Unit 6 - Response to Stimuli Flashcards
what changes in their environment do organisms respond to & what is the effect?
organisms detect & respond to internal & external stimuli
–> increases survival chances & increases chances of reproduction so passes on beneficial alleles
why is there always a strong selection pressure?
to avoid danger/predation
to detect prey
to avoid toxic build up e.g. CO2
to ensure effective O2 delivery by altering heart rate
what is the purpose of taxis & kinesis?
they are simple movements that can maintain a mobile organism in a favourable environment
describe kinesis
simple, non-directional movement of mobile organism
in response to unfavourable stimulus
changes the speed at which the organism moves & the rate at which it changes direction depending on conditions
in response to non-directional stimulus e.g. temperature
in kinesis, what happens if an organism is in favourable conditions (or has just moved from favourable to unfavourable conditions)?
rate of changing direction increases to increase chances of returning to favourable conditions quickly
in kinesis, what happens if an organism is in unfavourable conditions?
rate of changing direction decreases so organism moves in straighter line to increase chances of finding a location with favourable conditions (surrounded by +ve stimuli)
describe taxis
more advanced than kinesis
directional movement of mobile organism towards favourable conditions & away from unfavourable conditions
+ve taxis = towards stimulus
-ve taxis = away from stimulus
in response to directional stimulus e.g. light, chemicals, gravity etc.
describe tropism & example
plant growth response (or part of a plant)
in response to directional stimulus
enable favourable conditions for max. growth
e.g. shoots show +ve phototropism & -ve gravitropism
roots show -ve phototropism & +ve gravitropism & +ve hydrotropism
what causes tropism in plants?
uneven distribution of IAA auxin, which causes uneven cell elongation & growth
what do plants produce to control growth & responses to light & gravity?
hormones
what is the benefit of phototropism?
to aid photosynthesis
what is the benefit of gravitropism?
to obtain water, mineral ions & better anchorage
what does IAA stand for?
indolacetic acid
describe the response of shoots to light from directly above? (phototropism)
IAA diffuses evenly to both sides of the shoot
so even cell elongation & growth on both sides
so shoot grows straight up
describe the response of shoots to light from one direction? (phototropism)
IAA diffuses to shaded side of the shoot
so cells on shaded side elongate more & grow faster than cells on sunny side
so shoot grows towards light
what is the effect of the force of gravity on IAA?
the force of gravity causes IAA to accumulate on the underside of roots & shoots
describe gravitropism (response to gravity) in roots
- cells in root tip produce IAA
- IAA diffuses & accumulates on underside of root due to the force of gravity
- IAA inhibits cell growth & elongation on underside of root
- so cells on upperside grow faster & elongate more than underside cells
–> so roots grow downwards in the direction of gravity
+vely gravitropic
describe gravitropism (response to gravity) in shoots
- cells in shoot tip produce IAA
- IAA diffuses & accumulates on underside of shoot due to force of gravity
- IAA stimulates cell growth & elongation on underside of shoot
- so underside cells grow faster & elongate more than upperside cells
–> shoot grows upwards against gravity
-vely gravitropic
describe the organisation of the nervous system
CNS: brain, spinal cord
peripheral nervous system (PNS):
sensory pathways (S neurones from receptor to CNS)
motor pathways:
somatic/voluntary NS - conscious control e.g. movement
autonomic/involuntary NS - subconscious control e.g. heart rate: sympathetic - stimulate effectors & speed up
parasympathetic - inhibits effectors & slows down
what is a reflex & e.g.?
a rapid, short-lived, localised & involuntary response to a dangerous/harmful stimulus
e.g. removing hand from hot object
what makes a reflex rapid?
very few synapses (chemical message is slower than electrical impulse)
short neurone pathway
does not go to conscious part of brain
why are reflexes important? classic exam Q
to decrease or avoid damage - give e.g. related to Q
to escape from predators
to maintain balance/posture
role in homeostasis
describe the reflex arc (in exam, relate to Q)
- stimulus e.g. sharp pin
- receptor - pressure/mechanoreceptors in skin detect stimulus & generate potential in sensory neurone
- sensory neurone transmits action potential to spinal cord in CNS
- relay/intermediate neurone links sensory neurone to motor neurone
- motor neurone transmits action potential from spinal cord (CNS) to effector = muscle or gland e.g. muscles on finger/arm
- effector - muscle contracts/gland secretes e.g. finger/arm muscle contracts
- response e.g. pull finger/hand away from sharp object
from Seneca: function of dendrites, axon & cell body
dendrites carry impulse towards cell body
axon - away
cell body - where nucleus is located
what is the structure of a myelinated motor neurone?
one long axon
many dendrites - large SA for receiving action potentials (APs) from relay neurone
cell body - contains organelles, lots of RER & mitochondria for protein synthesis (channel proteins) & neurotransmitters
Schwann cells - wrap around axon, provide protection & electrical insulation & contains myelin sheath
nodes of Ranvier - gaps b/w Schwann cells where there is no myelin sheath
what are 3 functions of Schwann cells?
electrical insulation
phagocytosis
nerve regeneration
how does an AP travel along a neurone? (general structure)
by saltatory conduction
from one node of Ranvier to the adjacent node
what makes neurones excitable?
