neuronal communications Flashcards
what are receptor cells
specialised cells which respond to a specific stimulus by initiating an action potential (electrical impulse)
why is a receptor known as a transducer
it transforms stimulus energy into electrical responses (nerve impulses)
what do rods and cones do
generate an action potential and send it on to a sensory neurone
what is a pacinian corpuscle
location?
pressure receptor
at the ends of sensory neurones
rod and cone in retina:
stimulus
energy change involved
changes in light intensity
light to electrical
olfactory cells in nose
stimulus
energy change involved
chemicals in the air
chem to electrical
chemical receptors in taste buds
stimulus
energy change involved
chemicals in food
chem to electrical
pacinian corpuscles in skin
stimulus
energy change involved
changes in pressure on skin
kinetic to electrical
meissners corpuscles in skin
stimulus
energy change involved
touch and pressure
kinetic to electrical
organ of Ruffini
stimulus
energy change involved
heavier pressure
kinetic to electrical
proprioreceptors (stretch receptors)
stimulus
energy change involved
changes in muscle length
kinetic to electrical
hair cells in inner ear
stimulus
energy change involved
movement
kinetic to electrical vibration
vibration receptors in ear
stimulus
energy change involved
movement
kinetic to electrical
baroreceptors
stimulus
energy change involved
movement
kinetic to electrical
osmoreceptors
stimulus
energy change involved
solute conc of blood
chem to electrical
what is a sensory adaptation
neural or sensory receptors in the brain change/reduce their sensitivity to a continuous, unchanging stimulus
e.g. smells of house, weight of clothes
when may an organism show a decrease in response to a stimulus?
example?
after repeated presentations
e.g. animal may learn to ignore a stimulus which used to elicit stronger response due to repeat exposure (habituation)
what is sensitisation?
opposite of habituation: over time, an organism may become more sensitive due to exposure e.g. oversensitivity to noise
what is a nerve
an enclosed bundle of nerve fibres/neurones/cells
parts of human nervous system?
CNS (central)
PNS (peripheral)w
what is the CNS
brain
spinal cord
relay neurones
what is the PNS
cranial and spinal nerves containing sensory and motor neurones
parts of PNS?
autonomic NS
somatic NS
what is the somatic NS
voluntary movements and involuntary reflexes
output to skeletal muscle via motor neurones
what is the autonomic NS?
involuntary
output to smooth muscle, glands, cardiac muscle or internal organs
parts of autonomic NS?
parasympathetic NS
sympathetic NS
what is the sympathetic NS?
internal alarm: fight or flight responses
neurotransmitter is noradrenalaine
accelerator nerves
what is the parasympathetic NS?
relaxing responses: rest and digest
neurotransmitter is acetylcholine
many axons in the vagus nerve
what is the spinal cord
a column of nervous tissue running down the back
neurones feed into and come out of it
number of nerves connecting spinal cord w various body regions
31
what is a ganglion
swelling that contains lots of synapses/cell bodies
what is grey matter
synapses, unmyelinated relay neurones and numerous cell bodies
what is white matter
myelinated axons of neurones, relatively few cell bodies
what do pacinian corpuscles respond to
pressure
where are pacinian corpuscles found
the skin
what is at the centre of a pacinian corpuscle
what is at the end of this
a single sensory neurone
stretch-mediated sodium channels
mechanism of pacinian corpuscle sending AP
in resting state (resting potential of -65mV), SM Na+ channels are too narrow for Na+ to pass through
pressure is applied to pacinian corpuscle, stretching the capsule out of shape and deforming the capsule and the nerve ending inside of it. this causes the Na+ channels to open so it diffuses in
