Control and coordination' Flashcards
How are messages sent from the receptor to the coordinating
centre, and then to the effector?
Through nerve impulses and/or hormones!
The nervous system and the endocrine system work together to
monitor external/internal changes and coordinate responses
two parts of nercous system
1) Central Nervous System (CNS) → Brain & spinal cord
2) Peripheral Nervous System (PNS) → Neurones
Messages travel via
nerve impulses / action potentials
* Along neurones / nerve fibres
Impulse is passed from neurones to
target cells via a synapse
* Using neurotransmitters
Endocrine glands
- Secretory cells
- Releases secretions directly into blood
capillaries in the glands - Secretions: Hormones
- E.g. pituitary glands, thyroid, adrenal, ovary,
testes, pancreas
endocrine gland
Exocrine glands
- Secretory cells
- Releases secretion into ducts/tubes
(not blood capillaries) - Secretions: Not hormones
- E.g. stomach, salivary glands, pancreas
exocrine gland
Hormones
* Secreted by
endocrine glands
Hormones can be
globular proteins OR steroids
protein hormone
Insulin
steroid hormone
Testosterone
characteristics of hormones
nervous system and endocrine system both involve
- Cell signalling
- Signal molecule binding to receptor
- Both involve chemicals
Cell body of neurones
- Has a nucleus and cytoplasm
- Cytoplasm: Many mitochondria, ribosomes, RER, Golgi
Cytoplasmic processes
- Thin, cytoplasmic extension of cell body
Dendrites
- Carry impulses towards the cell body
- Axons
- Carry impulses away from the cell body
- Some enclosed with myelin sheath
Axon terminal / presynaptic knob
- Many mitochondria, synaptic vesicles
containing neurotransmitters, voltage
gated Ca2+ channels
presynaptic knob is part of a
synapse
synapse
= junction between
neurones / muscles
A synapse also includes:
* Synaptic cleft =
gap
→ has enzymes to breakdown
neurotransmitters
- Postsynaptic membrane
→ has receptor proteins for
neurotransmitters
Myelin sheath
- Insulates axons of many neurones
Myelin sheath function
Speeds up conduction of nerve impulses
Myelin sheath made up of
Schwann cells
→ Has nucleus
→ Layers of cytoplasm and plasma membrane spirals around the axon
Nodes of Ranvier
Between Schwann cells, no myelin
3 types of neurones
- Sensory neurone (afferent)
* Longer sensory axon / dendron
* Shorter axon - Motor neurone (efferent)
* Shorter dendrites
* Much longer axon - Intermediate / relay neurone
- Pathway where impulses are carried
along during a
reflex action
reflex arc example
knee jerk reflex, sneezing
advantages of reflex arc
- Fast
- Automatic, involuntary, without
conscious thought - Innate / instinctive, response is always
the same - Protects from harm
What are impulses?
→Brief changes to the distribution of electrical charge across
membrane (aka membrane potential)
At rest:
more negatively charged on inside than outside
* Resting potential = -70mV
When impulses are formed:
more positive on inside than outside
* Action potential / depolarization = +30mV
roles of sensory receptor cells
- Detect stimuli
- Acts as transducers
detect stimuli of sensory receptor cellls
- Receptors are specific to one-type
of stimulus - e.g. chemical, light, heat, sound, pressure
transducers of sensory receptor cells
- Converts stimulus energy to electrical energy
- Produce generator / receptor potential
→ Pass impulse along sensory neurone
Chemicals act as a
stimulus
Diff chemoreceptors are specific for diff
chemicals =
diff tastes
salt (NaCl)
- Na+ ions diffuse into cell via microvilli
→ Increase in positive charge inside cell - Membrane depolarized
→ Receptor / generator potential generated - Voltage-gated Ca2+ channels open
→Ca2+ enter cell - Trigger movement of vesicles
containing neurotransmitters
→ exocytosis occurs
→ neurotransmitter released - Neurotransmitter stimulate action
potential / impulse in sensory neurone
→ Send impulse to taste centre in brain
resting potential =
-70mV
At rest =
no stimuli, no impulses formed and transmitted
* Inside of axon more negatively charged than outside
* Neurone is polarized and maintained at -70mV
How is a resting potential maintained?