have resting potential & 3 protein transporters:
1. sodium-potassium pump
works all the time
all over the neurone
- open Na+ & K+ channels all over the neurone
there are more K+ channels than Na+ channels - membrane is more permeable to K+ - voltage-gated channels
sensitive to charge around them
all over axon
lots on axon hillock (mainly VgNa+)
describe the neurone when it has no membrane potential (theoretical)
- equal conc. K+ & Na+ inside & outside of axon
no membrane potential: 0mV
no diffusion of K+ & Na+
describe the neurone when decreasing membrane potential
sodium-potassium pump uses active transport to move 3 Na+ out & 2K+ into axon
–> increase conc. K+ & decrease conc. Na+ in axon
no K+ & Na+ diffusion
so overall decrease in # of positively charged ions in membrane –> decrease in membrane potential: -10mV
describe the neurone when creating & maintaining a resting membrane potential
sodium-potassium pump uses active transport to move 3 Na+ out & 2K+ into axon
K+ diffuses out of axon by fac. dif. via open channel proteins down electrochemical gradient
Na+ diffuses into axon by fac. dif. down electrochemical gradient
axon membrane is more permeable to K+ than Na+ so conc. of positive ions inside axon decreases to -65mV = resting potential
what are the essential factors for creating & maintaining resting potential?
- sodium-potassium pump actively transports 3Na+ out & 2K+ into axon using ATP
- axon membrane is more permeable to K+ (bc it has more K+ channel proteins) so more K+ diffuses out of axon than Na+ diffuses in
how is resting potential established (2 marker)?
- membrane is more permeable to K+ than Na+ bc it has more K+ channels
- sodium-potassium pump actively transports 3Na+ out & 2K+ into axon
establishes electrochemical gradient
what is a generator potential?
a small depolarisation of the neurone’s membrane potential, causing a deviation from the resting potential at -65mV
define depolarisation
the neurone’s membrane becomes less negative due to an influx of Na+ ions
where do generator potentials occur?
at receptor cells or sensory nerve endings e.g. in Pacinian corpuscle
what causes generator potentials?
energy transduction, where a receptor detects a stimulus in an energy form (as a result of an energy change)
this energy is used to open VgNa+
how is an AP caused (linked to generator potentials)?
if generator potential causes a large enough depolarisation of membrane (above -50mV) due to sufficient diffusion of Na+ into axon, AP triggered
what is the all or nothing law?
any stimulus that causes the membrane potential to reach/exceed the threshold value triggers an AP
all APs have the same magnitude
generator potentials below the threshold value of -50mV will not trigger an AP
describe the movement of Na+ ions when the stimulus is sub-threshold
- receptor detects a small energy change/stimulus
- some Vg Na+ channels open –> some Na+ diffuses into axon, down electrochemical gradient by fac. dif. –> membrane potential slightly less negative but does not reach threshold value of -50mV
- other VgNa+ channels do NOT open so no AP triggered
describe the movement of Na+ ions when the stimulus is above threshold
- receptor detects large energy change/stimulus
- many VgNa+ channels open –> lots of Na+ ions diffuse into axon down EC gradient –> large depolarisation of membrane
- this causes positive feedback = more VgNa+ channels to open –> greater influx of Na+ –> this reaches/exceeds the threshold value of -50mV so AP is triggered
all APs are the same amplitude no matter how large the initiating stimulus
what are the stages of the action potential?
resting potential
depolarisation
repolarisation
hyperpolarisation
restoring resting potential
what happens during resting potential?
-65 mV
sodium-potassium pump moving 3Na+ ions out & 2K+ ions into axon
VgNa+ & VgK+ channels closed
what happens during depolarisation?
generator potential up to -50mV
fac. diff. Na+ ions into cell down electrochemical gradient
membrane potential becomes more positive
at -50mV threshold, Vg Na+ channels open, causing influx of Na+
this causes positive feedback so more Na+ channels open
membrane potential increases to +40mV
what happens at +40mV?
Na+ equilibrium is reached at +40mV
VgNa+ channels close & VgK+ channels open
what happens during repolarisation?
VgNa+ channels close & VgK+ channels open
fac. diff. of K+ ions out of axon down electrochemical gradient
membrane potential becomes more -ve
what happens during hyperpolarisation?
when K+ ions diffuse out, membrane potential becomes more -ve than resting potential (as VgK+ channels are slow to close)
VgNa+ & VgK+ channels close
K+ equilibrium is reached at-90mV
what is the importance of the refractory period?
no AP can be generated in hyperpolarised parts of membrane
promotes separate impulses
ensures unidirectional impulse
creates a time delay b/w APs
limits frequency of AP
describe the passage of AP in an unmyelinated axon
- stimulus causes influx of Na+ ions so first section of membrane depolarises
- localised currents occur
- which causes VgNa+ channels further along membrane to open so neighbouring regions of membrane depolarise
- meanwhile, the previous region of membrane repolarises & is hyperpolarised then resting potential restored
describe the passage of AP in a myelinated axon
axon surrounded by myelin sheath produced by Schwann cells wrapping around axon
myelin is a mixture of lipids & acts as insulation
there are not VgNa+ or VgK+ channels in the axon membrane underneath the myelin
APs can only happen at Nodes of Ranvier, which are gaps b/w the myelin sheath
localised currents stretch b/w Nodes of Ranvier, speeding up the transmission of the impulse by 3 times
the impulse jumps b/w Nodes of Ranvier, which is saltatory conductance
what factors affect the speed of conductance of AP?