this depolarises the membrane and changes the potential difference (mV)
increased +ve charge inside the axon is called the generator potential
harder pressure= more channels open=greater generator potential
if pressure= big enough, gen. potential big enough to trigger action potential, which passes along sensory neurone
below threshold potential (-55mV), only LOCAL depolarisation caused so no action potential fired and no info to brain
as pressure increases, APs produced more frequently
describe ‘all or nothing’ repsonse
a certain level of stimulus, the threshold value, always triggers a repsonse
if this is not reached, no AP will be triggered
threshold value= minimum gen potential needed to generate an AP
the AP always has the same magnitude
summary of pacinain corpuscle mechansim
each PC surrounds a nerve ending on a sensory neurone
when vibration applied to PC, lamellae are compressed, stretching part of the neuronal membrane
this deformation enlarges SM Na+ channels, permitting the entry of Na+
this causes depolarisation of the membrane (change in electric potential, called a generator potential)
if GP large enough, will reach threshold potential, and an AP will be triggered, causing the neurone to fire
in this way, PC acts as a transducer bc converts kinetic stimulus to elec impulse
if stimulus intensity small, GP small, threshold not reached so no AP fired
what is a reflex
a response to a change in the environment that does not involve any processing in the Brian to co-ordinate the movement
same stimulus produces same response every time
allow the body to make
examples of reflex
knee jerk= somatic reflex involving the skeletal muscles
pupil reflex= autonomic reflex involving smooth muscle
why r reflexes useful
involuntary adjustments to changes in external environment to help control internal environment
what is a monosynaptic reflex
reflex arc containing only one synapse e.g. sensory->motor
what is a reflex arc
when the receptor and effector are in the same region
components of myelinated sensory neurone
synaptic endings and bulbs
axon (short)
cell body containing nucleus (outside CNS)
Schwann cell
nodes of ranvier
myelin sheath
dendron (long)
neurilemma
dendrites
components of motor neurone
cell body (in CNS)
dendrites
axon
nodes of ranvier
myelin sheath
Schwann cell
synaptic endings
synaptic bulbs
fraction of peripheral neurones that are myelinated
1/3
what is the myelin sheath made up of
Schwann cells (glial cell) wrapped tightly around the neurone
how does myelin sheath form
each time the Schwann cells grow around the axon, a double layer of phospholipid bilayer is laid down (20 layers of membrane)
myelin sheath kept alive by Schwann cell nucleus and cytoplasm which is squeezed into the periphery as the sheath forms
length of Schwann cell
1mm
name of gaps between Schwann cells
how long are the gaps
nodes of ranvier
2-3um
myelin sheath function
prevents ion movement across the neurone membranes so movement can only occur at the nodes of ranvier
so impulse jumps from node to node (saltatory conduction), making the conduction more rapid
non-myelinated neurone structure
enveloped by the Schwann cell but several neurones are enclosed loosely by the Schwann cell and there are no extra layers or wrapping or phospholipid bilayer so no myelin sheath is formed
non-myelinated neurone ion movement
ion movement is not prevented so the action potential travels across the neurone in a wave (continuous conduction) rather than jumping form node to node and so the transmission is slower
speed of transmission in myelinated vs non-myelinated neurone
100-120ms-1
2-20ms-1
length of myelinated vs non-myelinated neurones
long: up to 1m
shorter
myelinated vs non-myelinated neurones: associated w Schwann cells?
