor?

A

detect specific stimuli
(each detect one specific stimulus eg light or pressure)

resting potetial - difference in charge across membrane

stimulus excites membrane - more permeable to ions, more in and out

results in change of potential difference = generator potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is a pacinian corpuscle?

A

mechanoreceptor
only detect mechanical stimuli - eg pressure or vibrations
found in skin

sensory nerve ending wrapped in lamellae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

activation of a pacinian corpuscle

A
  • pressure deforms membrane
  • causes stretch mediated sodium ion channels to open
  • sodium ions flow in
  • depolarisation
  • leads to generator potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

control of heartbeat

A
  • SAN (wall of right atrium) sends wave of electrical activity over the atria
  • this causes both atria to contract at the same time
  • non-conducting tissue stops the impulse reaching the ventricles
  • waves transferred from SAN to AVN
  • AVN passes waves of electrical activity to bundle of His
    this carries waves from ventricles to apex of heart
  • bubble splits into pukinje fibres which carry waves up the muscular walls
  • causes ventricles to contract at same time from the bottom up

(slight delay before AVN reacts to allow atria to empty)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

control of heart rate

A
  • stimuli detected by chemoreceptors (chemicals) and baroreceptors (pressure)
  • in aorta and carotid arteries
  • impulse sent along sensory neurone in autonomic NS to medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

increasing heart rate

A

due to increased rate of respiration in muscles

  1. chemoreceptors detect rise in CO2
    or baroreceptor detect low blood pressure
    - in aortic arch or carotid arteries
  2. sends impulses to cardiac centre in medulla
  3. increased frequency of impulses to SAN along sympathetic NS
  4. noradrenaline released (bind to SAN) increases frequency of impulses from SAN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

decreasing heart rate

A

due to increased blood pressure or decreased respiration

  1. chemoreceptors detect high O2, pH or low CO2
    baroreceptors detect high blood pressure
    - in carotid arteries or aortic arch
  2. sends impulses to cardiac centre in medulla
  3. increased frequency of impulses to SAN along parasympathetic NS
  4. acetylcholine released (binds to SAN) decreases frequency of impulses from SAN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is a resting potential?

A
  • when the neurone isn’t being stimulated
  • outside of membrane more + than inside
    (more positive ions outside)
  • membrane is polarised (there’s a difference in charge across membrane)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how is a resting potential made?

A
  1. sodium potassium pump moves Na+ out of axon and K+ into axon
    - by active transport
  2. creates an Na+ electrochemical gradient, more Na+ out than in
  3. K+ diffuse out of axon
    - through K+ channels, by FD
    sodium ion channels closed (can’t get back in)

creates more + charge on outside than inside axon
- membrane is polarised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

action potenial

A
  1. stimulus triggers Na+ channels to open
    - Na+ diffuse down gradient into axon
  2. if potential difference reaches threshold, more Na+ channel open, more diffuse in
    - inside of axon becomes less -
    (depolarisation)

creates wave of depolarisation
- some Na+ diffuse sideways
- causes channels further down neurone to open

  1. repolarisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

repolarisation

A

getting neurone back to resting potential for next impulse

  1. Na+ channels close
  2. K+ channels open
    - so diffuse out down gradient

start to get membrane back to resting potential
- outside becomes more + again

  • hyperpolarisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is hyperpolarisation?

A

K+ channels slow to close
- too many K+ diffuse out axon
- potential difference becomes more - than resting potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the all or nothing principle?

A

once threshold is reaches, action potential will fire
- all same size

bigger stimulus doesn’t mean bigger action potential
- instead increases frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the refractory period + its purpose?

A

period of time after action potential when neurone cannot fire as membrane is not sufficiently polarised

means action potentials are:
- unidirectional
- cant overlap (discrete)
- limited frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is saltatory conduction?

A

action potential jumps between nodes of ranvier
on myelinated neurones
- increases speed of condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

3 factors that affect speed of conductance

A
  1. myelination
  2. axon diameter
  3. temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how does myelination affect speed of conductance?