the myelin sheath
axon diameter
temperature
how does the myelin sheath affect the speed of conductance?
causes nerve impulses to jump from one Node of Ranvier to another, called saltatory conduction
this increases the speed of transmission
how does the diameter of the axon affect the speed of conductance?
the greater the diameter, the faster the speed of impulse
bc less leakage of ions from larger axons
so easier to maintain membrane potential
how does temperature affect the speed of conductance?
the higher the temperature, the faster the speed of impulse up to a point
increased temp. = increased rate of diffusion of Na+ & K+ ions bc increased KE
increased temp. = increased rate respiration so increased atp production for sodium-potassium pump
greater strength of stimulus
= greater frequency of APs
what is the function of a synapse?
electrical impulse cannot travel over junction b/w neurones
neurotransmitters send impulses b/w neurones & to effectors
new impulses can be initiated in several different neurones for simultaneous responses
define synapse
the gap b/w 2 neurones
the point where one neurone communicates with another neurone or w an effector
describe the structure of a cholinergic synapse
presynaptic neurone:
presynaptic knob:
lots of mitochondria
SER
VgCa2+ ion channels
synaptic vesicles containing neurotransmitter/acetylecholine (ACh)
synaptic cleft:
gap b/w neurones
postsynaptic neurone:
receptors complementary to neurotransmitter/ACh
ligand-gated Na+ channels
describe how an impulse travels across a cholinergic synapse
- When AP arrives, Na+ enters through VgNa+ channel. depolarisation of membrane causes VgCa2+ channels to open.
- Ca2+ ions enter via fac. dif., causing vesicles containing ACh to move towards presynaptic membrane (requires ATP)
- vesicles fuse with presynaptic membrane & release ACh into synaptic cleft (exocytosis)
- ACh diffuses across synaptic cleft towards post-synaptic membrane
- ACh binds to complementary receptors on ligand-gated Na+ channels on post-synaptic membrane. ligand-gated Na+ channels open so Na+ diffuses in
- this causes depolarisation of post-synaptic membrane so VgNa+ channels open so Na+ diffuses into axon so new AP initiated
how does a synapse ensure unidirectionality of impulse?
1- neurotransmitter only produced in presynaptic neurone
2- ligand-gated Na+ channels are only in post-synaptic membrane
so impulse always goes from presynaptic to postsynaptic neurone
what happens when ACh binds to ligand-gated Na+ channels?
ACh binds to receptor site
which causes conformational change in protein (3 structure changes)
so Na+ enters
why is ACh recycled?
too slow & energy costly to produce new ACh every time
describe how neurotransmitter/ACh is recycled
- enzyme acetylcholinesterase (AChE) binds to ACh & hydrolyses ACh into acetyl + choline so it is released from receptors & ligand-gated Na+ channels close
prevents overstimulation of skeletal muscle cells
- choline is reabsorbed into presynaptic knob & recombined with acetyl in SER (requires ATP)
- ACh is packaged into vesicles for future use
define summation & name the 2 types
neurotransmitter from several sub-threshold impulses accumulate to generate an AP
temporal summation
spatial summation
define & describe the process of spatial summation
several simultaneous APs from different presynaptic neurones cause neurotransmitter release & converge onto one postsynaptic neurone
sub-threshold: if AP from only one presynaptic neurone, insufficient neurotransmitter is released
above threshold: if AP from more than one presynaptic neurone, sufficient neurotransmitter is released so AP triggered in postsynaptic neurone
define & describe the process of temporal summation
one presynaptic neurone has a high frequency of APs so releases neurotransmitter several times quickly
sub-threshold: no AP in postsynaptic neurone bc insufficient neurotransmitter released
above threshold: AP produced in postsynaptic neurone bc sufficient neurotransmitter released
what type of synapse is a cholinergic synapse?
excitatory
describe excitatory synapse
AP in presynaptic neurone increases chance of AP occurring in postsynaptic neurone
describe the process of transmission across an inhibitory synapse
AP in presynaptic neurone decreases the chance of AP occurring in postsynaptic neurone
1. neurotransmitter binds to & opens Cl- channels in postsynaptic membrane & K+ channels open
2. Cl- moves in & K+ moves out by fac. dif.
3. membrane potential becomes more -ve = hyperpolarised
4. reaching -50mV threshold for AP is less likely bc more excitatory neurotransmitter is needed
by what mechanisms do drugs increase & decrease synaptic transmission?
increase: inhibit AChE
mimic shape of neurotransmitter & bind to receptor site on ligand-gated Na+ channel so it opens
decrease: inhibit release of NT
decrease permeability of postsynaptic neurone to ions
hyperpolarise postsynpatic membrane
what is the function of receptors?