yes: wrapped around
yes: but surround many axons
myelinated vs non-myelinated neurones: myelin sheath/nodes of ranvier
both
neither
myelinated vs non-myelinated neurones: conduction of impulse
saltatory
continuous
myelinated vs non-myelinated neurones: function
carry AP over long distances quickly
co-ordinate actions where speed is less important e.g. digestion
what is speed of conduction of an impulse determined by>
diameter of axon
myelination
temperature
how does diameter of axon determine speed of conduction
greater diameter= faster transmission
(if narrow, there is increased resistance to flow of ions (current) so therefore it is slower)
how does myelination determine speed of conduction
120m/s myelinated, 0.5m/s nonmyelinated bc:
Na+ and K+ cannot diffuse through myelin sheath, so ionic movements can only occur at nodes of ranvier
therefore local currents (diffusion of Na+ down axon) are elongated from one node to next
AP jumps from node to node= saltatory conduction=faster transmission
how does temperature determine speed of transmission
increased KE so ions diffuse more quickly along axon
similarities between motor and sensory neurones
often long and can transmit APs over long distances
cell surface membranes contain gated ion channels that control entry/exit of Na+, K+, Ca2+
neurones maintain PD across plasma membrane
contain cell body w/ nucleus, mitochondria, ribosomes, ER
dendrites to connect w other neurones
axon carries impulses away from cel body
surrounded by Schwann cells
contain Na+/K+ pumps which use ATP to AT Na+ out and K+ into cell
differences between motor neurone and sensory neurone
MN have terminal cell body in CNS, SN have centralised cell body in PNS
MN have v long axon, carries AP to effector, SN have axon which is shorter than their dendron and carries AP to CNS
MN have no dendrons but have dendrites connected directly to cell body, SN has one long dendron which branches into dendrites
MN carries AP from CNS to effector, SN carries AP from receptor to CNS
MN starts at CNA and ends at motor end plate, SN starts at sensory recpetor and ends at CNS
what is the potential difference
inside a resting axon always has a slightly -ve elec potential compared w the outside (diff=potential difference, -65mV)
how is resting potential in axon maintained
due to distribution of various ions
while at rest, conc of Na+ ions higher on outside and once of K+ ions higher inside.
sodium potassium pump: 3Na+ OUT, 2K+ IN, ensures Na+ outside high, K+ inside high (SALTY BANANA)
membrane less perm to Na+ bc all VG channels closed
some K+ channels open so some diffuse out, adding to buildup of +ve charge outside
FD opposes AT of Na+/K+ pump: there is conc grad for Na+ ions to diffuse into axon and K+ to move out, but membrane more perm to K+ bc most of Na+ channels closed but K+ ones open (diffuse out down conc grad)
K+ ions leak out rapidly, cannot be replaced by sodium readily, influx of K+ never watched outflow of sodium: this combined w presence of -ve anions, which r too large to leave, results in inside of axon being -ve relative to outside
how can you investigate ionic basis of a nerve impulse
replace ions w radioactive isotope and trace movement across axon membrane
what is the change in the potential difference when a neurone is stimulated
action potential
(-65mV to +40mV)
magnitude of AP
+40mV
stages of action potential generation
resting potential
depolarisation
repolarisation
hyperpolarisation
redistribution of ions
describe resting potential
membrane polarised at -65mV inside compared to outside
the generator region of the neurone is stimulated (either due to actions at a synapse or receptor stimulation)
describe depolarisation
Na+ channels open and Na+ diffuses in
axon becomes less -ve= generator potential
if threshold (-55mV) is met/exceeded, +ve feedback occurs, so many VG Na+ channels open
many Na+ diffuse in down electrochemical gradient
electrical potential= +40mV
describe repolarisation
vG Na+ channels close and VG K+ channels open
K+ diffuse out down electrochemical gradient
PD returns to normal (-ve inside, +ve outside)
describe hyperpolarisation
PD undershoots slightly, making the cell hyper polarised (more -ve than at rest) e.g. 90mV
describe redistribution of ions
Na+/K+ pump restores the normal distribution of ions e.g. lots of Na+ outside/K+ inside
electrical potential returns to rest
what is the nature of a stimulus determined by
the position of the receptors and the sensory neurone bringing the information
action potential summary step by step
neurone stimulated at receptor or synapse
Na+ channels open: Na+ diffuse into axon, generator potential
threshold reached, +ve feedback, VG Na+ channels open, many Na+ diffuse in
PD reversed (depolarisation)
more +ve inside +40mV
Na+ gates close
K+ VG channels open, K+ diffuse out, inside axon returns to -ve
membrane hyper polarised, more -ve than resting potential (refectory period). wave of depolarisation continues to next section of membrane
Na+/K+ pump re-establishes normal resting potential as ions redistributed
why can an axon not transmit another impulse straight after transmitting one
resting Na+/K+ distribution needs to be restored
membrane has to be repolarised
what is the period of inexcitability after the transmission of an impulse called
the refectory period
how long does a refectory period last
5-10ms
parts of a refectory period?
