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control systems
9.5-6 nervous transmission
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structure of a neurone
cell body
dendrons
Myelin sheath
node of ranvier
axon terminal
cell body
contains
nucleus
and
organelles
dendrons
extensions from cell body
from
dendrite
to the
cell body
axon
extension
of the cytoplasm
from
cell body
to
axon terminal
myelin sheath
consists of
schwann
cells around axon
insulates
axon
prevents
movement
of ions
node of ranvier
gaps
between
schwann
cells
axon
terminal
releases
neurotransmitters
onto
cells
of target
organs
resting potential
Na
+ channels closed but
leaky
-
small
amount of sodium ions diffuse into neurone
K+
channels
closed
but
more
leaky - more ions diffuse out of neurone
Sodium-Potassium
ion pumps
actively
transport
3Na
+ ions out and
2K
+ ions in
more + ions are being pumped
out
cytoplasm of axon is more
negative
than outside
stops
action
potential
membrane is
polarised
-70mv
stages of an action potential
depolarisation
repolarisation
hyperpolarisation
return to
resting
potential
depolarisation
energy from
stimulus
received e.g
pressure
Na
+ gated channels
open
Na+
ions
diffuse down the
electrochemical
gradient INTO the cell via facilitated diffusion
potential difference across membrane now more +
-55mv = threshold potential reached. action potential initiated
Axon membrane is depolarised
other Na+ gated channels open
+40mv = max action potential reached. Na+ channels close. K+ channels open
repolarisation and hyperpolarisation
Na
+ channels close
K
+ channels open - causing other
K
+ channels to also open
K
+ ions diffuse OUT of neurone, down the electrochemical gradient
Charge of axon is
lowered
(
potential difference
across membrane is more -)
K+ channels are
slow
to close
overshoot
of K+ ions diffusing out
potential difference
across membrane more - than
resting
potential
charge in axon drops to
-90mv
membrane is
hyperpolarised
refractory
period
time in which
action
potential cannot be generated and
depolarisation
cannot occur
occurs after
hyperpolarisation
(
-80mv
)
2 types:
Absolute
and
relative
absolute refractory period:
membrane cannot be stimulated at all
relative refractory period:
membrane needs a
larger
than
normal
stimulus
importance of refractory period
limits frequency of impulse transmission
ensures
unidirectional
impulses (in one direction)
propagation of
unmyelinated
neurone
Na+
ions diffuse into axon via gated channels
inside of axon is more positive
Na+ ions diffuse laterally (both directions) along axon
first section of membrane is depolarised
local current established
caused by Na+ ions causing more gated channels to open and diffuse in
so threshold is reached in next section of membrane
impulses are conducted faster in
myelinated
neurones than unmyelinated neurones due to
saltatory conduction
saltatory conduction
Na+ gated channels are only present in the
nodes of ranvier
myelin sheath prevents
depolarisation
of membrane in all other areas
because there are no Na+ channels there so no
action potential
Na+ ions
diffuse
from one node to the other
so action potential jumps from
node
to
node
Factors affecting speed of transmission
axon diameter
- larger the diameter,
faster
the rate of transmission, less resistance to ion flow
temperature - larger the temp,
faster
the rate of transmission,
faster diffusion rate
synaptic transmission
action potential
reaches axon terminal - membrane is polarised
causes
Ca
+
gated
channels to open
Ca
+ ions diffuse into the
presynaptic
knob
which causes vesicles containing
neurotransmitters
(e.g. acetylcholine) to fuse with
presynaptic
membrane
neurotransmitters are released via
exocytosis
into the synaptic cleft and diffuse across
bind to
neuroreceptors
on the membrane of
postsynaptic
knob
causes
Na
+
channels
to open and diffuse into knob
causing membrane to become
depolarised
once
threshold
is reached,
action potential
is generated.
Excitatory Post synaptic potential
Na
+ channels open in post synaptic membrane
Na
+ ions diffuse into membrane
post synaptic cell becomes more +
charged
action
potential occurs
Inhibitory post synaptic potential
Cl-
channels open in post synaptic membrane
chloride
ions diffuse into membrane
post synaptic cell more -
charged
action potential
inhibited
role of neurotransmitter -
acetylcholine
causes muscle
contraction
causes
inhibition
of
parasympathetic
neurones
e.g.
decreased
heart rate
what happens to
acetylcholine
in
synaptic
cleft?
hydrolysed
by
acetylcholinesterase
into
acetate
and choline
diffuse
back into
presynaptic membrane
ATP used to
reform
them for
storage
in vesicle
role of neurotransmitter - noradrenaline
increases
rate of
heart contraction
and
breathing rate
increase
force of
skeletal muscle contraction
nicotine
mode of action:
mimics
acetylcholine
binds to
acetylcholine
receptors
effects:
increased
heart rate
and
blood pressure
stimulates
dopamine
release
causing
addiction
lidocain
mode of action:
blocks
Na
+
gated
channels
cannot enter
post synaptic
neurone
action potential is not generated -
inhibitory
effects:
anaesthetic
pain signals prevented to
brain
cobra venom
mode of action:
block
acetylcholine receptors
irreversibly
in
post synaptic membrane
na+ channels
permanently open
effects:
paralysis
(cant repolarise due to permanent opening)
death
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