neuronal, hormonal communication and plant/animal responses
endocrine system
the secretion of a chemical into the blood from a gland
hormone binds to a target cell, initiating series of reactions (cell signalling)
steriod hormones
lipid soluble
binding forms a hormone-receptor complex
- acts as a transcription factor, stimulates production of mrna, new proteins produced
non-steroid hormones
not lipid soluble
hormones are hydrophilic so cant pass through plasma membrane
bind to receptors on membrane
once bound, series of reactions triggered
reactions are mediated by cAMP
adrenal cortex
glucocorticoids- cortisol: regulates blood pressure
mineralocorticoids- aldosterone: regulates salt and water conc
androgens- low concs of male and female sex hormones
adrenal medulla
adrenaline- increases heart rate and rate of glycogen breakdown
noradrenaline- works with adrenaline, increases heart rate
pancrease- exocrine gland
produces and releases digestive enzymes
amylase, protease, lipase
pancreas- endocrine gland
control blood glucose conc using insulin and glycogen
endrocrine tissue is within islets of langerhans
islets contain alpha cells (produce and secrete glucagon) and beta cells (produce and secrete insulin)
effect of insulin
increase absorption of glucose
increase rate of respiration
increase rate of glucose->fat
increase rate of glucose->glycogen (glycogenesis)
inhibit glycogen release
effect of glycogen
increase use of fatty acids instead of glucose
increase glyogen->glucose (glycogenolysis)
production of glucose from other conpounds (gluconeogenesis)
insulin secretion
1. potassium and calcium channels open so potassium ions flow out
2. when blood glucose conc is high glucose moves into cell
3. glucose is metabolised to produce atp
4. atp closes potassium ion channels
5. accumulation of potassium ions alters potentail difference (less negative)
6. pd opens calcium ion channels
7. calcium ions cause vesicles to fuse with cell membrane
type 1 diabetes
the inability of fhe islet of langerhan b-cells to produce insulin
caused by autoimmune disease attacking b-cells
treat with insulin injections
type 2 diabetes
body cells not responding to insulin produced
linked eith excess body weight, physical inactivity
treatment- exercise
diabetes cure
pancreas transplant
use stem cells
seed germination
water stimulated production of gibberellins
gibberellins switch on genes for amylase and protease
leads to production of amino acids and glucose from food stores
auxins
hormones produced by cells
diffuse through plant and bind to receptors on plasma membrane
cause cell walls to become more flexible
apical dominance
in high concs auxins inhibit lateral growth and stimulate growth at apex only
further down the stem the auxin has diffused less so lateral growth can occur at lower concs
at very low concs aucin will stinulate root growth
stem elongation
gibberellins have role in elongation of stem
by increasing the internode length
leaf abcission
less light means less auxins
longer dark periods lead to reduction in auxin conc
leaves then produce ethene
ethene stimulate transcription of enzymes that weaken cell walls
xylem and phloem blocked by fats
wind blows leaves off plant
protection against freezing
freezing causes disruption to the plasma membranes and causes cells to die
so
cells put solutes that lower freezing points into vaccuole or cytoplasm
stomatal control
when leaves or roots have lack of water they release hormone ABA
controls opening of stomatal pores
ABA binds to receptor, changes the ionic conc
reduced water potential and lowers turgor of cells
physical and chemical defences
thorns, spikes, spines
unpleasant chemicals e.g. alkaloids, tannins
phototropism
the way plants respond to light as they grow
involved lateral movement of auxins away from light
auxins stimulate cell elongation
growing in the dark
plants grow more rapidly in dark than in light
driven by the need to grow up as quickly as possible
commercial plant hormones
ethene is used to ripen fruits
auxins are used to stimulate growth of roots
hormonal weed killers over stimulate growth of weeds so they die
general neurone structure
cell body- where neurotransmitters are produced
dendrons- detect electrical impulses
axons- carries electrical signal away
neurones