cells that detect stimuli (changes in the internal & external environment)
each receptor responds to…
thermo-
photo-
mechano-
chemo-
a different & specific type of stimulus
thermo- detect heat energy only
photo- detect light energy only
mechano- detect pressure only
chemo- detect chemicals only
define sensory reception & sensory perception
sensory reception: the function of receptors (receiving info.)
sensory perception: making sense of info. from receptors (interpretation) (largely the function of the brain)
describe 2 important features of receptors e.g. Pacinian corpuscle
- specific to a single type of stimulus: e.g. mechanical pressure only
- produces a generator potential by acting as a transducer
all stimuli involve change in energy
transducer/receptor converts this energy change into electrical nerve impulse/generator potential –> AP
e.g. PC transduces mechanical energy of stimulus into generator potential –> AP
where are PCs located?
deep in skin
lots in fingers & soles of feet
joints, ligaments & tendons where they allow organism to know which joints are changing direction (proprioperception)
what is the structure of PC?
see diagram
lamellae
capsule
blood capillary
sensory neurone ending
axon of sensory neurone
stretch-mediated Na+ channels
direction of AP
what are the lamellae of a PC?
layers of connective tissue with gel b/w them
how does the PC transduce mechanical energy into GP?
sensory neurone ending at centre of PC has stretch-mediated Na+ channels in CSM
when PC is deformed, the channels’ permeability to Na+ increases
describe the PC at resting state
the stretch-mediated Na+ channels are too narrow to allow Na+ to diffuse into the axon
PC has resting potential at -65mV
describe the process by which the PC causes an AP
when pressure is applied to the PC
lamellae are deformed & membrane around sensory neurone is stretched
this widens the stretch-mediated Na+ channels & Na+ diffuses into the axon of the sensory neurone
membrane depolarises & produces a GP
GP turns into AP if threshold value (-50mV) reached, which travels to CNS
what is the function of:
retina
fovea
blind spot
optic nerve?
retina: contains photoreceptors (rods & cones) & transmits APs to optic nerve
fovea: only cones, area of highest visual acuity
blind spot: no photoreceptors so light that falls on this spot is not perceived - exit of ganglion neurones of the optic nerve
optic nerve: transmits impulses generated in retina to cerebral cortex
what are the visual pigments of rods & cones?
rods: rhodopsin
cones: there are 3 different type of cone cells each with a different variant of iodopsin
what is the colour perception of rods & cones?
rods: monochromatic (black & white)
cones: trichromatic (blue, green & red bc of different iodopsin variants)
how many rods & cones are there in each eye?
120 million rods
6 million cones
what is the distribution of rods & cones?
rods: all over retina but not in fovea
exclusively rod cells in periphery of retina
cones: all over retina but greatest density at fovea
no cones at periphery
define visual acuity
clarity - ability to distinguish b/w 2 points close together
describe the visual acuity of rods
lower visual acuity
many rod cells converge onto one bipolar neurone = spatial summation = retinal convergence
2 points of light falling on retina are seen as one point bc only one AP sent
describe the visual acuity of cones
higher visual acuity
one cone cell joins to one bipolar neurone
2 points of light perceived as 2 distinct points
rod/cone –> bipolar neurone –>
ganglion neurone
describe rod cells’ sensitivity to light
more sensitive to light
bc rhodopsin breaks down more easily –> AP
also spatial summation effect of retinal convergence
/sufficient neurotransmitter released
= more likely to reach threshold value & trigger AP
describe cone cells’ sensitivity to light
less sensitive to light
as iodopsin breaks down less easily
to require higher light intensity to cause AP
also no retinal convergence
benefit to mammals of having different photoreceptor cells?
good all-round vision day & night
what is the autonomic nervous system & what 2 parts does it consist of?
part of the peripheral nervous system that controls involuntary processes
- parasympathetic nervous system - inhibits effectors –> slows down processes inc. decreases heart rate
- sympathetic nervous system - stimulates effectors –> speeds up processes inc. increases heart rate
describe cardiac muscle
makes up heart walls
myogenic - contraction is initiated from within itself (SAN) rather than from external impulses (like with skeletal muscles)
label diagram of the heart
see booklet
what is the cardiac cycle initiated by?
small area of cardiac muscle called the SAN/pacemaker which sets the rhythm for all other cardiac muscle ~65bpm resting hr
describe the sequence of events that control basic heart rate
- SAN send excitation wave of electrical activity over the atrial walls
- both atria contract
- the atrioventricular septum is non-conductive tissue that causes a delay b/w atrial & ventricular contraction
–> this allows atria to empty/ventricles to fill with blood fully - wave is conducted through the AVN
- AVN causes short delay before passing on the wave to Purkyne fibres that make up the Bundle of His
- the wave of electrical activity is transmitted to the apex the spreads upwards
- both ventricles contract from the apex upwards, pumping blood out the heart
what stimuli cause an increase in heart rate?
exercise (increased CO2)
stress/fear
low blood pressure
what are the functions chemo- & baro- receptors & where are they located?
chemoreceptors detect changes in pH
increased CO2 = decreased pH
baroreceptors detect stretch/pressure in blood vessels
both found in lining of blood vessels e.g. aorta & carotid arteries
what stimuli cause a decrease in heart rate?
recovery (decreased CO2)
rest
high blood pressure
how is heart rate increased?