absolute refectory period
relative refectory period
when is absolute refectory period
how long does it last
during depolarisation
1ms
what is the absolute reafctroy period
no additional stimulus (no matter how strong it is) can produce an action potential bc Na+ conc is high in axon, Na+ channels already open
when is relative refectory period
how long does it last
during depolarisation and hyperpolarisation
5ms
what is relative refactory period
only a more intense stimulus can produce an action potential
importance of refectory period
AP is only propagated forwards towards the region which is not in the refectory period, therefore in 1 direction only
separates APs, bc by the time the 2nd AP is generated, the first has passed further down: this sets an upper frequency limit
what is a nerve impulse
a wave of depolarisation that moves along the surface of a nerve cell
APs are propagated along the neurone by the effect of Na+ ions entering the neurone
step by step formation of local currents (transmission of impulse) in a non-myelinated neurone
VG Na+ channels open and Na+ diffuses in
localised depolarisation= +40mV action potential
Na+ diffuse along to next region via local current (v short) from high to low conc
causes a slight depolarisation further along which meets threshold, causing VG Na+ channels to open so region goes to +40mV
why is a new AP only generated in one direction (ahead)?
the region behind is still recovering from the AP it just had and the distribution of ions is not yet back to normal (conc of Na+ ions behind AP is still high)
this region is incapable of producing a new AP for a short time (refectory period)
step by step saltatory conduction
stimulus causes Na+ to diffuse in
threshold potential reached so +ve feedback causes Na+ channels to open
AP fired (+40mV)
Na+ diffuses to next node via longer local current
node reaches threshold potential (-55mV) so VG Na+ channels open and AP fired (+40mV)
region behind AP depolarises and redistributes Na+ and K+ ions
myelin insulates axon, preventing ion movement, Na+ leakage and dissipation
how is the strength of a stimulus determined by the brain
by the frequency of the impulses along the neurone and the number of neurones carrying the action potential
why is saltatory conduction quicker
ion channels
myelination stops leakage
why is saltatory conduction quicker than the wave (ion channels)
it takes time to open& close ion channels and saltatory conduction uses minimum no. of channels as AP jumps from node to node. myelinated neurones have longer sections w/o VG Na+ channels (only found at nodes) so depolarisation only at nodes, so time saved
why is saltatory conduction quicker than wave (myelination)
myelin sheath prevents dissipation of signal by preventing Na+ leaking out through membrane over longer local currents. therefore signal decreases v little in strength. in unmyelinated neurone, Na+ ions can only travel v short distances to trigger AP in next closest region before dissipating
why does saltatory conduction use less energy
less Na+/K+ channels needed bc these are only found at nodes, so depolarisation only required at nodes
components of pre-synaptic neurone
axon
myelin sheath
VG Na+ channels
mitochondria
VG Ca2+ channels
presynaptic membrane
SER
synaptic veiscles
microfilaments
presynaptic bulb
function of SER in presynaptic neurone
packaging neurotransmitter into vesicles
components of post-synaptic neurone
(synaptic cleft)
ligand gated Na+ channels
acetylcholine esterase
postsynaptic membrane
examples of neurotransmitters
acetylcholine
noradrenaline
dopamine
serotonin
acetylcholine site of action
throughout nervous system
e.g. somatic: skeletal muscle contraction
parasympathetic: vagus nerve
acetylcholine function
excitation or inhibition
effects of drugs on acetylcholine
atropine blocks action in parasympathetic NS
curare blocks action on muscles
nicotine mimics action
strychnine stops action
botulinum toxin prevents release
noradrenaline site of action
sympathetic NS
noradrenaline function
excitation
effects of drugs on noradrenaline
amphetamines stimulate release
imipramine inhibits reabsorption
reserpine reduces storage in synaptic knob
dopamine site of action
brain
dopamine function
excitation
effects of drug on dopamine
chlorpromazine blocks receptors of post-synaptic membranes
serotonin site of action
brain
serotonin function
excitation
effect of drug on serotonin
LSD affects synapses
step by step synapse transmission
AP arrives at synaptic bulb
AP causes VG Ca2+ channels to open, so Ca2+ diffuses into cytoplasm of presynaptic neurone
Ca2+ causes vesicles containing ACh to fuse w presynaptic membrane, emptying ACh into synaptic cleft by exocytosis
ACh is released and diffuses across cleft
ACh mols bind w complementary ligand gated receptors in post synaptic membrane, causing them to open Na+ channels
Na+ diffuse in, depolarising membrane, GP generated. if sufficient combine, threshold reached and new AP generated
acetylcholine esterase hydrolysed ACh to ethnic acid and choline, which are recycled entering the synaptic bulb and combined using ATP and stored in vesicles again
what would happen if ACh remained bound to post synaptic membrane?
