15. Control & Co-ordination Notes Flashcards
In mammals Nervous system: Transmission of nerve impulses 16.02.2021 Synapses 21.02.2021 Muscle contraction 24/26.02.2021 Endocrine system: Human menstrual cycle 24/26.02.2021 In plants Venus fly trap 02.03.2021 Auxin & gibberellin 03/05.03.2021
Structure of a sensory neurone & a motor neurone
Axons carry nerve impulses AWAY from cell body.
Dendrons carry nerve impulses TOWARDS cell body.
Body nervous system:
Central nervous system (CNS) = brain + spinal cord
Peripheral nervous system (PNS)
*Nerve impulse = an electrical signal that passes along a neurone in 1 direction {as a result of rapid movement of Na+ & K+ ions across CSM into/out of axon}
Sensory neurone
- Cell body, in DORSAL ROOT GANGLION (outside of spinal cord)
- contains nucleus, mitochondria, rough ER, Golgi body, ribosomes - Dendron is longer than axon, & has dendrites
- Has synaptic knobs
- Myelin sheath & nodes of Ranvier
Motor neurone
- Cell body (inside spinal cord; also Relay neurone)
- Has short dendriteS
- Axon longer than dendrites
- Has synaptic knobs
- with many mitochondria
- with many synaptic vesicles that contain neurotransmitters - Myelin sheath & nodes of Ranvier
Functions of sensory, relay and motor neurones in a reflex arc (+ describe)
Importance of reflex arc
- Fast and automatic
- response seen before impulse reaches brain, but impulse still gets transmitted to brain - Protect body from harm, eg. hot/sharp objects
- Response is Stereotypic - always the same to each specific stimulus
eg. knee jerk
Reflex arc: the pathway along which impulses are transmitted from a receptor to an effector, w/o involving the conscious regions of the brain
1. Very STRONG stimulus in receptor
eg. light, sound, heat
2. Action potential generated in sensory neurone
3. ❖Sensory neurone transmits impulse from RECEPTOR, through dorsal root of spinal nerve & into spinal cord, to CNS
- Action potential passes to relay neurone
4. ❖Relay neurone transmits impulse from sensory neurone –> motor neurone
5. ❖Motor neurone transmits impulse from relay neurone to EFFECTOR (muscle/gland)
+ impulses to brain
6. Response generated, aka reflex action
Roles of sensory receptor cells in detecting stimuli and STIMULATING the transmission of nerve impulses in sensory neurones
eg. Chemoreceptor cells found in human taste buds
- detect chemical energy {by specific receptor protein}
eg. rods & cones detect light energy
Regardless of intensity of stimulus,
- max action potential is +30mV - fixed size
- speed of transmission of action potential always same
BUT stronger stimulus increases:
- frequency of impulses/action potentials
- no. of neurones transmitting impulse
- Respond to stimuli (light, sound, touch, pressure, chemicals)
- Some receptors are the ends of sensory neurones; some are cells
- Are energy transducers: convert stimulus energy to electrical energy
- STIMULUS causes Na+ channels to open, Na+ enter cell
- Produce RECEPTOR POTENTIAL, depolarisation of membrane
❖ If receptor potential greater than threshold, action potential generated - all-or-nothing law - Increased stimulus strength increases frequency of action potential
In receptor cells,
- If receptor potential above threshold, voltage-gated Ca2+ channels open
- Ca2+ enter cell and cause release of neurotransmitter by EXOCYTOSIS
! Neurotransmitter stimulates action potential in sensory neurone, impulse passed along sensory neurone to brain
*if sensory neurone & not separate receptor cell, no need for Ca2+ channels; action potential stimulated by local current flow / local circuit
Transmission of an action potential in a myelinated neurone and its initiation from a resting potential
- action potential at any point in axon triggers production of action potential in adjacent region
- sodium-potassium pumps & ion channels are in fact still open during depolarisation and repolarisation stages (less significant)
❖ Resting potential
- Axon phospholipid bilayer impermeable to K+ & Na+
1. In a resting axon, SODIUM-POTASSIUM PUMPs (in CSM of neurone) actively pump 3 Na+ ions out and 2 K+ ions into axon - active transport, lots of ATP needed
2. CSM also has ion channels for facilitated diffusion (passive) across membrane - less Na+ channels & more K+ channels