- stimulus (specific to Q) is detected by receptors (specific to Q - chemo- detect increase in CO2 = decrease in pH or baro- detect stretch/pressure in blood vessels) in lining of blood vessels
- receptors send impulses to cardiac acceleratory centre in medulla
- more impulses are sent via sympathetic neurones e.g. cardiac nerve
- to the SAN
- then noradrenaline is released at an excitatory synapse
- this increases frequency of impulses to AVN
rate & force of contraction increases
cardiac output increases
blood pressure increases
what is the effect of increased cardiac output?
CO = HR X stroke volume (volume of blood pumped out the heart per beat)
more CO2 removed & more O2 delivered from muscles
how is heart rate decreased?
- stimulus (specific to Q) is detected by receptors (specific to Q - chemo- detect decrease in CO2 = increase in pH or baro- detect stretch/pressure in blood vessels) in lining of blood vessels
- receptors send impulses to cardiac inhibitory centre in medulla
- more impulses are sent via parasympathetic neurones e.g. vagus nerve
- to the SAN
- then acetylcholine is released at an inhibitory synapse –> K+ channels open, causing hyperpolarisation of post-synaptic membrane
- this decreases frequency of impulses to AVN
rate & force of contraction decreases
cardiac output decreases
blood pressure decreases
describe how muscles act in antagonistic pairs
muscles are usually found in antagonistic pairs
muscles are joined to the skeleton by tendons
muscles can only contract or relax - not push
contraction causes muscles to shorten & thicken
returning to long, thin state requires contraction of the antagonistic muscle
agonist vs antagonist
agonist = muscle that contracts
antagonist = muscle that relaxes
define voluntary muscle
controlled by nervous system
can be triggered voluntarily
describe the gross structure of skeletal muscle (see booklet for diagram)
tendon
connective tissue
muscle tissue is made up of thousands of muscle fibres
alternating light & dark bands
muscle fibres contain many myofibrils
define muscle fibre
many fused cells that form one continuous tubular cell with many nuclei (multinucleated)
define myofibril
individual contractile unit of a muscle made of actin & myosin
label & define parts of a single muscle fibre
sarcolemma - cell surface membrane
sarcoplasm - cytoplasm
sarcoplasmic reticulum - specialised form of SER. stores Ca2+ which is released to initiate muscle contraction
T(transverse)-tubules - in-folding of sarcolemma, which transmits action potentials into the fibre & close to each myofibril
many mitochondria - release ATP for muscle contraction (by sliding filament model) & active transport (of Ca2+)
define I band & how does it change when muscle contracts?
light band
only actin filament
narrower during contraction
define Z line & how does it change when muscle contracts?
thin, dark line in centre of I band where actin filament originate (think Zac)
move closer together during contraction
define A band & how does it change when muscle contracts?
dark band
myosin & actin overlap here
A band does not change size
define M line
thin, dark line in centre of A band (& H band) where myosin filaments are joined tail to tail
originate
define H band & how does it change when muscle contracts?
lighter section of the A band
only thick myosin filaments
decreases width as actin overlaps during contraction
define sarcomere & how does it change when muscle contracts?
functional unit of a myofibril
distance b/w 2 adjacent Z lines
sarcomere decreases during contraction as Z lines move closer together
what are the features of a contracted myofibril?
I band narrower - more overlap of actin & myosin
Z lines closer together - shorter sarcomere
H band narrower - more actin overlaps
NB A band stays same width as length of myosin filaments does not change
see booklet for diagram & electron micrograph
what is a neuromuscular junction?
where a motor neurone meets a muscle fibre
MN of somatic/voluntary nervous system
why are there many NMJ along the length of a muscle fibre?
to ensure different sections of muscle fibre contract together & powerfully, rather than weakly & as a wave of contraction
describe the process of transmission across a NMJ to cause a contraction of muscle fibre
1- AP arrives at presynaptic membrane
2- which causes Ca2+ ions enter neurone by facilitated diffusion
3- this causes ACh vesicles to fuse with presynaptic membrane & release ACh by exocytosis
4- ACh diffuses across the synaptic cleft & binds to ACh receptors on ligand-gated Na+ channels on the sarcolemma
5- ligand-gated Na+ channels open
6- Na+ enters & diffuses across sarcolemma & depolarises it
7- AP spreads along the muscle fibre membrane down T-tubules
this leads to contraction of the muscle fibre via sliding filament model
what are the similarities b/w a cholinergic synapse & NMJ?
similarities:
both have ACh neurotransmitter that is transported by diffusion
both have receptors that cause influx of Na+ when NT binds
both use a sodium-potassium pump to repolarise axon
both use enzymes to break down NT - AChE breaks down ACh
what are the differences b/w a cholinergic synapse & NMJ?
