animal and plant responses Flashcards
what does Mimosa pudica do?
carries out a thignomastic response (non-directional touch response)
due to threat of herbivores
how does Mimosa pudica respond to herbivores?
leaves curl up because cells in leaf becomes flaccid
mechanoreceptors are stimulated by change in pressure so ions are pumped out (active) of leaf cells and H2O follows down water potential gradient into stem
explain 2 structural defences (anatomical adaptations) a plant may have to discourage consumption by herbivores
spikes, thorns and barbs may cause pain or may introduce a poison/allergen into the herbivore
lignin=woody impermeable molecule so very difficult to eat and digest
examples of chemical defences
phenols
flavonoids
tannins
why do plants use chemical defences against herbivores
provide a bitter taste to the herbivore to deter it
poisonous so act as non-competitive enzyme inhibitors to disrupt enzymes
example of pheromone
ethene
what are pheromones w/ example
gases that influence the behaviour of members of same species or herbivore
e.g. tomato plants can ‘alert’ other plants of impending threat by herbivores so become bitter
tropism definition
a directional growth response towards a stimulus
4 types of tropism
thigmotropism
phototropism
hydrotropism
geotropism
what is a thigmotropism
example
function
response to touch
e.g. vine growing around a wooden pole
supportive for plant
what is a phototropism (both kinds)
positive: shoots grow towards light ti obtain light energy for p/s
negative: roots grow away from light to access water and minerals in soil and provide stability
what is hydrotropism
function
growth towards water
obtain H2O which is a reactant for p/s
what are both kinds of geotropism w/functions
positive: roots grow towards gravity so plant can gain water and mineral ions from soil and the plant has better anchorage and support
negative: shoots grow away from gravity to obtain light energy for p/s
nastic response definition
non-directional response to a stimulus which may or may not include growth
explain how M.pudica closes up its leaves in response to touch
mechanoreceptors stimulated by change in pressure
ions pumped out of leaf cells’ vacuoles (Cl- and K+) (active)
H2O follows out down water potential gradient (bc water potential outside cell is more negative)
the flexor cells stretch, extensor cells become flaccid
leaf curls and cells become flaccid so stomata close
how might thigmonastic response in plants help them to survive?
e.g. M.pudica
appear smaller to herbivores so less likely to be eaten
discourages predation by insects
protection against fire bc less SA exposed
suggest why plant growth regulators are called hormones although they are not produced in endocrine glands
plant hormones must still bind to specific receptors
they are transported from their site of synthesis to their target
explain why only certain tissues in a plant respond to a particular plant hormone
hormones bind to specific complementary receptors on plasma membrane of specific cells to trigger a response (series of reactions)
these receptors are only present in certain tissues
3 ways that plant hormones can move around the plant
diffusion
active transport
xylem (dissolved in water as transpiration stream) (facilitated)
what are IAAs
auxins
what is the role of auxin
cell elongation
mechanism of auxin step by step
auxin released from meristematic cells at shoot tip and diffuses down shoot tip from high to low concentration
auxin binds to specific receptors on plasma membranes of cells in the shoot
activates proton pumps to actively transport H+ into cellulose cell wall
presence of H+ ions in the cell wall reduces pH and activates expansions, which catalyse breaking of H bonds between cellulose macrofibrils and microfibrils
cellulose cell wall is now flexible and elastic
water enters the cells and elongates the cells as it enters the vacuole
characteristics of the zone of cell differentiation
higher pH as les IAA present
expansins denature and H bonds reform in cellulose (no longer flexible)
what does apical dominance ensure
that trees/plants grow tall and obtain as much light energy as possible
what is apical dominance
auxin released from the apical shoot tip/bud inhibits growth of lateral branches/shoots
how do some hormones overcome apical dominance
apply cytokinins to overcome apical dominance and promote cell division and growth of lateral shoots
experimental example of apical dominance
one intact shoot and one decapitated
intact shoot: IAA produced from shoot tip promotes apical dominance so sugars produced in p/s are not used to promote lateral growth
decapitated shoot: source of IAA removed so lateral shoots can grow and sugars like sucrose can be repaired to produce ATP for growht
what does germination require
O2 (aerobic respiration)
warm temperature (KE for enzymes)
water (activates gibberellins)
mechanism of gibberellins in germination step by step
water is absorbed by seed to soften seed coat to allow young root (radicle) and young shoot (plumule) to break out of seed
gibberellins (gibberellin acid) are activated in the embryo. they diffuse from embryo to the aleurone layer, bind to specific receptors on the plasma membranes of cells. they initiate transcription/translation of genes encoding digestive enzymes e.g. amylase, protease, maltase
starch in seed digested by amylase into maltose which is digested by maltase into alpha glucose. proteins are digested by proteases to produce amino acids
examples of plant responses to abiotic changes/stresses
stomatal closure
leaf loss/abscission in deciduous trees
photoperiodism
freezing conditions
examples of plant responses to abiotic changes/stresses: STOMATAL CLOSURE
prevents wilting
1. low soil water potential is detected by the roots
2. ABA synthesised and travels up the xylem via the transpiration stream to the leaves
3. ABA binds to a specific receptor on the plasma membrane of guard cell and stimulus stomatal closure. ATP is used to pump ions out of guard cells, reducing the water potential outside of the cell so water moves out by osmosis down the WP gradient
examples of plant responses to abiotic changes/stresses: LEAF LOSS/ABSCISSION IN DECIDUOUS TREES and fruit drop