- more K+ ions diffuse out, less Na+ ions diffuse into axon
3. ∴ inside of axon more negative than outside; resting potential ≈ -70mV –> axon membrane is POLARISED - Voltage-gated channels closed
❖ Depolarisation
- If resting potential above threshold potential -55mV, VOLTAGE-GATED sodium ion channels open, Na+ enter axon
- Inside of axon becomes less negative –> depolarised
- Na+ continue to enter until potential difference raised to +30mV
- Voltage-gated sodium ion channels close
❖ Repolarisation
- VOLTAGE-GATED potassium ion channels open, K+ move out of axon
- Inside of axon becomes more negative again - repolarised
❖ Hyperpolarisation
- K+ continue to exit until potential difference is very negative -80mV –> hyperpolarised
- Voltage-gated potassium ion channels close
- Sodium-potassium pumps restore p.d. by pumping out Na+ and pumping in K+
- Resting potential -70mV achieved again; action potential can occur again
- Myelin sheath insulates axon & prevents ion movement
- Action potential ONLY occurs at nodes of Ranvier
- LOCAL CIRCUITS set up between nodes {movement of Na+ from +ve to -ve region, across axon}
- saltatory conduction occurs, in which action potential jumps from node to node
- One way transmission of action potential due to…
- …Refractory period at previous node
^action potential only generated ahead, NOT behind it
^region that has just had action potential cannot trigger a new action potential for a short time (in recovery)
Importance of the myelin sheath (saltatory conduction) in determining the speed of nerve impulses and the refractory period in determining their frequency
+ larger diameter / thicker axons transmit impulses faster than thin ones, due to lower resistance
- Uncovered areas between Schwann cells = nodes of Ranvier
- Schwann cells contain a nucleus
- not all axons and dendrites have myelin sheath
- Made up of Schwann cells that wrap around axons (and dendrons, but axons more important )
- Sheath mainly lipid {+ some proteins}
1. Insulate axons & Prevent ion movement (b/c impermeable to Na+ & K+)
2. Action potentials/Depolarisation can ONLY occur at nodes of Ranvier
3. LONGER local circuits set up between nodes; nodes are 1-3mm intervals apart {Na+ move from +ve to -ve region, across axon}
4. Saltatory conduction occurs, action potentials jump from node to node
5. Speed of transmission of impulse in myelinated neurone 100ms-1, approx. 50x faster than unmyelinated
6. Speed in unmyelinated neurone 0.5ms-1
Structure of a cholinergic synapse and explain how it functions
*nerve impulses cannot jump across synapses; signals passed across by chemicals called neurotransmitters
Structure
1. Synaptic cleft = gap between two neurones
2. Vesicle containing neurotransmitter
3. Neurotransmitter receptor proteins
4. Synaptic knob has many mitochondria to produce ATP for:
- neurotransmitter synthesis
- vesicle formation
- vesicle movement
- exocytosis
+ removal of Ca2+ from pre- neurone by active transport
Function
- When action potential reaches synaptic knob, VOLTAGE-GATED calcium ion channels open in presynaptic membrane
- Ca2+ enter {diffuse} synaptic knob & induce vesicles containing acetylcholine (ACh) to move towards PREsynaptic membrane
- Vesicles fuse with pre- membrane & release Ach into synaptic cleft (exocytosis)
- Ach DIFFUSEs across synaptic cleft & binds to complementary receptor on POSTsynaptic membrane
- Ligand-gated sodium ion channels open & Na+ enter post- neurone
- Postsynaptic membrane is depolarised
- Action potential generated in postsynaptic neurone
- synaptic cleft contains ACETYLCHOLINESTERASE; hydrolyse ACh –> acetate + choline
- stops continuous production of action potentials in post- neurone
- choline combines with acetyl CoA –> Ach again in presynaptic neurone (ATP needed)
4 roles of synapses in the nervous system
❖Ensure transmission in 1 direction
- vesicles containing neurotransmitters ONLY in presynaptic neurone & receptor proteins ONLY in postsynaptic membrane
❖Allow interconnections of many nerve pathways
- allows wide range of responses
- Involved in memory and learning
- due to new synapses being formed
- summation - Filter out less frequent impulses / low level stimuli (to avoid overloading neurones)