1- NMJ only excitatory vs CS can be excitatory or inhibitory
2- NMJ only involves motor neurones vs CS can involve motor, sensory & relay neurones
3- at NMJ ACh binds to receptors on sarcolemma vs at CS ACh binds to receptors on CSM on post-synaptic neurone
4- NMJ only links neurones to muscles vs CS links neurones to neurones or neurones to effector organs
5- AP ends at NMJ vs new AP might be produced along another neurone in CS
if lots of motor units are triggered to contract,
a large force is produced
describe the sliding filament model
1- AP/depol. of sarcolemma at motor end plate passes along sarcolemma down T-tubules
2- this causes Vg Ca2+ channels in sarcoplasmic reticulum membrane to open
3- Ca2+ is rapidly released from SR & Ca2+ ions diffuse into myofibril down conc. grad.
Ca2+ binds to spec. receptor (troponin), which causes tropomyosin to change shape, which exposes myosin binding site on the thin actin filament
4- myosin head attaches to actin binding site forming actin-myosin cross-bridge
ADP must be bound
5- detachment of ADP changes the angle of myosin head so actin filament is pulled along, which is the powerstroke generating force
6- ATP binds to myosin head causing detachment from actin binding site
hydrolysis of ATP resets myosin to original position
7- myosin can then bind to the next binding site on actin & continue to move the thin actin filament
what is tropomyosin?
long protein strand wrapped around actin
myosin is an ATPase
diagram of sliding filament model
see booklet
describe the process of muscle relaxation
when muscle is no longer stimulated by motor neurone:
1- Ca2+ is actively transported, using ATP, back into SR
2- low conc. of Ca2+ causes tropomyosin to change back to original shape & cover myosin binding site on actin filaments
3- myosin heads bind to & hydrolyse ATP, detaching from actin filaments & cannot re-bind
4- muscle can be stretched back, as actin filaments are pulled out of myosin filaments, to its original length by gravity or contraction of antagonistic muscle
describe muscle contraction under anaerobic conditions
most ATP generated by aerobic respiration in mitochondria, but active muscle might not get sufficient O2 to maintain sufficient ATP production
so it is important muscle function can be maintained under anaerobic conditions
but, glycolysis can only continue alongside lactic acid fermentation, which affects proteins involved in muscle contraction, which decreases force generated
describe the role of phosphocreatine in muscle contraction
PCr stored in muscles
PCr system provides an additional way of rapidly regenerating ATP under anaerobic conditions without lactic acid build up
provides phosphate to make ATP
ADP + PCr –> ATP + Cr
ATP –> PCr (store of P) at rest
short-term PCr store
PCr –> ATP during exercise
draw & explain graph of energy sources used in muscle during exercise
see booklet
define slow twitch muscle fibres
contract with less power & slower over a longer period of time
how are slow twitch muscle fibres adapted for endurance?
- contain many mitochondria for aerobic respiration
- lots of myoglobin O2-binding protein
- richer blood supply to provide O2 for aerobic respiration
- found in lower legs & back muscles - to maintain posture
define fast twitch muscle fibres
contract rapidly & powerfully over short period of time (but increased lactic acid = fatigue faster)
how are fast twitch muscle fibres adapted for explosive strength?
- more myosin filaments to generate greater contractile force per second
adapted for anaerobic respiration: - large PCr store
- large glycogen store to supply anaerobic respiration
used for weightlifting & sprinting - found in biceps, triceps etc.
define homeostasis
the maintenance of a constant internal environment within restricted limits, involving physiological control systems
describe the role of hormones in homeostasis (general)
hormones are produced in glands & secreted into blood stream - carried in plasma
they act on target cells which have specific receptors (3y) on CSM complementary to the specific hormone
effective in low concentrations
widespread & long-lasting effects
sometimes secondary messenger model
why is homeostasis important for enzymes?
change in temp causes change in 3y structure - H, ionic & disulfide bonds & change in function
change in pH causes “
why is homeostasis important for the water potential of the blood?
more -ve water potential (hypertonic - high blood glucose conc.) causes water to move out of cells & into blood by osmosis - cells shrivel & die
more +ve water potential (hypotonic - low blood glucose conc.) causes water to move out of blood into cells by osmosis - cells burst
blood should be isotonic so no net osmosis
outline the homeostatic control system
- receptor detects stimulus
- control centre coordinates information & response
- effector brings about response that returns conditions back to optimum = -ve feedback
- muscles contract
- glands secrete
define positive feedback
deviation from the normal causes changes that result in an even greater deviation from the normal/optimum
e.g. influx of Na+ during AP
define negative feedback
the change produced by the control system, to restore a variable back to the optimum, opposing the original deviation
e.g. blood glucose control, blood water potential control & thermoregulation
(most common)
describe thermoregulation as an example of negative feedback - when too hot
vasodilation of arterioles
more blood flow into capillaries near skin surface
so more radiation of heat from body
sweat more
increased evaporation of water
causes heat loss from body
describe thermoregulation as an example of negative feedback - when too cold
vasoconstriction of arterioles
less blood flow into capillaries near skin surface
so less radiation of heat from body
shivering = rapid muscle contraction
increased rate of respiration
exothermic reaction
produces heat
why is control of blood glucose important?
glucose is needed for respiration to produce ATP
in blood, glucose lowers water potential causing water to move out of cells by osmosis
describe the hormones that are involved in the control of blood glucose conc.
glucagon is produced by alpha cells in the islets of Langerhans in the pancreas
insulin is produced by beta cells in the islets of Langerhans in the pancreas
glucagon & insulin work antagonstically
only 1 acts at a time
have opposite effects
what is the role of the liver (the 3 main functions)?