APs would fire continuously (Na+ channels would remain open)
leads to continuous contraction is muscles, so muscle fatigue, disrupting normal functions e.g. breathing
how long does synapse transmission take
from initial AP arrival to reformation of ACh, takes 5-10ms
what are cholinergic synapses
where are they located
synapses that use ACh
at neuromuscular junctions, in brain and spinal cord and within parasympathetic NS
what is ACh synthesised from
choline and acetyl-coA
packed into synaptic vesicles
how does cocaine affect synapses
prevents dopamine being recovered from synapses and taken back into presynaptic neurones
(dopamine= excitatory NT and its buildup leads to over-activation of its receiving cells)
how does heroin affect synapses
heroin inhibits release of GABA from presynaptic neurones
so fewer GABA molecules bind to post-synaptic receptors
GABA is an inhibitory NT so without its effect there is an increased probability of post synaptic APs
how does curare affect synapses
toxins from curare plant inhibit ACh receptors at neuromuscular junctions so blocks ACh binding so prevents muscle contraction
components of a neuromuscular junction
T-tubule
sarcolemma
motor end plate
(junctional folds of sarcolemma at motor end plate)
synaptic cleft
describe excitatory post synaptic potential
where membrane potential of post synaptic neurone moves closer to the threshold due to a small depolarisation as an NT causes opening of channels which allow +ve charges to enter the post synaptic neurone
describe inhibitory post synaptic potential
where membrane potential of post synaptic neurone moves away from the threshold due to a small hyper polarisation as an NT causes opening of channels which allow -ve charges (Cl-) to enter the post synaptic neurone and or positive charges (K+) to leave
what decides whether a certain NT is excitatory or inhibitory at a given synapse
which of its receptors are present on the postsynaptic cell
e.g. ACh has inhibitory effect on heart muscle but excitatory effect on skeletal muscle
is GABA inhibitory or excitatory
site of action
inhibitory in brain
roles of synapses
allow neurones to communicate
ensures 1 way transmission between neurones
divergence
summation
memory and learning
synaptic fatigue prevents overstimulation
allows weak background stimuli to be filtered out as only stimulation strong enough is passed on
roles of synapses: ALLOWS NEURONES TO COMMUNICATE
neuronal communication is a type of cell signalling
roles of synapses: ENSURES 1 WAY TRANSMISSION BETWEEN NEURONES
release of NT at pre-synaptic membrane and location of receptors on the post-synaptic membrane ensures the nerve impulse can only be transmitted in 1 direction
roles of synapses: DIVERGENCE
1 presynaptic neurone might diverge to many post synaptic neurones so 1 AP can be transmitted to several parts of the body and/or brain
e.g. reflexes: one pathway might cause response and another might inform brain
what is summation
a type of neuronal integration whereby all input from several post synaptic potentials are added together
what are the 2 types of summation
spatial summation (convergence)
temporal summation
roles of synapses: SPATIAL SUMMATION
a post synaptic neurone may receive excitatory and inhibitory potentials from many presynaptic neurones
the post synaptic neurone summates all the stimuli from all the neurones and produces a coordinated response
if the sum of the EPSPs overcome the sum of the IPSPs to reach threshold potential, an AP is generated (if IPSPs>EPSPs, membrane hyper polarises and no AP)
roles of synapses: TEMPORAL SUMMATION
repeated stimulation of the same synaptic ending in rapid succession may occur until sufficient NT is released to allow EPSPs to combine to reach threshold potential and produce an AP
this ensures only stimulation that is strong enough is passed on
if a low level stimulus is persistent it can be amplified
roles of synapses: MEMORY AND LEARNING
strengthening of specific pathways in the nervous system is the basis of memory
if the brain frequently receives information about 2 things at same time, new synapses form in the brain between the neurones involved