when auxin levels are high, leaves do not drop
when auxin levels drop, ethene levels increase, which triggers the transcription and translation of cellulase genes
cellulase digests cellulose cell walls and leaves/fruits drop/ are abscised
examples of plant responses to abiotic changes/stresses: PHOTOPERIODISM
a plant’s photoperiod related to the number of daylight hours required for flowering
controlled by a set of proteins called PHYTOCHROMES
examples of plant responses to abiotic changes/stresses: FREEZING CONDITIONS
some plants can synthesise antifreeze proteins in low temps, lowering the freezing point of the vacuole cell sap, enabling survival in cold winter months
ALSO in cold temps, SER synthesises cholesterol which intersperses itself between phospholipids, increasing the fluidity of the phospholipid bilayer
commercial uses of plant hormones
auxin to produce flowers, grow cuttings, produce seedless fruit and kill weeds
gibberellins to produce fruit, brew beer, produce cane sugar and breed plants
cytokinins to reduce lettuce wastage and clone plants
ethene
how are auxins used to produce flowers
prevents leaf and fruit drop so flowers can remain on shelves for longer
how are auxins used to grow cuttings
cutting taken between 2 nodes at an angle
lower leaves
cut stem dipped in rooting powder containing auxin
cut stem replanted in moist soil and covered with a transparent polythene bag
how are auxins used to produce seedless fruit
known as parthenocarpy
treat unpollinated flowers w/ auxin
promotes ovule growth and auxin release in the developing fruit
no seeds remain in the fruit
how are auxins used to kill weeds
promote excessive shoot growth (cell elongation) so stem cannot support itself, buckles and dies
how are gibberellins used to produce fruit
applied to grapes to elongate stalks, allowing grapes more space to grow. larger and less compact bunches w/ larger grapes produced
applying gibberellins can delay senescence (ageing) in citrus fruits to improve shelf life
working synergistically w/ cytokinins to elongate and improve shape of apples
how are gibberellins used to brew beer?
speeds up germination of barley seeds (amylases and maltase are produced quicker)
barley then turns into malt
how are gibberellins used to produce cane sugar?
gibberellins cause stem elongation between the nodes
sugar cane stores sugar in cells in the internodes so elongation makes more available from each plant
how are gibberellins used to breed plants?
gibberellins can speed up seed production and germination in young conifer plants
seed companies can induce early seed formation in biennial plants (produce seeds after 1 year)
spraying gibberellins biosynthesis inhibitors can keep plants short and stocky to prevent lodging
how are cytokinins used to reduce lettuce wastage
applying cytokinins prevents yellowing of lettuce leaves after they have been picked
how are cytokinins used to clone plants
used as a growth hormone in micropropagation
promote bud & shoot growth by stimulating cell division in explants
describe the commercial uses of ethene
speeding up of fruit ripening in tomatoes, citrus fruits and apples
promoting fruit drop in cherry, cotton and walnut
promotes lateral growth in some plants
restricting ethene can prevent fruit ripening which is useful for storage and transport of bananas
effect of gibberellins on amylase produced in isolated tissues from barley seeds
exposure increases rate of amylase synthesis
gibberellins are activated in barley seeds’ embryo and diffuse to aleurone layer, and bind to specific receptors on PMs of cells
initiate transcription/translation of genes encoding amylase (enables starch to be digested into maltose)
w/ no treatment, amylase production is much slower and therefore plants need gibberellin for germination to occur
why would temperature be controlled in an experiment investigating auxin
higher temperature means higher KE of molecules so faster rate of diffusion
auxins site of production
shoot tips
root
shoot
apical bud
auxins effects
promotes cell elongation in shoot tips
inhibits cell elongation in root
inhibits leaf abscission (ethene production) in shoot
promotes apical dominance in apical bud
gibberellins site of production
seeds
stem
gibberellin effects
stimulates germination of seeds by causing digestive enzymes to be synthesised
work synergistically w/ auxins to promote stem elongation (internal growth) and promote lateral shoot growth
(effects of gibberellin are greater than effects of auxin on stem elongation)
ethene site of production
leaves
ethene effects
stimulates abscission/ fruit drop
abscisic acids site of production
roots
leaves
seeds
abscisic acids effects
inhibits cell division and therefore growth of roots
promotes stomatal closure in leaves
inhibits germination of seeds
cytokinins site of production
applied artificially to apical bud
cytokinins effects
overcomes apical dominance
used as growth hormone in micropropagation (promote bud and shoot growth by stimulating cell division in explants)
what does myogenic mean
initiates its own beats at regular intervals (doesn’t need to receive elec impulses from a neurone to make it contract)
how does SAN act as a pacemaker
initiates wave of excitation that sets the pace and rhythm for cardiac muscle cells to contract
typical resting heart rate
75bpm
path of wave of excitation in heart
SAN
AVN
bundle of his
purkyne fibres
step by step heart contraction
SAN initiates wave of excitation which spread over both atria simultaneously
short delay before AVN transmits WoE so atria can finish contracting
AVN transmits WoE to the ventricles
Bundle of His carries wave of excitation down the septum to the apex
purkyne fibres carry WoE over the surface of the ventricles and allow the ventricle walls to contract from apex upwards
where is the cardiovascular centre found
medulla oblongata
what is the heart rate controlled by
autonomic nervous system (involuntary) reflex action
nerves (motor neurones) run from cardiovascular centre to SAN
what is HR increased by
the accelerans nerve (sympathetic NS)
what is HR reduced by
vagus nerve (parasympathetic NS)
does parasympathetic or sympathetic NS dominate at rest?