- glycogenesis - the conversion of glucose to glycogen by the liver when blood glucose conc. is too high
caused by insulin - glycogenolysis - the breakdown of glycogen into glucose by the liver when blood glucose conc. is too low
caused by glucagon & adrenaline - gluconeogenesis - the production of glucose from glycerol & AAs (non-carb sources) when blood glucose conc. is too low
caused by glucagon
the liver is a target organ
it is where insulin & glucagon have the biggest effect
describe the process of the secondary messenger model - how glucagon & adrenaline work to increase blood glucose conc.
- adrenaline binds to receptor protein in the liver cell’s CSM
- binding of adrenaline causes protein on inside of CSM to change shape (3y)
- this activates adenylate cyclase enzyme, which converts ATP to cyclic AMP (cAMP)
- cAMP binds to protein kinase, which changes its shape & activates it
- activated protein kinase enzyme catalyses the conversion of glycogen to glucose (glycogenolysis)
glucose moves out of liver cell into bloodstream by facilitated diffusion
what is the purpose of insulin?
to decrease blood glucose conc.
what happens when insulin binds to glycoprotein receptor on the CSM of liver & muscle cells (target organs)?
- insulin binds to receptor on CSM causing a change in 3y structure of glucose channel proteins in membrane so they open
glucose moves in by fac. dif. from bloodstream - insulin causes vesicle with glucose channel proteins in membrane to fuse with CSM
more glucose channel proteins in CSM increases permeability of cell to glucose so increased uptake of glucose by fac. dif. - insulin activates enzymes that convert glucose to glycogen within cell = glycogenesis
how does the action of insulin reduce blood glucose conc.?
increases glucose absorption into liver & muscle cells
increases rate of glycogenesis
increases rate of respiration - uses up more glucose, which increases uptake into cells (maintains conc. grad.)
increases rate of conversion of glucose to fat
what happens, in terms of insulin, when blood glucose conc. has decreased?
beta cells stop producing insulin
-ve feedback
describe the role of glucagon
purpose: to increase blood glucose conc.
works by:
attaching to specific receptor proteins on CSM of liver cells (target organ)
activates enzymes that convert glycogen into glucose = glycogenolysis
activating enzymes that are involved in converting AAs & glycerol into glucose = gluconeogenesis
same mechanism as adrenaline
glucose released into bloodstream by fac. dif. & alpha cells stop producing glucagon -ve feedback
describe type 1 diabetes & its treatment
insulin dependent
disorder in which the body cannot produce insulin (due to beta cell damage & often autoimmune)
uncontrolled high blood glucose conc. & treated with insulin injections & managing carb. intake & exercise
describe type 2 diabetes & its treatment
insulin independent
obesity is a risk factor
body stops responding to insulin
due to glycoprotein receptors on CSM of body cells being lost or unresponsive
treated with carb. controlled diet & exercise regime
describe the structure of the kidney (gross)
renal cortex:
lighter-coloured outer layer of the kidney
contains Bowman’s capsule, PCT & DCT & blood vessels
medulla:
darker-coloured inner layer of the kidney
contains loop of Henle, collecting ducts & blood vessels
fibrous capsule - protects the kidneys
ureter - tube that carries urine to the bladder
renal vein - returns blood to the heart via the vena cava
renal artery - supplies blood to the kidneys from aorta
describe the structure of the Bowman’s capsule
at the start of the nephron
surrounds a bundle of glomerular capillaries called the glomerulus
what happens at the glomerular capillary?
filtrate is forced out of capillaries through pores due to hydrostatic pressure
what are the functions of the afferent arteriole & the efferent arteriole?
afferent: supplies the nephron with blood from renal artery
large diameter
efferent: carries blood away from Bowman’s capsule
small diameter
describe the structure & function of the proximal convoluted tubule
series of loops of tubule surrounded by capillaries
site of reabsorption of glucose & AAs
describe the structure of the loop of Henle
long hairpin shaped tubule that extends from cortex into medulla & surrounded by capillaries
descending limb - highly permeable to water
ascending limb - impermeable to water
describe the structure & function of the distal convoluted tubule
series of loops of tubule surrounded by capillaries
site of reabsorption of ions & some water
describe the structure & function of the collecting duct
DCT (from multiple nephrons) empties filtrate into collecting duct
ADH affects the permeability of the collecting duct, which has a vital role in osmoregulation
filtrate in collecting duct is now urine & is taken to bladder via ureter
describe the formation of glomerular filtrate by ultrafiltration
- blood enters Bowman’s capsule in afferent arteriole, passes through capillaries that form the glomerulus & exit via the efferent arteriole
- the diameter of the afferent arteriole is greater than that of the efferent arteriole which causes high hydrostatic pressure in capillaries
- small molecules e.g. water, glucose, AAs, ions & urea pass through pores in capillaries’ endothelial cells, the basement membrane & spaces b/w podocytes
- proteins & blood cells are too large so cannot pass through/stay in capillaries
describe the process of selective reabsorption of glucose, AAs & water by the PCT
- Na+ ions are actively transported out of epithelial cells by Na+-K+ pump, which reduces their conc. & establishes a conc. grad. of Na+ ions in epithelial cells
- Na+ ions move down conc. grad. by fac. dif. from lumen of PCT through co-transport proteins which carries other molecules e.g. glucose/AAs with it
- glucose/AAs move by fac. dif. into blood through channel proteins in basal membrane
NB waste products are not reabsorbed
how is the PCT adapted to its function?