synaptic membranes are adaptable: e.g. made more sensitive to ACh by addition of more receptors so more likely to fire AP
roles of synapses: SYNAPTIC FATIGUE PREVENTS OVERSTIMULATION
synaptic transmission becomes progressively weaker with prolonged and intense excitation
constant stimulation leads to a reduction in NT release from a synapse: the synapse is said to be fatigued and we have become habituated to the stimulus
over time the number of NT receptors in the plasma membrane can decrease too
roles of synapses: ALLOW WEAK BACKGROUND STIMULI TO BE FILTERED OUT AS ONLY STIMULATION STRONG ENOUGH IS PASSED ON
constant background stimuli e.g. smell of house are filtered out: only changes in the intensity of the stimuli are significant to the nervous system
a low-level stimulus may generate an AP in the presynaptic neurone which may be unlikely to cause an AP in the postsynaptic neurone bc several vesicles of NT must be released for this to occur
a more intense stimulus may lead to an increased frequency of APs which leads to more NT release and an AP firing in the postsynaptic neurone
what is multiple sclerosis
the immune system attacks the protective sheath (myelin) around neurones
Demyelination disrupts the messages travelling along nerve fibres. It can slow them down, jumble them, accidentally send them down a different nerve fibre or stop them from getting through at all.
effects of MS
communication problems between your brain and the rest of your body. Eventually, the disease can cause permanent damage or deterioration of the nerve fibers.
numbness, weakness, lack of coordination
describe and explain how the resting potential is established and how it is maintained in a sensory neuron
Na+/K+ pump uses ATP to pump 3Na+ out and 2K+ into the neurone
membrane is less permeable to Na+ as fewer Na+ channels are open (VG ones closed)
K+ can diffuse freely out of neurone
large numbers of negative anions inside
positive ions build up outside
symptom of MS
difficulty co-ordinating movement/speech/swallowing
features of synapse= only allow transmission in one direction
how is this achieved
only presynaptic neurone releases NT
only presynaptic neurone has Ca2+ channels
only postsynaptic neurone has receptors for NT
NT broken down at postsynaptic membrane
importance of acetylcholine esterase at synapses
breaks down ACh to acetate and choline, which return to presynaptic neurone for recycling
prevents constant stimulation of post synaptic membrane
explain how Ca2+ ions enter neurone
depolarisation causes VG Ca2+ channels to open
Ca2+ diffuses through channels in the membrane via facilitated diffusion
explain why there is a delay between impulse arriving at sensory neuron and depolarisation of next neruone
cleft between them
Ca2+ enter synaptic bulb
movement of synaptic vesicles
diffusion of NT
receptor/channels opening on postsynaptic membrane
explain why NTs must be removed from postsynaptic receptors and from synaptic cleft
to allow repolarisation to occur
prevents Na+ channels remaining open
so new AP can be generated
to avoid continuous contraction
to allow recycling of NT
botulinum toxin stops nerve impulse transmission at synapses
suggest how this may occur
inhibits ACh synthesis/ secretion
prevents uptake of Ca2+ so no ACh crosses synaptic cleft so no AP
or blocks Na+ channels so threshold not reached so no AP
or inhibits acetylcholine esterase so no removal of ACh from receptors so no repolarisation
describe roles of synapses in nervous system
pass APs between neurones one-way
filters out weak stimuli (high threshold)
amplification (lower threshold)
temporal summation (several impulses at high frequency can be integrated from one presynaptic neurone)
spatial summation (several impulses from different neurones arriving at same post synaptic neurone integrated)
learning and memory form new synapses
explain what transmembrane ligand gated ion channel means
spans cell surface membrane
opened by binding of specific substance e.g. GABA
pore through which ions like Cl- can pass