sensory- cell body in middle, carry impulse from receptor to coodination centre or relay
relay- cell body surrounded, impulse from sensory to motor
motor- cell body at end, impulse from coordination centre or relay to effector organ
schwann cell
insulating layer around neurone
speeds up impulse transmission up to 100 times
pacinian corpuscle
when detects pressure changes shape which deforms membrane surrounding the neurone
when this happens, sodium ions are able to diffuse into neurone
causes neurone to be depolarised
reflex arc
stimulus
receptor
sensory n
relay n
motor n
effector
response
resting potential
normal state of neurone when its not transmitting an impulse
in this state, membrane is polarised with higher positive charge outside
pd is roughly -70mV
resting and action potential process
1. resting potential- k+ channels and na+ channels close, na+/k+ pump is working, causing a pd across membrane
2. na+ voltage gated channels open, na+ moves in, membrane is depolarising, more na+ channels open
3+4. more na+ channels open bc more na+ ions diffuse in, increasing pd (positive feedback)
5. at +40mV, na+ channels close, k+ channels open
6+7. k+ moves out, repolarisation, pd decreases
8. cell overshoots, hyperpolarisation
9. resting potential is reached bc of acrions of k+ ion channels closing and na+/k+ pump working
impulse transmission along a neuron
1. Resting potential
2. Action potential reverses charges, Membrane is depolarised, Sodium ions diffuse along axon
3. Alters PD causing voltage gated sodium channels to open, Sodium ions diffuse along axon, Depolarises membrane
4. Process repeats, First selection of axon repolarises, overshoots and is hyperpolarised (Refractory period), Stops impulse travelling in wrong direction
5. Impulse continues along axon, First section returns to resting potential
saltatory conduction
schwann cell Insulates neuron and prevents ion movement, So action potentials can only occur at the nodes of ranvier
Action potential jumps from node to node and dramatically speed up transmission of the impulse along the neurone
Wider neuron will transmit impulse quicker
synapse
Junction between neurons where Message is converted from electrical impulse into chemical impulse and back into electrical impulse
Diffusers across synaptic cleft
Neurotransmitters can be excitatory or inhibitory
cholinergic synapse
acetylcholine
acetylcholinesterase
role of synapse
Ensures impulses unidirectional
Allows impulse from one presynaptic neuron to stimulate many postsynaptic neurons
^ spatial summation
temporal- 2 weak signals arriving shortly after each other trigger the neurone to fire
controlling heart rate
The medulla oblongata monitors the pressure (baroreceptors) and pH (chemoreceptors)
Increased metabolic activity-> More CO2-> Blood pH is lowered-> Speed heart rate and increases frequency of impulses to SAN-> SAN increases heart rate-> CO2 level returns to normal
Brain
cerebrum- voluntary actions, learning, memory, personality
Cerebellum- Unconscious functions
Medulla oblongata- Controlled heart and breathing rate
Hypothalamus- Regulates temperature and water levels
pituitary gland- Hormonal control centre
knee jerk
spinal reflex bc relay is in spine
maintain balance
blinking reflex
cranial reflex as relay neurone is in brain not spinal cord
initiated by touching cornea, bright light, loud sounds
skeletal muscle
mde of long interconnected cells that share sarcoplasm
cells are surrounded by plasma membrane called sarcolemma
sarcolemma has infolds called t-tubules
cells contain modified ER called sarcoplasmic reticulum
each cell are long organelles called myofibrils
myofibrils composed of 2 proteins actin and myosin
sliding filament theory
thin (actin) filaments slide between thick (nyosin) filaments within each sarcomere
changes sarcomere length from 2.5 micrometers to 2.0 micrometers
sliding filament theory process
1. Calcium ions move tropomyosin by attaching to troponin exposing binding site on actin
2. my head (with ADP attached) binds to Actin
3. ADP releases causing myosin head to move (power stroke)
4. ATP attaches to myosin causing myosin had to detach
5. ATP is converted to ADP causing myosin head to move back
6. If there is calcium ions, Myosin head will attach to another binding site