- Na+/K+ pump
* 3 Na+ pumped out, 2 K+ pumped in
* ATP needed
* Axon phospholipid bilayer impermeable to K+ / Na+
* Electrochemical gradient is set up = difference in both charge and chemical
ions across membrane
→ So K+ diffuse out, Na+ diffuse in
→ via channel proteins - More K+ channels open than Na+ channels
* Membrane more permeable to K+ than Na+
* More K+ leaves than Na+ enter
* Leaking K+ is responsible for resting potential
→Inside becomes relatively more negative than outside
P/S: these channel proteins are open all the time. But voltage-gated
K+ and Na+ channels are closed
Depolarisation (-70 mV → +30mV)
- Voltage-gated K+ channels remain closed
- Voltage-gated Na+channels open
→ Channels change shape when membrane potential changes when action
potential arrives from previous section
*Na+ enter cell
*Membrane becomes less negative / depolarized →+30mV
→ Action potential is generated
* Size of action potentials is fixed at +30 mV
* The higher the strength/ intensity of the stimulus, the higher the
frequency of action potentials
* Also – the more neurones are depolarised
Repolarisation (+30mV → -70mV)
- Voltage-gated Na+ channels close
- Voltage-gated K+ channels open
*K+move out of cell
*Inside becomes negative /repolarised → -70mV
Depolarisation spreads to next region due to movement
of +ve ions to -ve regions. A “local circuit” is set up.
Hyperpolarisation / Refractory Period
(less than -70mV)
- Voltage-gated Na+ channels remain closed
- Voltage-gated K+channels close
*But slight delay so excess K+ions have moved out of axon
When membrane is hyperpolarized = refractory period
*Membrane is insensitive to any depolarisation
*No action potential can be generated
→ Function: ensure one-way transmission
* Due to the refractory period, action potentials are discrete events /
do not merge into one another
→ Function: Length of refractory period limits maximum frequency of
action potentials
* E.g. longer refractory period = lower maximum frequency
Return to Resting Potential (-70mV)
*Na+/K+pump acts again
→ Membrane can be depolarized again
→ Action potential can be generated again
How action potentials are transmitted
along a non-myelinated axon?
- Depolarisation spreads to next region due to movement of positive
ions to negative regions
→A “local circuit” is set up
→This causes voltage-gated Na+ channels to open in the next region
→Causing next action potential
How action potentials are
transmitted along a myelinated axon?
But with the MYELIN SHEATH… there is an increased speed of conduction!
* Myelin insulates axon
→ Does not allow movement of ions
→ Lengthens local circuits
* Passage of ions only at nodes of Ranvier
→ Action potential / depolarization only at nodes of Ranvier
→Local circuit is set up between nodes
→Action potential ‘jumps’ from node to node
→This is called saltatory conduction
Saltatory Conduction
Faster transmission because myelin sheath insulates axons
→Local circuit is set up between nodes
→Action potential ‘jumps’ from node to node
Threshold Potential (-50mV)
- Minimum potential needed for action potential to be generated
→ Only depolarisation that reaches threshold produces an action potential
If depolarisation <-50mV
action potential is not generated
→ only local depolarisation occurs
Only if depolarisation >= -50mV,
action potential is generated
→ Size of action potential is fixed at +30mV
→ all-or-nothing law
synapse=
junction between neurones
/ muscles
- Presynaptic knob
→ Many mitochondria, synaptic vesicles
containing neurotransmitters, voltage
gated Ca2+ channels
Synaptic cleft
= gap
→ has enzymes to breakdown
neurotransmitters
Postsynaptic membrane
→ has receptor proteins for
neurotransmitter
role of synapses
- Ensure one-way transmission
- Allow interconnection of nerve
pathways - Involved in memory and learning
- Filter out low-level stimuli
how do synaspses Ensure one-way transmission
- Receptors only on postsynaptic neurone
- Neurotransmitter vesicles only on
presynaptic neurone
how do synapses allow interconnection of nerve apthways
- Nerve impulses can diverge / integrate
- Allow wider range of behaviour / action in
response to a stimulus
how are synapses involved in memory and learning
- Due to new synapses being formed
how do synapses Filter out low-level stimuli
- Weaker stimulus cause release of low
quantities of neurotransmitters - No impulse generated in postsynaptic
neurone →brain - Prevent brain from being overloaded with
sensory information
The Cholinergic Synapse
Neurotransmitter = acetylcholine (ACh)
1. Action potential reaches presynaptic
membrane
2. Voltage-gated Ca2+ channels open
→ Presynaptic membrane becomes
