15 - Nervous Coordination & Muscles

• Neurones:

  1. In its resting state, the outside of the membrane is positively charged as there are more positive ions outside
  2. The membrane is therefore polarised (has a difference in charge across it)
  3. Resting potential = -70 mV
  4. The resting potential is maintained by sodium potassium pumps & potassium ion channels in the membrane
• How are resting potentials maintained?

  • Sodium-Potassium pumps move Na+ ions out the neurone. The membrane is impermeable so they cannot move back in, creating a Na+ ion electrochemical gradient
  • The sodium-potassium pumps move K+ ions into the neurone & they diffuse back in through potassium ion channels
  • Making the outside positively charged
• How do sodium potassium pumps work?

  They move 3 sodium ions out the neurone by active transport for every 2 potassium ions moved in. Requires ATP

  
• How do Potassium ion channels work?

  Potassium ions move out the neurone by facilitated diffusion, down the concentration gradient

  
• Steps of an action potential:

  1. Stimulus - this excites the neurone, causes sodium ion channels to open. More sodium ions enter the neurone, makes the neurone less negative
  2. Depolarisation - potential reaches the threshold (around -55 mV), sodium channels open & ions diffuse into the neurone
  3. Repolarisation - at potential difference of +30 mV the sodium ion channels close & potassium ions open. Potassium ions diffuse out
  4. Hyperpolarisation - potassium ions channels are slow to close, slight overshoot (i.e. less than -70 mV)
  5. Resting Potential - ion channels reset back to resting potential

  
• Action Potentials move along the wave:

  1. When an action potential occurs, some of the sodium ions that enter the neurone diffuse sideways
  2. This causes sodium ion channels in the next region to open & for sodium ions to diffuse in
  3. Causes a wave of depolarisation to travel along the neurone
  4. Wave move away during refractory period because these parts can't fire an action potential.

  
• Discrete Impulses:

  1. During refractory period, ion channels are recovering & can't be opened
  2. So the refractory period acts as a time delay between one action potential & the next. This means that

  • action potentials don't overlap & are separate impulses
  • there's a limit to the frequency at which the nerve impulses can be transmitted
  • action potentials are unidirectional (can only travel in one direction)
• All-or-Nothing Nature:

  1. Once the threshold is reached, an action potential will always fire with the same change in voltage, no matter how large the stimulus
  2. If the threshold isn't reached, action potential won't fire
  3. A bigger stimulus won't cause a bigger action potential , but it causes them to fire more frequently

  
• How does Myelination affect speed of conduction?

  1. Myelin sheath is an electrical insulator, the sheath being made from Schwann Cells
  2. Between Schwann cells are nodes of Ranvier where Sodium Ion channels are concentrated
  3. In a myelinated neurone, depolarisation only happens at nodes as the impulse 'jumps' from node to node (called saltatory conduction)
  4. Otherwise the wave must travel along the whole length of the axon membrane

  
• How does Axon Diameter affect speed of conduction?

  Action potentials are conducted quicker along axons with bigger diameter because there's less resistance to the flow of ions
• How does Temperature affect speed of conduction?

  Speed of conduction increases with temperature as ions diffuse faster. This reaches a limit around 40C as proteins begin to denature
• Synaptic Transmission:

  1. When an action potential reaches the presynaptic neurone, it causes neurotransmitters to be released into the synaptic cleft
  2. They diffuse across & bind to receptors on the postsynaptic neurone
  3. This might trigger muscle contraction (in a muscle cell) or a hormone to be secreted (from a gland)
  4. Neurotransmitters are removed by the cleft to prevent the response from happening again e.g. either recycled into presynaptic neurone or broken down by enzymes

  
• Across a Cholinergic Synapse (1):

  1. Cholinergic Synapses use acetylcholine
  2. The action potential stimulates voltage-gated calcium ion channels to open & calcium ions diffuse into the synaptic knob

  
• Across a Cholinergic Synapse (2):

  1. The influx of calcium ions into the synaptic knob causes the synaptic vesicles to move into the presynaptic membrane & they then fuse with the membrane
  2. The vesicles release the neurotransmitter acetylcholine into the synaptic cleft
  3. This is called exocytosis

  
• Across a Cholinergic Synaptic (3):

  1. Acetylcholine diffuses across the synaptic cleft & binds to specific cholinergic receptors on the postsynaptic membrane
  2. This causes sodium ion channels in the postsynaptic neurone to open
  3. The influx of sodium ions generates an action potential in the postsynaptic neurone
  4. ACh is removed from the synaptic cleft so the response doesn't keep happening. It's broken down by the enzyme acetylcholinesterase & the products are re-absorbed into the presynaptic neurone and are used to make more ACh

  
• What do excitatory transmitters do ?