A

myelin sheath acts as an electrical insulator
- made of Schwann cells with nodes of ranvier between (bare membrane)
- Na+ channels concentrated there

SPEEDS UP rate of conductance

depolarisation only happens at nodes of ranvier and jumps between them

in non mylenated neurones, depolarisation must happen along whole axon, slower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does axon diameter affect speed of conductance?

A

larger diameter = faster

less RESISTANCE to flow of ions in cytoplasm

means depolarisation can reach other parts of membrane faster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how does temperature affect speed of conductance?

A

increased temperature = faster

ions have more kinetic energy so can diffuse faster

but only increased to certain temperature
- proteins begin to denature (in carriers)
- speed decreases

21
Q

2 types of summation

A

temporal
- 2 or more impulses arrive in quick succession from SAME presynaptic neurone
- action potential more likely as more NTs released into synapse

spatial
- many presynaptic neurones can join to one post synaptic neurone
- small amounts of NTs released from each can be added to reach threshold
- therefore more likely to trigger AP

22
Q

what is summation?

A

NTs released from one neurone may not be enough to reach threshold

NTs released from multiple impulses/ neurones added tighter to reach threshold
and fire an action potential

23
Q

Excitatory neurotransmitters

A

Depolarise lost synaptic membrane
Fires action potential if threshold met

24
Q

Inhibitory neurotransmitters

A

Hyperpolarise post synaptic membrane
(Potential difference more negative)
Prevents it firing action poteinal

25
Q

difference between inhibitory and excitatory neurotransmitters

A

inhibitory
- hyperpolarise postsynaptic membrane more
- prevents an action potential

excitatory
- depolarise postsynaptic membrane
- action potiential more likely to be fired, if threshold met

26
Q

transmission across a synapse

A
  1. action potential reaches synaptic knob
    - causes calcium ion channels to open
  2. calcium ions diffuse into presynaptic neurone
    - influx causes vesicles (containing NTs) to move to presynaptic membrane and fuse
  3. vesicles release acetylcholine into synaptic cleft
  4. diffuses across and binds to specific receptors on post synaptic membrane
  5. causes Na+ channels to open in postsynaptic
    - influx causes depolarisation
    - if threshold met, action potential fired
  6. acetylcholine broken down (acetyl and choline) by acetylcholinesterase - products reabsorbed into presynaptic knob
27
Q

why is transmission across a synapse unidirectional?

A

specific receptors only on postsynaptic - can only bind to one side
neurotransmtter only released from one side

acetylcholine broken down and removed from synapse - stops reaction happening

28
Q

transmission across a neuromuscular junction

A

synapse between neurone and muscle cell (sarcomere)

works the same as a normal synapse
but:

  • spreads dwon t tubules
  • postsynaptic membrane has more receptors than other synapses
  • has folds called clefs which store acetylcholinesterase
  • acetylcholine always excitatory - more likely to trigger action potential and therefore response in muscle

leads to depolarisation of sarcomere and musce contraction
sarcomere has t tubules

29
Q

how can drugs affect synapse transmission?

A

drugs can:

block receptors
- can’t be activated
- reduces transmission

mimic neurotransmitters
- same shape
- more receptors activated
- increase transmission

stimulate/ inhibit release of NTs
- more/ less receptor activated
- increase/ decrease transmission

inhibit enzyme that breaks down NTs
- more left in synapse to bind to receptors
- increase transmission

30
Q

structure of skeletal muscles

A

made of muscle fibres
- large bundles of long cells
- membrane called sarcolemma

contain myofibrils - organelles
made of actin and myosin

parts of sarcolemma fold inwards into sarcoplasm - t tubules

sarcoplasmic reticulum in sarcoplasm
- sots and releases Ca+

  • many mitochondria to provide ATP
31
Q

structure of myofibrils

A

contain myosin - thick myofilaments
actin - thin myofilaments

A bands - dark
- thick myosin and overlapping actin
I bands - light
- thin actin filaments

myofibril made of short units - sarcomeres
z line - end of each sarcomere
m line - middle of each sarcomere (and middle of myosin)
h zone - only myosin filaments (around m line)