Ultrastructure of striated muscle with particular reference to sarcomere structure
- striated muscle cells / muscle fibres / myofibres
- multinucleate syncytium
- Sarcolemma - equivalent of CSM
- Sarcoplasm - equiv. of cytoplasm; many mitochondria
- Sarcoplasmic reticulum *equiv. of ER but diff. function
- stores high conc. of Ca2+ ions
- many protein pumps on its membrane for active transport of Ca2+ - T tubules (transverse system tubules)
- infolding of sarcolemma
- usually close to a sarcoplasmic reticulum - In a muscle fibre, many myofibrils made of actin + myosin
❖Actin: THIN filament attached to Z lines/discs
- globular protein
- has binding site for myosin head
- troponin & tropomyosin attached
❖Myosin: THICK filament attached to M lines
- fibrous protein w/ globular protein head (ATPase)
❖Sarcomere: distance between Z lines
- I band - only actin (lightest)
- H band - only myosin (lighter)
- A band
- overlapping regions of actin + myosin (darkest & thickest)
- includes H band
Roles of neuromuscular junctions, transverse system tubules and sarcoplasmic reticulum in STIMULATING contraction in striated muscle
- Neuromuscular junction = junction between motor neurone & muscle fibre
Action potential reaches NEUROMUSCULAR JUNCTION / motor end plate, same events as in synapse earlier (eg. synaptic cleft)… then
- Acetylcholine binds to receptors in SARCOLEMMA, Na+ channels open, Na+ enter muscle fibre
- Sarcolemma is DEPOLARISED (& initiates action potential)
- Depolarisation spreads down T TUBULES
* sarcoplasmic reticulum near T tubules - Induce calcium ion channels on membrane of sarcoplasmic reticulum to open
- Ca2+ diffuse out of SARCOPLASMIC RETICULUM
- Ca2+ bind to troponin
- Troponin changes shape & tropomyosin moves, exposing myosin-binding site on actin
Sliding filament model of muscular contraction
including the roles of troponin, tropomyosin, calcium ions and ATP
- If Q asks about role of Ca2+ in the coordination of muscle contraction:
1. when impulse arrives at neuromuscular junction, voltage-gated Ca2+ channels open; Ca2+ enter; stimulate vesicles to fuse with pre- membrane; impulse in sarcolemma/T-tubules stimulates release of Ca2+ from sarcoplasmic reticulum
2. bind to troponin… when no action potential, Ca2+ pumped back into sarcoplasmic reticulum
- Ca2+ released from sarcoplasmic reticulum
- Ca2+ bind to troponin
- Troponin changes shape & moves tropomyosin, exposing binding site on actin
- Myosin head binds to site & forms CROSS BRIDGE
- Myosin head has ATPase; hydrolyses ATP –> ADP + Pi
- When ATP binds to myosin head, myosin head detaches from actin
- When ATP hydrolysed, myosin tilts head
- Myosin head binds to actin again
- When ADP + Pi released, POWER STROKE occurs, in which myosin head pulls actin & goes back to previous orientation
- each power stroke moves 10nm; combined effect of power stroke allows contraction - Process repeated
- Sarcomere shortens (A band remains same length)
Roles
❖Troponin has binding site for Ca2+
❖Tropomyosin covers/uncovers binding site on actin
When there is no action potential,
> Ca2+ channels on membrane of sarcoplasmic reticulum close
❖Ca2+ pumped back into sarcoplasmic reticulum by active transport using ATP
- Ca2+ are removed from troponin
- Tropomyosin moves & blocks binding site on actin
> No cross bridge between actin and myosin - muscle relaxes
Compare the nervous and endocrine systems as communication systems that co-ordinate responses to changes in the internal and external environment
3 similarities + 7 differences
Similarities
- Both involve cell signalling
- Chemicals (neurotransmitters/hormones)
- Signalling molecules bind to receptors
Differences ✦ form & mode of transmission - Electrical impulses travelling along neurones vs Chemicals called hormones travelling in blood ✦ nature of communication - Electric and chemical vs Chemical ✦ response destination - Muscle/gland vs Target organs ✦ effect is... - Localised vs Widespread ✦ transmission speed - Faster vs Slower ✦ longevity of effect response - Short-lived vs Long-lived ✦ receptor location - On CSM vs Either on CSM or within cell
Human menstrual cycle
roles of the hormones FSH, LH, oestrogen and progesterone in controlling changes in the ovary and uterus