VAGUS NERVE
although both provide slight stimulation
medulla oblongata nerve types
has excitatory and inhibitory nerves
how does vagus nerve act
releases acetylcholine (ACh) at synapses between neurones
causes hyperpolarisation of cardiac muscle
how does accelerans nerve act
releases noradrenaline at synapses between neurones
causes depolarisation of cardiac muscle
baroreceptors role
detect changes in blood pressure
chemoreceptors role
detect change in blood pH (CO2 content)
what do stretch receptors in skeletal muscles and joint capsules detect?
what does this trigger?
movement of limbs
sends elec impulses to medulla oblongata via sensory neurone
increase sympathetic nerve activity and decreases parasympathetic activity
HR increases so more oxy blood supply to muscles
where are chemoreceptors
carotid arteries
aorta
brain
chemoreceptors mechanism during exercise
CO2 conc in blood increases
chemoreceptors send impulses to medulla oblongata via sensory neurone
increase sympathetic and decrease parasympathetic nerve activity
increase HR and remove more CO2 from blood
after exercise, less CO2, blood pH increases so sympathetic nerve activity decreases
where are baroreceptors found
aortic arch
carotid artery
vena cava
baroreceptors role when BP increases
BR stimulated
more impulses to medulla oblongata
more stimulation of SAN
increased HR and SV
vena cava baroreceptors:
source of stimulation
nerve involved
outcome on heart
increased blood volume returning to the heart due to strenuous activity
more accelerans nerve stimulation
increased HR
aortic arch and carotid artery baroreceptors:
source of stimulation
nerve involved
outcome on heart
increased cardiac output
decreased accelerans and increased vagus nerve stimulation
decreased HR
2 branches of nervous system
central NS
peripheral NS
what is CNS made up of
unmyelinated grey matter (mostly)
white matter= axons of unmyelinated neurones
what is PNS made up of
somatic (voluntary)
autonomic (involuntary)
describe somatic NS
output to skeletal muscles via motor neurones
acetylcholine
includes somatic reflexes
autonomic NS output
glands, smooth muscle, cardiac muscle
branches of autonomic NS
parasympathetic
sympathetic
describe parasympathetic NS
rest and digest
conservaiton of energy
NT= acetylcholine
vagus nerve
descrie sympathetic NS
fight/flight response
internal alarm
NT= noradrenaline
accelerant nerve
somatic vs autonomic NS: control
S= volunatry
A= involuntary
somatic vs autonomic NS: neurones
S- sensory neurons form sense organs and motor neurones to skeletal muscles
A- input form internal receptors via sensory neurones to motor neurones that supply internal organs
somatic vs autonomic NS: target
S- skeletal muscles
A-cardiac muscle, smooth muscle, glands
somatic vs autonomic NS: ganglia
S-only 1 motor neurone, cell body in CNS
A- cell bodies of 2nd motor neurones are in ganglia outside the spinal cord: preganglionic neurone carries AP from CNS to ganglia, postganglionic neurone carries AP to target effector
somatic vs autonomic NS: myelination
S- most neurones are myelinated, allowing for fast responses. somatic reflexes r faster
A- most neurones unmyelinated. rapid response not as important for autonomic reflexes
parasympathetic vs sympathetic NS: origin of neurones
P: emerge from cranial and sacral regions of CNS
S: emerge from thoracic and lumbar regions of CNS
parasympathetic vs sympathetic NS: position of ganglion
p; close to effector
S; close to spinal cord
parasympathetic vs sympathetic NS: length of neurones
P; preganglionic is long, postganglionic is short
S; preganglionic short, postganglionic long
parasympathetic vs sympathetic NS: transmitter substance released at effector
P: acetylcholine
S: noradrenaline
parasympathetic vs sympathetic NS: time of greatest activity
P: rest/digest
S: fight/flight
parasympathetic vs sympathetic NS: effects on heart via SAN
P; lower HR and force of contraction
S; higher HR and force of contraction
parasympathetic vs sympathetic NS: effects on blood vessels
P; maintains steady muscle tone in arterioles to gut, smooth muscle, brain and skeletal muscle
S; dilates arterioles to brain and skeletal muscle, constricts arterioles to gut
parasympathetic vs sympathetic NS: effect on lungs
P: lower BR and depth
S: increased ventilation rate and depth
parasympathetic vs sympathetic NS: effect on eyes
P: pupils narrow
S: pupils dilate
parasympathetic vs sympathetic NS: effects on digestive system
P: stimulates peristalsis, stimulates secretion of juices from glands, inhibits contraction of sphincter muscles (faeces are passed), glycogenesis in liver
S: inhibits peristalsis, little effect on glands, contraction of sphincter muscles, gluconeogenesis and glycogenolysis in liver
parasympathetic vs sympathetic NS: effects on skin
P: no effect on sweat glands, erector muscles or arterioles
S: increased sweat production, hair erector muscles contract so hairs raise, constriction of arterioles to skin
describe reflex actions:
(determined by what?)