more permeable to Ca2+
→ Ca2+ ions enter presynaptic neurone
3. Vesicles containing ACh move towards
and fuse with presynaptic membrane
→ Exocytosis occurs
→ ACh released into synaptic cleft
4. ACh diffuse across synaptic cleft
5. ACh binds with receptor proteins
on postsynaptic membrane
6. Receptor proteins change shape and
Na+ channels open
→ Na+ enter postsynaptic neurone
* Postsynaptic neurone depolarized
* Action potential is generated
* As long as ACh binds with receptors,
Na+ channels will stay open
→ Continuous transmission of action
potential
→ Can cause synaptic fatigue / paralysis
7. ACh breakdown by acetylcholinesterase at synaptic cleft
* ACh→ acetate & choline
* ACh is recycled (ATP needed)
* Depolarisation stops in
postsynaptic membrane
→ stop continuous action potential
3 types of muscles
cardiac
skeletal
smooth
2 types of striated muscle
cardiac and skeletal
Striated Muscles
- Striated = striped under microscope
- Attached to bones by tendons
- Many long, cylindrical muscle fibres
→Multinucleated
→Each muscle fibre is made up of myofibrils
Muscle fibres have
- Plasma membrane = sarcolemma
- Cytoplasm = sarcoplasm
- Specialised ER = sarcoplasmic reticulum
muscle fibres have Plasma membrane = sarcolemma
→ sarcolemma infoldings = transverse
system tubules (T-tubules)
→ can conduct action potentials
muscle fibres have Cytoplasm = sarcoplasm
→ Many parallel myofibrils
→ Fibres are multinucleated
→ Manymitochondria
muscle fibres have Specialised ER = sarcoplasmic reticulum
→ have protein pumps
→ have a lot of Ca2+
Two types of myofilaments:
- Thick filaments = made of myosin
- Thin filaments = made of actin
- Thick filaments = made of myosin
→fibrous protein with globular
protein head
→ Attached to M line
Thin filaments = made of actin
→chain of globular protein molecules
→ has binding site for myosin
→ troponin and tropomyosin is
attached to actin
→ Attached to Z line
Sarcomere
Interdigitation of thick and thin filaments give striated appearance
Myosin attached to
M line
Actin attached to
Z line
scaromere between
2 Z lines
- Distance between Z line decreases
during muscle contraction
I band
light band
* Only thin filaments
* Shortens during muscle contraction
H band
light band at centre of dark
band
* Only thick filaments
* Shortens during muscle contraction
A band =
dark band
* Overlap of thick and thin filaments
* Stays the same during muscle contract
Muscle Contraction begins at
neuromuscular junction
→ Cholinergic synapse between a motor neurone and a muscle fibre
* Terminal knobs of motor neurone = motor end plate
* Neurotransmitter = acetylcholine (Ach)
neuromuscular junction
- Cholinergic synapse of neuromuscular junction
- Action potential arrives the presynaptic membrane
- Voltage-gated Ca2+ channels open
- Ca2+ enter presynaptic knob
- Vesicles containing ACh fuse with presynaptic
membrane - AChreleased by exocytosis into synaptic cleft
- ACh diffuses across synaptic cleft
- AChbind to receptors on sarcolemma
(muscle cell membrane) - Na+ channel opens
- Na+ ions enter sarcoplasm of muscle cell
sarcolemma - Sacrolemma depolarised
- Depolarisation and Ca2+
- Depolarisation spreads via T-tubules → sarcoplasmic reticulum (ER)
- Sarcoplasmic reticulum depolarized
- Voltage-gated Ca2+ channels open
- Ca2+ diffuse out from sarcoplasmic reticulum → sarcoplasm
- Ca2+ initiates muscle contraction
When muscle is relaxed:
- Troponin = attached to tropomyosin
- Tropomyosin = blocks myosin-binding
site on actin
When muscle contracts:
- Ca2+ in sarcoplasm bind to troponin
→ Troponin changes shape and moves tropomyosin
→ Exposes myosin-binding site on actin
→ Allows myosin head to attach and form cross-bridge with actin
Sliding Filament Model
1) Myosin head with ADP and Pi form
cross-bridges with actin
→ Pi is released
2) Myosin head tilts and pulls actin
→ Power stroke moves actin towards M line
→ Myofibril / sarcomere shortens
→ ADP released from myosin head
3) ATP binds to myosin head
→ ATPase hydrolyses ATP into ADP and Pi
→ Myosin head lets go of actin
→ Myosin moves back to original position
4) Process repeated at site further along actin molecule
Sarcomere shortens during
muscle contraction
* H band shortens
* I band shortens
* A band remains the same
Muscle Relaxation
When action potential stimulation
stops….
- Ca2+ is actively pumped into
sarcoplasmic reticulum
→ Ca2+ do not bind to troponin on
actin filament
→ Tropomyosin moves to block
myosin-binding sites on actin
filament
→ Filaments slide back to original
position
→ Muscle relaxes
Muscles uses a lot of
ATP
* Only small amount of ATP present in muscle
More ATP is synthesized by….