epithelial cells have
1. microvilli, which gives a large SA for:
more channel proteins for fac. dif. & co-transport
more carrier proteins for AT
2. infoldings at base, which gives large SA for reabsorption into blood
3. lots of mitochondria to produce ATP for AT for Na+-K+ pump
4. lots of RER/ribosomes for high rate proteinsynthesis for lots of carrier & channel proteins
what is the function of the loop of Henle?
where water is reabsorbed into surrounding blood capillaries from the collecting duct, which concentrates urine so it has a lower water potential than the blood
what is the conc. of urine directly related to?
the length of the loop of Henle
the longer the loop of Henle, the more water can be reabsorbed by osmosis –> small vol. of v conc. urine
e.g. desert animals longer LOH than humans
compare the structure & function of the descending limb & ascending limb of LOH
descending limb - narrow & thinner walls
highly permeable to water
water leaves filtrate & goes into blood
ascending limb - wider & thicker walls
impermeable to water
Na+ pumped out from filtrate
counter-current multiplier
the LOH acts as a counter-current multiplier so maintains a water potential gradient for the whole length of the collecting duct
describe the process of maintaining a gradient of Na+ ions in the medulla by the loop of Henle
- Na+ ions are actively transported out of the ascending limb of LOH, using ATP
- this generates a lower WP in the interstitial region. thick walls impermeable to water so little water escapes
- descending limb is highly permeable to water so water moves out of the filtrate into capillaries by osmosis (–> heart by renal vein)
- the filtrate progressively loses water, lowering the WP inside the descending limb & reaches the lowest WP at the hairpin
- at the base of the ascending limb, Na+ ions move out by diffusion & further up by AT so WP increases
- in interstitial tissue, there is a gradient of WP b/w the ascending limb & collecting duct with the highest WP in the cortex & increasingly lower WP further into the medulla
- collecting duct is permeable to water so as water moves through, it passes out by osmosis into capillaries (& –> by renal vein)
- as water passes out filtrate, WP decreases & WP of interstitial tissue decreases so water continues to move out by osmosis down the whole length of the collecting duct = the counter current multiplier effect
describe the process of reabsorption of water by the DCT & collecting ducts
overall function of DCT: to make final adjustments to water & ions/salts that are reabsorbed into the blood & to control the pH of the blood by selectiving which ions are reabsorbed
first part of DCT = same function as LOH: reabsorption of ions into blood - final adjustment of blood ion conc.
2nd part of DCT = same function as collecting duct: water reabsorbed into blood
DCT & collecting duct have ADH receptors on CSM
how is the DCT adapted to its function?
cells that form the walls of the DCT have microvilli & many mitochondria to allow reabsorption ions rapidly from filtrate by AT out of DCT - see PCT
what are the causes of a decrease in water potential of the blood?
- too many ions or too little water being consumed
- overheating so lots of sweating
what are the causes of an increase in water potential of the blood?
- large vol. of water being consumed
- salts used in metabolism & excreted but not replaced from food
describe the process of osmoregulation in response to a decrease in water potential of the blood
- osmoreceptors in hypothalamus in brain detect decrease in WP
–> H2O is lost from osmoreceptors into blood by osmosis - hypothalamus sends more impulses to posterior pituitary gland, which is the effector
- pituitary gland releases more ADH into the blood & travels to kidneys
- ADH increases the permeability of the DCT & CD to water
- more water is reabsorbed into blood by osmosis, producing a smaller vol. of more conc. urine - conserves water
describe the process of osmoregulation in response to an increase in water potential of the blood
- osmoreceptors in hypothalamus in brain detect increase in WP
–> H2O enters osmoreceptors from blood by osmosis - hypothalamus sends fewer impulses to posterior pituitary gland, which is the effector
- pituitary gland releases less ADH into the blood & travels to kidneys
- permeability of the DCT & CD to water & urea decreases
- less water is reabsorbed into blood by osmosis from CD, producing a larger vol. of more dilute urine - removes excess water
describe how ADH increases the permeability of the collecting duct to water
- ADH binds to prot. receptors on CSM of DCT & CD, which activates phosphorylase
- phosphorylase causes vesicles containing aquaporins to fuse with CSM of DCT & CD
- more aquaporin channels increases the permeability to water so more water leaves CD & is reabsorbed by osmosis
(4. ADH increases urea permeability so more urea moves into interstitial region from CD = lowers WP of ISR)
–> smaller vol. of more conc. urine
define aquaporin
specific channel protein for water