(is Brain involved?)
rapid automatic response
involuntary (no conscious thought)
follows a specific pattern in response to a given stimulus
it is determined by the presence of an inherited pattern of neurones forming spinal and cranial reflex arcs
brain may be informed that reflex has happened, but is not involved in co-ordinating response
usually have some sort of survival value
examples of neurone pathways of reflex actions
SN-MN
SN-RN-MN
SN-RN-RN-MN
SN-RN-MN-MN
what is a stimulus
detectable change in the environment
what does a receptor do
(transducer) detects and coverts stimulus energy to an electrical input
survival importance of reflexes?
prevent body being harmed of reduce severity of damage
how do reflexes increase chances of survival
bc they are involuntary so decision-making regions of the brain are not involved so response is quicker
being present form birth means they dont have to be learnt and therefore provide immediate protection (innate behaviours)
they are extremely fast (reflex arc is as short as possible and normally only involves 2 synapses. some reflexes are monosynaptic)
examples of reflexes (stimuli)
smell of food
hot plate
food in throat
bright light
tap on patella tendon
reflex: smell of food:
receptor
effector
response
cranial/spinal?
olfactory cells in nose
salivary glands
secrete salia
cranial
reflex: hot plate:
receptor
effector
response
cranial/spinal?
thermoreceptors in skin
bicep muscle
move hand away
spinal
reflex: food in throat:
receptor
effector
response
cranial/spinal?
touch receptors in pharynx
smooth muscle of pharynx
swallow food
cranial
reflex: bright light:
receptor
effector
response
cranial/spinal?
photoreceptors in retina
circular iris muscles contract
pupils narrow
cranial
reflex:tap on patella tendon:
receptor
effector
response
cranial/spinal?
stretch receptors in quadreceps
quad muscle contracts
lower leg lifts
spinal
blinking may be stimulated by sudden changes in the environment e.g.:
foreign object touching cornea
drying out of cornea
sudden bright light
loud sounds
sudden movement
stages in blinking reflex
foreign body stimulates mechanoreceptors in cornea
AP transmitted along SN
AP passes along RN in lower brain stem (pons)
AP sent along branches of MNs
Obicularis Oculi (facial) muscle around eye pulls eyelid inward helping to close the eyelid
how can blinking reflex be overriden/inhibited
involves 2 synapses so can be overridden by inhibitory signals from the cerebral cortex
higher centre can send inhibitory impulses much more rapidly than non-myelinated relay neurones in the pons
the inhibitory action can prevent AP forming in the MN
(essential for people who wear contact lenses)
describe knee jerk reflex
stretch receptors in quadriceps muscles detect that muscle is being stretched
AP transmitted along SN
SN synapses directly w MN
MN transmits impulse to effector (quadriceps) causing it to contract and lower leg moves forward quickly
an inhibitory relay neurone inhibits MN to the antagonistic hamstring muscle causing it to relax (would interfere w reflex response otherwise)
what type of reflex have monosynaptic reflex arcs
only stretch reflexes
can the knee jerk reflex be inhibited
no because there are no relay neurones involved
polysynaptic arcs are required for a reflex to be inhibited as inhibition relies on the rapid myelinated neurones carrying APs to synapse before the MN is stimulated
therefore absence of this reflex may indicate NS problems
what part of the brain is responsible for conscious thought and memory
(largest part)
cerebrum
what is cerebrum divided into (and what are these connected by)
2 hemispheres: connected via the corpus callosum
corpus callosum contains what and allows for what?
contains over 250 million nerve fibres
allows the 2 hemispheres of the cerebrum to communiacte
cerebrum outer layer makeup
outermost layer (surface area 2.5m^2), is folded and consists of a layer of nerve cell bodies known as the cerebral cortex
where is cerebral cortex more highly developed
what does it control
in humans
higher brain functions
what higher brain functions does the cerebral cortex control
conscious thought and voluntary actions and emotional responses
ability to override some reflexes
features associated w intelligence e.g. reasoning, judgement, interpreting and learning
control of speech and visual processing
hypothalamus function
regulates the autonomic nervous system
controls most of the body’s homeostatic mechanisms
in-depth hypothalamus functions w parts responsible
osmoreceptors: responses mediated by pituitary gland
thermoregulatory centre: monitors blood temperature: responds via NS or hormonal via pituitary
regulates digestive activity: gut secretions/peristalsis controlled
regulates endocrine glands via the pituitary gland (thyroid and adrenal cortex)
involved in melatonin release to induce sleep
what is medulla oblongata responsible for controlling (brief) so thus what is consequence
vital functions
damage here is fatal
what does medulla oblongata form a link between
brain and spinal cord
what does medulla oblongata control action of
non skeletal muscles (therefore used in autonomic control)
examples of how medulla oblongata is used in autonomic control
contains respiratory centre- controls breathing and regulates rate and depth of breathing
contains cardiac centre- regulates heart rate
contains vasomotor centre- controls blood pressure and regulates circulation
what does cerebellum co-ordinate
balance and learned sequences of movement (unconscious functions)
what is cerebral cortex divided into
sensory areas
association areas
motor areas
what do sensory areas of cerebral cortex do
receive impulses indirectly from receptors via sensory neurones
what do association areas of cerebral cortex do
compare sensory inputs with previous experience
what do motor areas of the cerebral cortex do
send AP to various effectors
what does frontal lobe of cerebrum contain and do
contains somatic motor associated area so co-ordinates movement
what is occipital lobe of cerebrum responsible for
visual association
what is parietal lobe of cerebrum repsonsible for
somatic sensory (touch) association
what is temporal lobe of cerebrum responsible for
auditory association
functions of the hypothalamus
regulation of thirst (osmoregulation), temperature (thermoregulation)
monitors chemical and hormone levels in the blood
controls the release of hormones eg ACTH from the anterior pituitary gland
produces hormones like ADH and oxytocin and causes their release from the posterior pituitary
pathways of hormones from anterior pituitary gland
TRH stimulates TSH release, travels to thyroid which secretes thyroxine
CRH stimulates ACTH release, travels to adrenal cortex which secretes cortisol
compare anterior and posterior lobe of pituitary gland
A: no direct nerve connection w the hypothalamus, P: direct nerve connection w hypothalamus
A: connected via portal blood system, P: no portal blood system
A: release TSH and ACTH into blood when a releasing factor from portal system binds, P: no releasing factors, AP from hypothalamus triggers release of ADH
describe pathway of release of cortisol (negative feedback)
hypothalamus releases CRH
CRH travels in portal blood system to anterior pituitary
ACTH released and travels in blood to adrenal cortex
cortisol released from zona fasciculata
cortisol inhibits the release of CRH and ACTH (negative feedback), so switches off its own production
parts of fight or flight response stimulated by hypothalamus
SYMPATHETIC NS:
impulses sent via motor neurones activate glands, smooth muscles, cardiac muscles
adrenal medulla activated to secrete adrenaline and noradrenaline
HORMONE RELEASE VIA ANTERIOR PITUATARY GLAND
TRH, pituitary secretes TSH, thyroid gland secretes thyroxine
CRH, pituitary secretes ACTH, cortisol released by adrenal cortex
elements of fight/flight response (caused by sympathetic NS and hormone release)
more blood flow (vasodilation) to brain so more mental activity
dilated pupils (radial muscles contract)
higher HR, SV, BP so higher CO and more O2 to tissues
hairs stand up, more sweat production
vasodilation to muscles heart brain, vasoconsitrciton to gut and skin
increased BGL
increased BR so more O2 in
how does activation of the fight/flight response affect voluntary muscle
breathing/intercostals contracting/diaphragm contracting faster
more blood flow to skeletal muscles
leg muscles primed for action
glycogenolysis in muscles
how does activation of the fight/flight response affect involuntary muscle
arteriole smooth muscle relaxes to increase blood flow to the brain= vasodilation (caused by adrenaline)
radial smooth muscle in pupils contracts, pupils dilate (caused by adrenaline)
thyroxine increases metabolic rate and sweat production
arterioles contract/dilate to alter blood flow/pressure (less blood to gut/skin, less gut secretions and pale skin)
smooth muscle in airways relaxes so airways widen
how does a stroke cause problems with coordination of movement, loss of memory/speech, paralysis of body below the neck
disruption of O2/glucose supply to brain cells for aerobic respiration
lack of O2/glucose/blood supply/damage to:
cerebrum/cerebral cortex so loss of speech/memory
cerebellum so problems w co-ordination/ movement
medulla oblongata so paralysis of body below neck
explain why the cerebral cortex is a tissue whereas the brain is an organ
cerebral cortex is made up of a group of similar types of cell, working together to perform a similar function
the brain consists of several tissues carrying out more than one function
state the region of the brain where the hypothalamus is found
forebrain
list brief functions of hypothalamus
homeostasis
autonomic NS control
thermoregulation
hormone release
sleep control
pituitary gland control
osmoregulation
melatonin release
region ion brain responsible for learning and memory
cerebrum
region of brain responsible for control of balance and fine movement
cerebellum
what part of the brain is involved with the ability to see
cerebral hemisphere
hormone that stimulates glycolysis
adrenaline
part of the brain that has nervous control of the heartbeat
medulla oblongata
what are the 3 types of muscle
voluntary (skeletal)
cardiac
involuntary (smooth)
description of voluntary/skeletal muscle
cell membrane=sarcolemma
cytoplasm=sarcoplasm
many mitochondria
multinucleate
extensive SER
number of myofibrils (organelles) make up contractile units called sarcomeres arranged end to end
description of cardiac muscle
cells form branched fibres with cross bridges
cells separated by intercalated discs (specialised gap junctions that allow co-ordinated contraction) joining cells at ends
good supply of capillaries
abundant mitochondria (more reliant on aerobic respiration)
description of involuntary/smooth muscle
spindle shaped
tapered at both ends
contains bundle of actin and myosin
single nucleus
forms sheets
numerous mitochondriav
voluntary/skeletal muscle appearance under microscope
striated or striped or banded
cardiac muscle appearance under microscope
striated or striped or banded due to myofibrils
involuntary/smooth muscle appearance under microscope
unstriated bc no myofibrils (actin and myosin arranged differently)
voluntary/skeletal muscle innervation
somatic nervous system (somatic reflexes)
cardiac muscle innervation
myogenic but autonomic NS and hormones control rate
involuntary/smooth muscle innervation
autonomic NS (sympathetic and parasympathetic)
voluntary/skeletal muscle contraction
quick and powerful
cardiac muscle contraction
quick
w/o NS (myogenic)
involuntary/smooth muscle contraction
slow and sustained
voluntary/skeletal muscle fatigues…
quickly
cardiac muscle fatigue
does not fatigue due to lots of mitochondria
involuntary/smooth muscle fatigues ….
slowly (doesn’t tie easily)
where is voluntary/skeletal muscle found and what is its function
voluntary movements
attached to skeleton via tendons
contraction shortens the muscle and force is transmitted to bona via tendon and bone pulled
also somatic reflexes (involuntary)
where is cardiac muscle found and what is its function
in heart
contract to decrease volume in heart chambers to pump blood into ventricles or out of heart via arteries
where is involuntary/smooth muscle found and what is its function
intestine walls for peristalsis
uterus walls
arterioles to regulate BP and distribution of blood e.g. during exercise and temp regulation
reflexes e.g. in iris of eye
describe structure of a skeletal muscle cell
each fibre/cell contains many nuclei and many organelles called myofibrils, which are embedded in the muscle fibre sarcoplasm and are surrounded by sarcoplasmic reticulum
T-tubules (infoldings of the sarcolemma)
what are myofibrils composed of
protein filaments called myofilaments
what does sarcoplasmic reticulum do
stores and secretes Ca2+
released to cause muscle contraction
what do T-tubules allow to happen
allow APs propagating along the surface membrane to also travel throughout the interior of the muscle
why does a muscle/fibre contain many nuclei
embryonic cells fused together to form individual muscle fibres
what are myofibrils
long cylindrical organelles made of proteins called actin and myosin which are lined up in parallel
the myofibrils are the contractile elements of the muscle cells
why are there many mitochondria between myofibrils
(each smaller than one sarcomere)
provide ATP for muscle contraction
name of cytoplasm within muscle fibre
sarcoplasm
what is each myofibril divided along its length into
repeating units called sarcomeres (contractile until of the muscle)
what gives rise to the striped/striated appearance of muscle fibres
within the sarcomeres are 2 protein filaments and the overlap of these filaments gives rise to striped/striated appearances
what are muscle fibres’ thin filaments
actin
what are muscle fibres’ thick filaments
myosin
what/where is the Z line
boundaries between sarcomeres (between actin filaments)
what does I band contain
actin only
what does H zone contain
myosin only
what/where is the A band
overlap of actin and myosin (
what does the M line contain
proteins which anchor the myosin filaments
where is titin
along Z lines
describe what happened to lengths when the muscle contracts
sarcomere gets shorter
I band decreases
H zone disappears
A band remains the same
what do myosin filaments have
protein projections/cross bridges/ “bulbous heads” which extend towards the actin filaments
what do myosin heads contain
an actin binding site
an ATP binding site (ATPase enzyme)
myosin heads when muscle at rest?
not connected to the actin filaments
an ATP molecule is bound to the free end of each cross bridge
what are actin filaments associated with
2 other proteins:
troponin
tropomyosin
(involved in the contraction process)
what are actin filaments made up of
2 actin chains twisted around each other
what does troponin do
holds tropomyosin in place (binds to action tropomyosin and calcium)
what does tropomyosin do
blocks binding sites for myosin head on actin
step by step sliding filament mechanism
Ca2+ bind to troponin which changes shape. troponin and tropomyosin move away from myosin binding site so myosin heads (which have ADP and Pi attached) can bind to actin active site and muscle fibre can contract
conformational change in myosin head and it tilts from 90 to 45, which forces actin the move in relation to myosin (ADP and Pi released)
ATP now binds w myosin head
myosin head hydrolyses ATP to ADP and Pi, which provides the energy to released the myosin head from the actin.
the head detaches and flips away and returns to its original 90 position
then binds further along and process repeats
what happens to sliding filament mechanism if ATP runs out
myosin heads do not detach
filaments cannot slide so become locked in position
when does rigor mortis occur
48-60 hours after death
what happens when myosin heads bend
actin and myosin filaments move past each other and muscle is shortened
what happens during relaxation of muscle
Ca2+ returns to resting level (ATP used to pump Ca2+ back into sarcoplasmic)
active sites of actin are blocked
what is a motor end plate
a highly excitable region of a muscle fibre
where do motor neurones interact with muscles
neuromuscular junction/ motor end plate
nervous stimulation of skeletal muscle
skeletal muscle is under the control of the voluntary NS
a single MN innervates many muscle fibres
each muscle fibre is controlled by a branch from only 1 MN
step by step sequence of events in stimulation of a muscle fibre
an AP arrives
AP causes uptake of Ca2+ ions by MN
Ca2+ cause vesicles containing ACh to fuse w presynaptic membrane
ACh released and diffuses across synaptic cleft
ACh molecules bind w receptors in sarcolemma of muscle fibre, causing them to open Na+ channels
Na+ ions flood in, depolarising membrane and initiating AP which spreads along membrane down T-tubule (carried to centre of muscle fibres)
Ca2+ channels open so Ca2+ diffuse out of sarcoplasmic reticulum
Ca2+ bind to troponin, causing tropomyosin to move and expose the binding sites for myosin on actin filaments
myosin head binds (with ADP and Pi attached) so sliding filament mechanism occurs
what happens when AP stops arriving at neuromuscular junction
T tubules no longer depolarised so Ca2+ channels in SR close
Ca2+ ions moved back into SR rapidly by transporter proteins
Ca2+ bound to troponin is released, so tropomyosin binds back to normal position covering myosin binding sites
myosin can no longer bind
muscle is relaxed
similarities between synapses and neuromuscular junctions
NTs located in vesicles in presynaptic cytoplasm
arrival of ATP causes Ca2+ to move in and NT to move into cleft
NT diffuses across cleft and binds to complementary receptors on postsynaptic membrane
binding of NT results in opening of Na+ channels on post synaptic membrane
enzymes e.g. acetylcholinesterase present on the post synaptic membrane break down NT
differences between synapses and neuromuscular junctions
S: post synaptic stimulation leads to AP in next neurone, NMJ: post synaptic stimulation leads to depolarisation of sarcolemma and contraction
S: neurone to neurone, NMJ: neurone to muscle
S: synaptic bulb rounded and small, NMJ: membrane of end plate has increased SA bc folded
where does energy for muscle contraction come from (4 sources)
ATP
creatine phosphate
anaerobic metabolism
aerobic metabolism
what system of energy supply dominates during tennis serve
ATP hydrolysis releases energy
ATP= small, soluble, relatively unstable so cannot be stored easily
what system of energy supply dominates during 100m sprint
creatine phosphate
can supply more ATP to allow us to run for a few seconds
what system of energy supply dominates during a 400m sprint (strenuous exercise)
anaerobic metabolism
cannot continue indefinitely bc of lactic acid buildup
also aerobic metabolism
what system of energy supply dominates during marathon
aerobic metabolism
and anaerobic metabolism
describe energy release during short burs of exercise e.g. tennis serve
ATP produced in respiration is required for the sliding filament mechanism
small amount of ATP are found in the sarcoplasm which can be hydrolysed
this ATP runs out within a few seconds
ATP to ADP, Pi and energy
describe energy release during 100m sprint
replenishing ATP w creatine phosphate
most muscle fibres store creatine phosphate, a chemical that phosphorylates ADP to ATP
this reaction maintains the muscle’s supply of ATP during vigorous exercise
creatine phosphate is regenerated once energy becomes available
what is the amount of ATP that creatine phosphate reaction can form limited by?