32
Q

outline sliding filament theory

A

muscle contract as myosin and actin slide over each other

  • myofilaments themselves don’t contract
  • sarcomeres do
33
Q

how is ATP made for muscle contraction

A

aerobic respiration
- most generated by oxidative phosphorylation in mitochondria
- only works with oxygen, long periods of low intensity exercise

anaerobic repiration
- ATP made by glycolysis
- glycolysis makes pyruvate with is made into lactate
- builds up in muscle causing fatigue, good for short periods of intense exercise

phosphocreatine
(see next)

34
Q

how is phosphocreatine used to make ATP?

A

ATP made from phosphorylating ADP
- adding a phosphate from phosphocreatine

  • stored inside cells, generates ATP fast
  • used up very fast - used for short vigorous bursts

doesn’t require oxygen
doesn’t create lactate

35
Q

slow twitch muscle fibres

A
  • contract slowly
  • work for long period of time - without tiring
  • good for endurance activities eg maintaining posture
  • energy released slowly by aerobic respiration (many mitochondria and blood vessels for O2)
36
Q

fast twitch muscle fibres

A
  • contract quickly
  • get tired very fast
  • good for fast, short movements eg sprinting
  • energy released fast by anaerobic respiration using glycogen (few mitochondria and blood vessels)
37
Q

2 respiratory substrates

A

amino acids
fatty acids and glycerol from lipids

38
Q

how are amino acids used as a substrate?

A

deaminated =
3c molecule used to make pyruvate
4/5c compounds used in Krebs cycle

39
Q

how are lipids used a substrates?

A

glycerol phosphorylated
= triose phosphate
fatty acids converted to acetyl

40
Q

How do photoreceptors work?

A

Covert light to electrical impulses

Light absorbed by light sensitive optical pigments
Light bleaches pigments, causing chemical change
- change alters membrane permeability to Na+
Generator potential created if reaches threshold, impulse along bipolar neurone

41
Q

Cone cells

A

Concentrated in fovea
Colour vision

less sensitive to light (best in bright)
- one cone joins one neurone
- takes more light to reach threshold to trigger action potential (not added)

high visual acuity
- close together and one cone joins one neurone
- light from 2 points generates 2 action potentials (one from each cone) so point can be distinguished

42
Q

Rod cells

A

Peripheral parts on retina
Black and white

sensitive to light (work well in dim)
- many rods join to one neurone
- many weak generator potentials combine to reach threshold for action potential

low visual acuity
- many rods join same neurone
- light from two close points can’t be told apart, only generate one action potential

43
Q

activation of rod cells

A
  • rhodopsin breaks down when light shines on it
  • into retinal and opsin
  • results in generator potential produced

ATP needed to resynthesise rhodopsin

44
Q

How is colour seen?

A

Rod and cones have differential optical pigments -> sensitive to different wavelengths of light

3 types of cone cells, with different optical pigments
Red, green and blue SENSITIVE

Stimulated in different proportions to see different colours

45
Q

On a graph… why does potential/charge increase?

A

Sodium ion channels open
Influx of sodium ions
Have positive charge (so increase charge)

46
Q

On a graph… why does potential/charge decrease?

A

Sodium ions channels close
Potassium ion channels open, diffuse in

47
Q

Potential difference of membrane (on graph)

A

Resting potential (flat section)
- potential difference across membrane
- polarised
- outside more positively charge (more + ions)

Action potential (going up)
- depolarises membrane
- Na+ channels open, diffuse in
- makes inside of neurone less negative
- increased PD across membrane

Repolarisation (going down)
- Na+ channels close and K+ open
- membrane back to resting
- more + on outside

Hyperpolarisation (dip after peak)
- K+ channels slow to close
- too many K+ diffuse out
- potential difference more negative then resting

48
Q

what is a generator potential?

A

change in potential difference (across a membrane) due to a stimulus

bigger stimulus excites membrane more (potential difference changes more) so bigger generator produced

if generator potential big enough (threshold met) - triggers action potential

Biology 🧬 (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions