BIOLOGY- stimuli and response

stimulus

A change in the internal or external environment

receptors

detect stimuli, can be cells or proteins on cell surface membranes

effectors

cells that bring about a response to a stimulus to produce an effect
include muscle cells and cells found in glands and pancreas

sensory neurones

take electrical impulses from receptors to CNA (brain and spinal cord)

Motor neurones

take electrical impulses from CNS to effectors

Relay/ intermediate neurones

take electrical impulses from sensory to motor neurons

reflexes

body responds to stimulus without making conscious decision to respond. protect the body as they're rapid

reflex arc

pathway of neurons linking receptors to effectors in reflex

eg reflex response to heat

1. thermoreceptors in skin detect heat stimulus
2. sensory neuron carries impulses to relay neuron
3. relay neuron sends impulse to motor neuron
4. motor neuron sends impulses to effector
5- muscle contracts, you withdraw your hand to stop pai and damage

3 features of reflexes

fast- very few synapses
fixed- same in everyone, effective from birth
involuntary- no conscious thought, speeds and response for protection from harm

electrical impulse movement

electrical impulse reaches end of neuron, neurotransmitters secreted to target cells so nervous response is localised. neurotransmitters are quickly removed, so are short lived. response is rapid, allows animals to react quickly to stimuli

how do plants increase chances of survival

responding to environmental changes.
eg sense direction of light and grow towards it to maximise light absorption for photosynthesis

tropism

The response of a plant to a directional stimulus.
respond to stimuli by regulating their growth

positive tropism

Growth towards a stimulus

negative tropism

growth away from a stimulus

phototropism

growth of a plant in response to light
shoots\= +vely phototrophic
roots\= -vely phototrophic

gravitropism

growth of a plant in response to gravity
shoots\= -vely gravitropic
roots\= +vely gravitropic

how do plants respond to directional stimuli

Using specific growth factors
produce in growing regions of the plant eg shoot tips leaves

auxin

growth factors that stimulate growth of shoots by cell elongation
cell walls become loose and stretchy so they get longer
high conc in roots might inhibit growth

Indoleacetic acid (IAA)

plant growth regulator
produced in tips of shoots in flowering plants + roots.
moves around plant to control tropisms, moves by diffusion and active transport over short distances and via phloem over long distances
tip detects stimulus, results in uneven distribution of IAA (different conc) \= uneven distribution of growth

IAA in phototropism

moves to shaded side of
shoots- IAA conc increases on shaded side. cells elongate and shoot bends towards light (+ve)
roots- IAA conc increases on shaded side. growth inhibited so root bends away from light (-ve)

IAA in gravitropism

moves to underside
shoots- IAA conc increases on lower side- cells elongate and shoot grows upwards (-ve)
roots- IAA conc increases on lower side- growth inhibited so root grows downwards (+ve)

taxis/tactic

directional behavioral response in a moving organism
eg woodlice move away from light (-ve phototaxis), helps them survive by keeping them in damp conditions- reduced water loss

kinesis/ kinetic

non-directional behavioural response in a moving organism
eg woodlice move slowly and turn less often in humidity and faster in dry air to improve survival

choice chambers

investigate animal responses
container with different compartments- can control different environmental conditions- test how animals respond to conditions like light intensity or humidity

choice chambers method

2 halves- distilled water on one side and calcium chloride (drying agent) on another (investigating tactic responses for humidity levels)
leave chamber to stabilise before adding woodlice in center of chamber and cover with a lid
after 10 mins, record how many woodlice are on each side

for light intensity, cover half of the lid with black paper, makes 1 side dark. put damp filler of both sides, put 10 woodlice in center, repeat steps from before

receptors are specific

only detect 1 type of stimulus eg light pressure
different types for different stimuli
some are cells (eg photoreceptors) some proteins on cell surface membrane (eg glucose receptor)
they are transducers
initiate an impulse (generator potential) in sensory neuron, only when certain threshold is reached

transducers

changes energy from one form to another

how receptors work in nervous system

nervous system receptor in resting state (not stimulated)
there is a difference in charge between inside and outside of cell- generated by ion pumps and ion channels \= voltage across membrane (potential difference)
when cell at rest, potential difference\= resting potential

when stimulus detected, cell membrane is excited\= more permeable- allows more ions in and out\= alters potential difference
generator potential\= potential difference due to stimulus
bigger stimulus\= excites membrane more\= bigger movement of ions\= bigger change in potential difference\= bigger generator potential

if generator potential big enough to reach threshold level- triggers action potential (electrical impulse in a neurone)

if stimulus too weak, generator potential won't reach threshold\= no action potential

action potential

all 1 size
unidirectional
always fire with same change in voltage
bigger stimulus won't cause bigger action potential
strength of stimulus measured by frequency of action potentials (no of action potentials triggered in a certain time period)
don't overlap due to refractory period
all-or-nothing \= threshold reached, action potential fired. not reached, not fired

Pacinian corpuscles

mechanoreceptors- detect mechanical stimuli eg pressure and vibrations
found in skin
contain end of sensory neurone (sensory nerve ending), wrapped in lots of layers of connective tissue (lamellae)
at rest sodium ion channels in cell membrane of neurone ending is closed

How pacinian corpuscle works

pacinian receptors stimulated (eg pressure) lamellae deformed, press on sensory nerve ending
sensory neurone cell membrane stretches, deforming stretch-mediated sodium ion channels.
channel ions open and na+ diffuses into cell
sudden influx of na+ depolarises (changes potential) of membrane- creates generator potential
if reaches threshold, triggers action potential in sensory neurone

photoreceptors

light receptors in eye
light enters through pupil. amount of light controlled by muscles in iris
light rays focused by lens onto retina (contain photoreceptor cells that detect light)
fovea\= area of retina that has lots of photoreceptors
nerve impulses from photoreceptor cells carried from retina to brain by optic nerve (bundle of neurone)
where optic nerve leaves eye\= blind spot- no photoreceptors\= not sensitive to light

convert light into electrical impulses

light enters eye, hits photoreceptors, absorbed by light-sensitive optical pigments
light bleaches pigments, causing chemical change + alter membrane permeability to sodium ions
generator potential created- if reaches threshold action potential \= nerve impulse sent along bipolar neurone
bipolar neurone\= connect photoreceptors to optic nerve, takes impulses to brain

rods

rod shaped
greater number
found mainly at peripheral part of retina
contain rhodopsin
only give info in black and white (monochromatic)

cones

cone shaped
fewer number
concentrated at fovea
contain iodopsin- 3 types (red green and blue sensitive)
gives info in colour (trichromatic vision)

sensitivity of rods and cones

rods- more sensitive to light- sensitive to low light levels
fire action potential in dim light, many rods join to one neurone, so weak generator potential combine to reach threshold and trigger action potential

cones- only sensitive to high light levels- fire action potential in bright light. one cone joins to one neurone- takes more light to reach threshold and trigger action potential

visual acuity

ability to tell apart points that are close together

rods- poor visual acuity- rods join to same neurone\= light from 2 points close together can't be told apart

cones\= high visual acuity\= cones close together and one cone to one neurone. when light from 2 points hits 2 cones, 2 action potentials (1 from each cone) go to brain- can distinguish 2 point close together as 2 separate points

Control of heartrate

heart\= myogenic- contracts and relaxes without receiving signals from nerves.
Pattern of contractions control the regular heartbeat

sino-atrial node

pacemaker of the heart
in wall of right atrium
initiates impulses on its own.
cause atria and ventricles to contract at around 70bpm

atrioventricular node

responsible for passing waves of electrical activity to bundle of his because band of non-conducting collagen prevents waves of electrical activity being passed directly from atria to ventricles
slight delay before AVN reacts- males sure atria have emptied before ventricles contract

bundle of his

A group of muscle fibres in the heart
conducts waves of electrical activity between ventricles to apex (bottom).
bundle splits into thinner fibres in left and right ventricle walls

Purjinke fibers

carry electrical waves to muscular walls of right and left ventricles
contract simultaneously from bottom up

rate at which SAN fires is controlled by

medulla oblongata

medulla oblongata

made up of cardio-acceleratory centre and cardio-inhibitory centre

cardio acceleratory center

linked to SAN by sympathetic nerve

Cardio inhibitory center

linked to SAN by parasympathetic nerve

pressure receptors

baroreceptors in aorta + carotid arteries
stimulated by high and low blood pressure
detect stimuli

chemical receptors

chemoreceptors in aorta, carotid arteries and medulla
monitor o2 level, co2 and ph levels
detect stimuli

high blood pressure in heart

detected by baroreceptor
impulses sent to cardio-inhibitory centre in medulla
sends impulses along parasympathetic neurone
secretes acetylcholine (neurotransmitter)
binds to receptors on SAN\= decreases heart rate and reduces bp

low blood pressure in heart

detected by baroreceptors
impulses sent to cardio-acceleratory centre in medulla
impulses sent along sympathetic neurones
secrete noradrenaline
binds to receptors on SAN \= heart rate speeds up and bp increases

high O2, low CO2, high pH

detected by chemoreceptors
impulses sent to cardio-inhibitory centre
impulses sent along parasympathetic neurones
secrete acetylcholine
binds to receptors on SAN\= decreases heart rate \= returns 02, c02 and ph to normal

low O2, high CO2, low pH

detected by chemoreceptors
impulses sent to cardio-acceleratory centre
impulses sent along sympathetic neurones
secretes noradrenaline
binds to receptors on SAN\= increases heart rate\= 02, c02 and ph goes back to normal

neurone cell membranes

polarised at rest
resting state\= outside of membrane +vely charged compared to inside
more +ve ions outside than inside of cell\= potential difference across membrane

resting potential of a neuron

-65 to -70 mv
maintained by sodium-potassium pump and potassium ion channels

sodium-potassium pump in neurone

carrier protein in axon membrane
- active transport (ATP needed) moves 3Na+ ions out of axon for every 2K+ put in
- membrane not permeable to Na+\= can't diffuse back in so sodium ion electrochemical gradient made- more Na+ outside cell than inside
- na+/k+ pump lets K+ in, but membrane permeable to K+, so facilitated diffusion allows them out in potassium ion channels
this means outside of cell +ve charged compared to inside of cell

depolarisation when stimulated steps

stimulus-sodium ion channels open- if big enough- rapid change in potential difference\= action potential

1. stimulus
2. depolarisation
3. repolarisation
4. hyperpolarisation
5. resting potential

1. Stimulus (action potential)

excited neurone cell membrane= sodium ion channels open, membrane becomes more permeable to sodium. Na+ diffuses down Na+ electrochemical gradient into neurone. Inside of neurone = less -ve

2. Depolarisation (action potential)

if potential difference reaches threshold, (around -55mv), more sodium ion channels open\= more Na+ rapidly diffusing into cell

3. Repolarisation (action potential)

at potential difference of around +30-40mv, Na+ channels close (if don't, would stay depolarised) k+ channels open.
membrane\= more permeable to k+, so k+ diffuse out down k+ concentration gradient.
membrane starts to go back to resting potential

4. hyperpolarisation (action potential)

k+ channels\= too slow to close\= too many k+ ions diffuse out
potential difference\= lower than resting potential

5. resting potential (action potential)

ion channels reset, na+/k+ pump returns membrane to resting potential until excited by another stimulus

refractory period

membrane can't be excited again straight away. ion channels 'recovering', can't be made to open
action potentials don't overlap- pass along as discrete impulses
limit to frequency at which they can be transmitted

wave of depolarisation

when action potential happens, some na+ ions that enter diffuse sideways\= na+ channels in next region open + na+ diffuse.- causes wave of depolarisation to travel along neurone
wave move away from some parts of membrane in refractory period because these parts can't fire action potential

factors that effect speed of conduction of action potential

myelination
diameter of axon
temp
number of synapses

myeilnation

myelin sheath\= electrical insulator- made of schwann cell
bare membrane between patches\= nodes of ranvier
na+ channels concentrated at nodes
in myelinated neurone\= depolarisation only happens in nodes of ranvier (na+ can get through membrane)
neurones cytoplasm conducts enough electrical charge to depolarise next node, so impulse jumps
saltatory conduction
non-myelinated neurone\= impulse travels as wave along whole length of axon membrane \= slower than saltatory conduction

saltatory conduction

the jumping of action potentials from node to node

diameter of axon

bigger diameter\= faster transmission
action potential conducted quicker because less resistance to flow of ions than in cytoplasm with smaller axon
less resistance\= depolarisation reaches other parts of neurone quicker
bigger axon- smaller s.a:v ratio

temperature

temp increase\= ions diffuse faster
after 40- proteins denature so speed decreases
greater temp- faster transmission- more kinetic energy- diffuse faster

number of synapses

greater number- slower transmission

synapse

junction between 2 neurones or between neurone and effector cell

synaptic cleft

gaps between cells at synapse

synaptic knob

Contains synaptic vesicles of neurotransmitters

synaptic transmission process

action potential reaches end of presynaptic neurone (knob)
ca2+ channels open and ca2+ move into knob
synaptic vesicles fuse with presynaptic membrane + neurotransmitter released into cleft (exocytosis)
neurotransmitters diffuse to post-synaptic neurone and bin d to specific receptors
when bind, might trigger action potential, causes muscle contraction, or secrete a hormone
neurotransmitter removed from cleft so doesn't continue- re-uptake by pre-synaptic neurone or broken down by enzymes
receptors only on post synaptic membrane\= unidirectional

Ach across cholinergic synapse

action potential arrives at the synaptic knob of the presynaptic neurone.
action potential stimulates voltage-gated ca2+ channels in the presynaptic neurone to open. Ca2+ diffuse into the synaptic knob. (They're pumped out afterwards by active transport.)
The influx of ca2+ into the synaptic knob causes synaptic vesicles to move to the presynaptic membrane. They fuse with the presynaptic membrane. The vesicles release the neurotransmitter acetylcholine (ACh) into the synaptic cleft (exocytosis)
ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the postsynaptic membrane.
causes na+ channels in the postsynaptic neurone to open.
influx of na+ into the postsynaptic membrane causes depolarisation.
An action potential on the postsynaptic membrane is generated if the threshold is reached.
ACh is removed from the synaptic cleft so the response doesn't keep happening. broken down by an enzyme called acetylcholinesterase (AChE) and the products are re-absorbed by the presynaptic neurone and used to make more ACh.

excitatory

neurotransmitters depolarise post-synaptic membrane- will fire action potential if threshold reached

inhibatory

neurotransmitters hyperpolarise post synaptic membrane (potential difference more -ve) prevents it from firing an action potential

summation

effect produced by the accumulation of neurotransmitters from two or more neurones

spatial summation

many neurones connect to 1 neurone
small amount of neurotransmitter released from each of these neurones can be enough altogether to reach threshold in post-synaptic neurone and trigger action potential
if some neurones release inhibitory neurotransmitter, total effect of all neurotransmitters\= no action potential

temporal summation

2 or more nerve impulses arrive in quick succession from same presynaptic neurone
makes action potential more likely- more transmitter is released into synaptic cleft

neuromuscular junctions

between motor neurone and muscle
use ACh neurotransmitter and binds to nicotinic cholinergic receptors

differences between neuromuscular junctions and other synapses

post synaptic membrane\= folds that form clefts. stores enzyme to break down ACh
post synaptic membrane has more receptors than other synapses
ACh always excitatory at neuromuscular junctions. when motor neurone fires an action potential, normally triggers a response in muscle cell- not always the case between two neurones

how drugs effect action of neurotransmitters

same shape as neurotransmitters
block receptors
inhibit enzyme that breaks down neurotransmitters
stimulate release
inhibit release

drugs same shape as neurotransmitters

mimic action at receptors
drugs\= agonists
means more receptors are activated

drugs block receptors

can't be activated by neurotransmitters fewer receptors are activated

drugs inhibit enzymes that break down neurotransmitters

more neurotransmitters in synaptic cleft to bind to receptors- neurotransmitters are there for longer

drugs that stimulate

stimulate release of neurotransmitters from pre-synaptic neurone\= more receptors are activated

drugs that inhibit

inhibit release of neurotransmitters from pre-synaptic neurone\= fewer receptors activated

muscles

act as antagonistic pairs
skeletal muscles attached to bones by tendons
pairs of skeletal muscles contract and relax to move bones at a joint
bones of skeleton are incompressible, so act as levers, giving muscle something to pull against

ligaments

attach bones to other bones to hold them together

antagonistic pairs

muscles that act on opposite sides of a joint- work together to move a bone

contracting muscle

agonist

relaxing muscle

antagonist

eg of antagonistic pair

lower arm
bones in lower arm attached to bicep muscle and tricep muscle by tendons
biceps contract (agonist) - tricep relaxes (antagonist)- arm bends at elbow

biceps relax(antagonist)- tricep contracts (agonist)- arm straightens

skeletal muscle is made of

long muscle fibres
muscles act as effectors- stimulated to contract by neurones

sarcolemma

cell membrane of a muscle fibre
some folds inwards across muscles fibre and stick into sarcoplasm (transverse t tubules) help spread electrical impulses in sarcoplasm to reach all parts of muscle fibre

sarcoplasm

cytoplasm of a muscle fibre

sarcoplasmic reticulum

network of internal membranes. runs through sarcoplasm, stores and releases ca2+ that are needed for muscle contraction

muscle fibres

lots of mitochondria\= provide ATP needed for muscle contraction
multinucleate (contain many nuclei)
lots of long cylindrical organelles- myofibrils- made of proteins\= highly specialised for contraction

myofibrils

contain thick and thin filaments- move past each-other and make muscles contract