- Aerobic respiration in mitochondria
- Lactate pathway in sarcoplasm
- Creatine phosphate in sarcoplasm
* Immediate source of energy once ATP is used up
Similarities between mammals and plants about electrical coomunication
- Have electrochemical gradients
- Plant cells have sodium-potassium pumps
- Have resting potential
- Membrane depolarises → action potentials
differences between mammals and plants about electrical coomunication
venus fly trap
- Sensory hair cell is receptor and detects touch
* If 2 hairs are touched / 1 hair is touched twice within 35 seconds…
* Ca2+ ion channels open @ cells at base of hair
* Ca2+ flow in
* Cell membrane depolarised
→ Action potential occurs
* Depolarisation spreads over leaf / lobe
→ to midrib / hinge cells - Acid growth @ hinge cells
* H+ pumped out of cells into cell walls
* Cross-links in cell wall broken
* Calcium pectate of middle lamella dissolves
* Cell wall loosens
* Ca2+ enter hinge cells
* Water enters hinge cells by osmosis
* Cells expand / become turgid
* Lobes change from convex to concave
* Trap shuts quickly in 0.3s
* Elastic tension released - Further deflections of sensory hairs
* Trigger action potentials → seal trap
* Stimulate entry of Ca2+ into gland cells
* Ca2+ stimulate exocytosis of vesicles containing digestive enzymes
* Trap stays shut for up to 1w for digestion - After digestion, cells of upper surface of midrib grow slowly
* Leaf reopens and elastic tension builds in the cell walls of midrib
Venus Fly Trap
Two adaptions to conserve energy and avoid closing unnecessarily:
- Stimulation of single hair does not trigger closure
→ At least two hairs must be touched OR one hair touched twice
within 35 seconds
→ Prevent trap from closing when raining or when debris fall into trap - Gaps between stiff hairs allow very small insects to crawl out
→No energy wasted on digesting a very small meal
Chemical Communication in Plants
- Plant hormones/plant growth regulators
- Produced in a variety of plant tissues
- Not in endocrine glands
- Plant hormones interact with receptors
inside/outside cell and initiate a signaling cascade
Movement of plant hormones:
a) Directly from cell to cell
→By active transport or diffusion
b) Via phloem/xylem vessels
E.g. Auxins, gibberellins, abscisic acid
Auxins (IAA) short
- Growth by cell elongation at tips of roots and shoots
- Inhibits lateral growth / branching– i.e. apical dominance
- Via acid growth hypothesis
- Group of several chemicals
- Main auxin = IAA (indole 3-acetic acid)
- Synthesized in growing tips of shoots & roots
→ Aka apical meristems where there is active mitosis
- Gibberellins (GA) short
- Seed germination
- Stem elongation
- Causes breakdown of DELLA proteins, which are inhibitors of cell growth
and seed germination - Plant growth regulator / plant hormone
- Synthesized in young leaves, seeds & stems
- Abscisic acid (ABA) short
- Respond to water stress
- Stimulate closure of stomata
- Uses Ca2+ as second messenger
Role of auxin
- Stimulate cell elongation
- Inhibits lateral growth / branching – i.e. apical dominance
→ Cause plants to grow taller towards light
P/S: Auxin not solely responsible for apical dominance
* There is interaction between auxin and other plant growth regulators
* Gibberellin enhances IAA
Role of Auxin in Cell Elongation
The Acid Growth Hypothesis
- Auxin binds to receptors in cell surface membrane
- Stimulates proton pumps in cell surface membrane
* By active transport
* H+ from cytoplasm into cell wall
* Cell wall become more acidic - pH-dependent enzymes (expansins) activated to weaken cell wall
* By breaking H bonds between cellulose microfibrils
* Cell wall loosens → more elastic, can stretch - Ions enter cell and water potential of cell decreases
* Water enter cell by osmosis
* Increase in turgor pressure
* Cell wall expands
* Cause elongation of cell
why is the acid growth hypothesis supported
Hypothesis supported bcs….
1. Cell elongation can be prevented by neutralising the acidity of cell
wall using a buffer
2. Can cause cell elongation by acids
3. Protons released from cells in response to auxin
Uneven distribution of auxin can cause
stem / root to bend in
respond to stimuli
→ Higher concentration of auxin, more cell elongation
→ E.g. auxin causes shoots to bend towards sunlight
* Auxin inhibits lateral growth at
growing tips of shoots
→ The act of pruning removes auxin
→ Allows branching and produces bushier plants
roles of GA
- Seed germination
- Stimulates cell division and cell elongation in stem
Gibberellin enhances
IAA
for seed germination to happen
- Seed is dormant / metabolically inactive
→DELLA proteins act as inhibitors of cell growth and seed germination
→Maintain seed dormancy
- Seed absorbs water by osmosis
→Water stimulates production of gibberellin by embryo
