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A2 Biology
Chap 15: Control and Coordination
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How myelin sheath increases the speed of conduction
of
nerve impulses.
Myelin
insulates
axon
Action
potential
(AP) only at
nodes
of
Ranvier
Local
circuits
set up between
nodes
Saltatory
conduction → AP/impulses
jump
from node to node
Importance of the myelin sheath in the transmission of action potentials:
Myelin sheath
insulates
axon,
preventing
ions from passing through
Allows for
saltatory conduction
, where the impulse travels/jumps from node to node
Action
potential
only occurs at the
node
of
Ranvier
Transmission of impulses is
faster
Longer
local circuits are produced between nodes
Events at a synapse leading to the release of acetylcholine:
Action potential
occurs at the
presynaptic membrane
Ca2+ channels open
, allowing
Ca2+
ions to
enter
the presynaptic neuron through
facilitated diffusion
Vesicles
containing
acetylcholine
(
ACh
)
move
and
fuse
to the
presynaptic membrane
Exocytosis
of
ACh
releases it into the
synaptic
cleft
Role of acetylcholinesterase in the synapse:
Breaks down
ACh
in the synaptic cleft and
recycles
them
ACh leaves the
binding site
, stopping
depolarization
in the
postsynaptic membrane
Stops continuous
action
potential
Roles of synapses in the nervous system:
Ensures
one-way
transmission of impulses
Interconnects
nerve pathways
Integrates
impulses
Involved in
memory
and
learning
How an action potential arriving at the neuromuscular junction can result in depolarization of the sarcolemma:
Ca2+
channels
open
in the
presynaptic
membrane
Ca2+
enters the presynaptic neuron
Vesicles
containing
ACh
/
neurotransmitters
move
towards and
fuse
with the
presynaptic
membrane
ACh is released through
exocytosis
and diffuses across the synaptic cleft
ACh
binds
to
receptors
on the
sarcolemma
Na+
channels open, allowing
Na+
to enter the
sarcoplasm
and causing
depolarization
Describe how the response of the sarcoplasmic reticulum to the arrival of an AP leads to the contraction of striated muscle.
When sarcoplasmic reticulum (SR) is
depolarised
Voltage gated
Ca2+
channels open
Ca2+
diffuses
down the concentration gradient
Binds
to
troponin
which
changes
shape
Tropomyosin
is displaced/
moves
Binding sites are
exposed
Allows
globular
heads
of
myosin
to bind to
actin
(cross bridges formation)
Power stroke
→ myosin
moves
and
pulls
actin
Main features of thick and thin filaments in the sarcomere
Thick filaments
Myosin
Fibrous
protein
Globular
heads
M
lines
Thin filaments
Actin
Globular
protein
Consists of
troponin
and
tropomyosin
Z
lines
Describe how tropomyosin and myosin are involved in the sliding filament model of muscle contraction.
Tropomyosin:
Covers
myosin
binding sites
on
actin
When
calcium
ions bind to
troponin
/
tropomyosin
→
moves
/changes shape
Allows myosin to
bind
to actin → forming
cross bridges
Myosin:
ATP
hydrolysis
Myosin head
pivots
Myosin heads
binds to actin and forms
cross
links
with
actin
ADP and Pi
detaches
Myosin head returns to
previous
position
Actin is
moved
New
ATP
binds
Myosin
detaches
from actin and cross bridges
break
Explain the role of ATP in the contraction of striated muscle.
Myosin head
binds to
actin
→ forms
cross bridges
ADP
released causes motion of
myosin heads
Actin moves -
power stroke
ATP binds to
myosin heads
Myosin
head
detaches
from actin
Myosin head moves back to
original
position
ATP
needed to pump Ca2+ back into
SR
Describe the role of calcium ions in the contraction of striated muscles.
Voltage gated
Ca2+
channels
open
Ca2+
diffuses out of
SR
and into
sarcoplasm
Ca2+
binds to
troponin
which causes it to change shape
Tropomyosin
moves/displaces
Exposes
myosin-binding
sites
Globular
heads of
myosin
binds to these site (
actin
) and
cross
links
Power
stroke,
myosin
moves and
pulls
actin →
contraction
of muscle
Describe how the production of AP in the leaf cells of the Venus fly trap can result in the leaves closing and trapping the cell. [5]
AP
reaches
lobe
-
hinge
cells
H+
pumped out of the cell/into the cell
wall
Cell
wall
loosens and
cross-links
are broken
Calcium pectate
dissolves
Ca2+
enters cell,
decreases
WP
Water
enters through
osmosis
Cells
expand
and become
turgid
Leaves become
concave
Describe how venus fly trap produces AP to digest insects.
2
sensory hairs stimulated within
30
seconds //
1
sensory hair stimulated
twice
AP
travels
Ca2
+ channels open → Ca2+
diffuses
into
gland
cells
Stimulates
vesicle-containing
digestive
enzymes
to
move
and
fuse
to CSM
Exocytosis
of digestive enzymes → digest insects
Describe sequence of events that follows the uptake of water by grain wheat
Embryo
produces/releases
gibberellin
Gibberellin moves into
aleurone
layer
Gibberellin
stimulates production of
amylase
Amylase moves into
endosperm
Hydrolyse
/break down
starch
to
maltose
Maltose converted to
glucose
Glucose moves into
embryo
For
respiration
/
ATP
production
For
growth
Describe how auxin contributes to elongation growth.
Auxin
binds to
receptors
on
CSM
Stimulates
ATPase proton pumps
to pump
H+
ions → from
cytoplasm
to
cell wall
Acidify
cell wall,
decreasing
pH
Activates
expansins
→
loosen bonds
between
cellulose microfibrils
K+ channels
open
, K+ diffuses in → Influx of
K+
Decrease
WP, increase osmosis of water through
aquaporins
Cell
elongates
due to an
increase
in internal pressure
How is resting potential maintained?
Sodium-potassium pumps in axon membrane - 3 Na+ out, 2 K+ in
Many large, negatively charged molecules in axon - attracts K+ ions
Impermeability of axon membrane - Na+ cannot diffuse through axon membrane when neurone is at rest
Closure of voltage gated channels
How membrane potential changes
Impulse
reaches
threshold
potential
(
-50mV
)
Depolarisation
Repolarisation
Hyperpolarisation
Refractory
period
Resting
state
When action potential is stimulated:
Sodium
channel proteins
open
Na+ ions pass
into
the axon down
electrochemical
gradient
Depolarisation
:
decreases
potential difference, inside becomes less negative/more positive and reaches
threshold potential
(
-55mV
)
All
or
nothing
principle
Positive feedback - triggers
more
voltage gated
sodium
channels
to
open
,
more Na+ enters
- reaches
30mV
Action potential
is generated
Repolarisation and refractory period
After
1
ms, all
Na
+ voltage gated channels
close
K
+ voltage gated channels
open
- K+ diffuses
out
Repolarisation: returns to
potential difference
(-70mV)
Short period of
hyperpolarisation
K+ voltage gated channels
close
,
refractory
period -
recovery
and
unresponsive