≈ 28 days; 1st day = start of menstruation
1st half of cycle (follicular phase) - secondary oocyte produced
2nd half of cycle (luteal phase) - uterus prepares for implantation
FSH & LH secreted by pituitary gland
oestrogen & progesterone secreted by ovaries
*endometrium = uterus lining
- Hypothalamus releases GnRH (gonadotrophin releasing hormone) to pituitary gland
- so anterior pituitary gland secretes FSH into blood
✦target: ovary, to stimulate development of a primary follicle - As follicle develops, it secretes oestrogen into blood
- [oestrogen] increases
3 targets:
✦uterus: repair & thicken endometrium, increase in blood vessels
✦anterior pituitary gland: inhibit FSH & LH at LOW level of oestrogen (negative feedback)
✦hypothalamus: inhibit GnRH
- oestrogen level high just before ovulation
- HIGH level of oestrogen triggers FSH & LH secretion - LH & FSH released in a SURGE
✦ovary: LH triggers ovulation (day 14) - release of secondary oocyte from ovarian follicle/Graafian follicle
- Remains of ovarian follicle develop into a corpus luteum - Corpus luteum secretes progesterone & oestrogen (lower level)
3 targets of progesterone:
✦uterus: maintain endometrium
✦anterior pituitary gland: inhibit FSH & LH secretion
✦hypothalamus: inhibit GnRH - If fertilisation does not occur,
- Corpus luteum degenerates b/c production of FSH & LH, which are needed to survive, are inhibited by progesterone & oestrogen
- As corpus luteum degenerates, levels of oestrogen & progesterone decrease
- Endometrium not maintained & breaks down –> menstruation occurs
- FSH no longer inhibited, so can stimulate development of new primary follicle
Cycle can start again
If fertilisation occurs,
- Corpus luteum receives hCG (human chorionic gonadotrophin) hormone from implanted embryo
- hCG allows corpus luteum to sustain w/o FSH & LH
- Corpus luteum continues to secrete progesterone & oestrogen to maintain endometrium (until placenta develops and secretes progesterone throughout pregnancy)
Biological basis of contraceptive pills containing oestrogen and/or progesterone
- Synthetic hormones used, as they do not get broken down quickly
- taken daily for 21 days then stop for 7 days to allow menstruation - Oestrogen & progesterone conc. remain high
- Negative feedback on anterior pituitary gland to Inhibit secretion of FSH & LH
- Ovarian follicle does not develop & ovulation is inhibited
- Thickens CERVICAL mucus to prevent entry of sperm
- Endometrium is thin, so prevents implantation
Rapid response of the Venus fly trap to stimulation of hairs on the lobes of modified leaves + how the closure of the trap is achieved
- live where soil conditions lack nitrogen; so obtain nitrogen for growth by trapping and digesting insects
- lobes are connected by hinge cells in the middle
- each lobe has 3 sensory/trigger HAIRS
(Electrical communication in plants)
- Mechanical energy converted to electrical…
- …by sensory hair cells - receptors that detect touch
- Cell membrane depolarises {b/c Ca2+ channels open, Ca2+ enter, generate receptor potential}
- If (at least) 2 hairs touched within 35 seconds OR 1 hair touched twice within 35 seconds,
- Action potential occurs & spreads over leaf/lobe, to HINGE cells {spread through leaf cells via plasmodesmata; plants do not have neurones}
- H+ pumped out of cells into cell walls
- Cell wall loosens (due to low pH)
- CALCIUM PECTATE dissolves in the middle lamella
- Ca2+ ions enter cells & water enters cells by OSMOSIS, down the ψ gradient
- (hinge) Cells become turgid and expand
- Lobes change from convex to CONCAVE
- Trap shuts quickly in 0.3s
Role of auxin in (cell) elongation growth by stimulating proton pumping to acidify cell walls
(Chemical communication in plants)
*Auxin, gibberellin = plant growth regulators
- based off Acid-growth hypothesis
- Auxin binds to a receptor on the CSM
- Auxin stimulates proton pumps in CSM…
- …To pump H+ (from the cytoplasm) into the cell wall by active transport
- pH of cell wall decreases
- pH-dependent enzymes - EXPANSINS - activated
- Bonds between cellulose microfibrils broken
- Cell wall loosens & becomes more elastic
- More water enters cell & turgor pressure increases
- so Cell wall expands