link to athletes
the initial concentration of creatine phosphate in the cell
for this reason, many athletes in sports that require rapid power output consume creatine supplements to increase the pool of immediately available ATP in their muscles
describe energy release during strenuous exercise
anaerobic respiration dom (glycolysis) produces net 2 ATP
glucose ->2 lactic acid + 2NAD
NAD allows glycolysis to continue
if lactic acid builds up, muscles fatigue
(substrate level phosphorylation)
describe energy release during marathon
aerobic respiration dom
glycolysis -> link reaction -> Krebs -> ETC
oxidative phosphorylation
greater yield of ATP than anaerobic resp
when are slow twitch muscle fibres used
during endurance activities
bc they contract slowly and can work over long periods of time
when are fast twitch muscle fibres used
for short bursts of activity
bc contractions are powerful and quick
slow vs fast twitch muscle fibres: ATP
slow have more
slow vs fast twitch muscle fibres: contraction time
slow= contract longer time
fast= short burst contraction
slow vs fast twitch muscle fibres: fire____
slow= fire slowly
fast= fire rapidly
slow vs fast twitch muscle fibres: respiration method
slow= aerobic
fast= anaerobic
slow vs fast twitch muscle fibres: fatiguing
slow= fatigue slowly
fast= fatigue quickly
why do fast twitch muscle fibres fatigue quickly
lactate produced as a by-product of aerobic respiration causes fast-twitch fibres to become fatigued quickly
slow vs fast twitch muscle fibres: blood supply
slow= good blood supply
fast= poor blood supply
slow vs fast twitch muscle fibres: mitochondria
slow= high numbers of mitochondria
fast= low numbers of mitochondria
result of low number of mitochondria in fast-twitch muscle fibres
rely more on glycogen
slow vs fast twitch muscle fibres: myoglobin
more myoglobin in slow so bright red
less myoglobin in fast so paler
good blood supply, high no.s of mitochondria and more myoglobin in slow twitch muscle fibres helps w what?
help to maintain aerobic resp in the tissue
so slow twitch fibres are v slow to fatigue
HOWEVER, ATP gen is slower than in fast twitch fibres (contraction of slow twitch fibres is weaker)
slow vs fast twitch muscle fibres: density of myofibrils
slow= low density myofibrils (low myosin ATPase activity)
fast= high density myofibrils
slow vs fast twitch muscle fibres: diameter
slow= small diameter
fast= large diameter (thicker, more myosin)
slow vs fast twitch muscle fibres: resistance to lactic acid
slow= low resistance to lactic acid
fast= high resistance to lactic acid
how to measure fatigue
electrical activity of muscles can be investigated using an electromyograph (EMG)
the more powerful the contraction, the higher the amplitude
the amplitude decreases as the muscle fatigues
suggest why a lack of ATP may lead to muscle rigidity
myosin heads cannot detach from actin (cross bridge not broken)
so filaments cannot slide and become locked in position
prevents relaxation/ muscle stays contracted
muscles cannot elongate again (relax) without an ________
(EXPLAIN TOO)
antagonist
sometimes the antagonist is another muscle, sometimes it is elastic recoil air hydrostatic pressure in a container
e.g. elastic recoil & BP in blood and heart walls
e.g. elastic recoil in airways
muscle fatigue definition
a decrease in maximal force or power production in response to contractile activity
what is fatigue
when a muscle fibre is repeatedly stimulated, there is a decrease in tension and the muscle is said to be fatigued
how does an increased conc of H+ ions lead to a reduction in the force of contraction of a muscle
as H+ conc increases, pH decreases so proteins in muscle denatured change shape
Ca2+ channels in sarcoplasmic reticulum change shape due to low pH-> can no longer allow Ca2+ to diffuse out into sarcoplasm
therefore insufficient Ca2+ to bind to troponin, so tropomyosin not moved so binding sites for myosin on actin filaments not exposed
less myosin heads can bind to actin , so less sliding filament mechanism ( conformational change in less myosin heads so less cross bridges form, so less heads bend so muscle shortens/contracts less)
power stroke strength decreased/ less power strokes
actin pulled past myosin w less force
H+ may denature any proteins e.g. actin/myosin
suggest what might cause muscles to fatigue
lack of ATP: needed for Na+/K+ pumps, exocytosis, myosin head detachment and return to the 90 degree angle, pumping Ca2+ back into sarcoplasmic reticulum
lack of blood flow to the muscles
lack of O2 or glucose to muscle leads to lack of ATP
NT not released from presynaptic motor neurone
sarcolemma does not depolarise
damage to muscle fibres: prolonged/ intense muscle activity can cause damage to the muscle fibres, including micro-tease in muscle tissue. this damage can trigger an inflammatory response, leading to swelling and pain in the affected muscles, contributing to fatigue
accumulation of metabolic byproducts like H+ or lactic acid (these can disrupt normal cellular processes within muscle fibres, leading to fatigue. in addition, accumulation of H+ in muscle tissue can decrease pH of the muscle, further impairing muscle function)
functions of cerebrospinal fluid (CSF), which surround the Braun and fills the central cavities
mechanical protection
removes excess heat/ cools brain
supplies O2
advantage of cerebral cortex being highly folded
more neurones in given space
more processing power