  They depolarise the postsynaptic membrane, making it fire action potentials if the threshold is reached. E.g. acetylcholine is an excitatory neurotransmitter at cholinergic synapses in the CNS - it binds to cholinergic receptors which causes an action potential
• What do inhibitory neurotransmitters do?

  They hyperpolarise the postsynaptic membrane which prevents it from firing an action potential. E.g. acetylcholine is an inhibitory neurotransmitter at cholinergic synapses in the heart. When it binds to receptors, it causes potassium ion channels to open on the postsynaptic membrane, hyperpolarising it.
• What is Spatial Summation?

  1. Sometimes many neurones connect to one neurone
  2. The small amounts of neurotransmitters add together & trigger an action potential
  3. If some neurones release an inhibitory neurotransmitter, than the total effect may be no action potential

  
• What is Temporal Summation?

  Temporal Summation is where 2 or more nerve impulses arrive in quick succession from the same presynaptic neurone, This makes an action potential more likely because more neurotransmitter is released into the synaptic cleft

  
• Neuromuscular Junctions:

  1. A neuromuscular junction is a synapse between a motor neurone & a muscle cell
  2. Neuromuscular junctions use acetylcholine, which binds to cholinergic receptors called nicotinic cholinergic receptors

  • The postsynaptic membrane has lots of folds that form clefts. These clefts store acetylcholinesterase
  • Postsynaptic neurone has more receptors
  • ACh is always excitatory at a neuromuscular junction. So when the motor neurone fires an action potential, it will trigger a response in the muscle cell.

  
• Drugs (Same Shape)

  • Some drugs bind to receptors as they're same shape (called agonists).
  • Means more receptors are activated
  • E.g. nicotine mimics acetylcholine, binding to nicotinic cholinergic receptors in the brain

  
• Drugs (Block receptors)

  • These drugs called antagonists
  • This means fewer receptors are activated.
  • E.g. curae blocks acetylcholine at neuromuscular junctions, resulting in paralysis

  
• Drugs (Inhibitors)

  • They inhibit the enzyme that breaks down neurotransmitters
  • Results in more neurotransmitters in the synaptic cleft binding to receptors
  • E.g. nerve gases stop acetylcholine from being broken down, resulting in loss of muscle control

  
• Drugs (Stimulants)

  • Some drugs stimulate the release of neurotransmitters from the presynaptic neurone so more receptors are activated e.g. amphetamines
• Drugs (Neurotransmitter Inhibitors)

  • Some drugs inhibit the release of neurotransmitters from the presynaptic neurone so fewer receptors are activated e.g. alcohol
• Muscles act in Antagonistic Pairs:

  1. Skeletal muscle is the type of muscle used to move e.g. biceps & triceps move the lower arm
  2. Skeletal muscles are attached to bones by tendons
  3. Ligaments attach bones to other bones
  4. Pairs of skeletal muscles contract & relax to move bones at a jones. As bones are incompressible, they act as levers, giving the muscles something to pull against
  5. Muscles that work together to move a bone are called antagonistic pairs. Contracting muscle = Agonist, Relaxing muscle = Antagonist

  
• Example of Antagonistic Pairs:

  1. Bones of the lower arm are attached to a biceps muscle & a triceps muscle by tendons
  2. The biceps & triceps work together to move your arm - as one contracts, the other relaxes

  
• Muscle Fibres:

  1. Skeletal muscles are made of Muscle Fibres, with their 'cell membrane' is called the sarcolemma
  2. Bits of the sarcolemma fold inwards across the muscle fibre called the transverse (T) tubules & they help to spread electrical impulses.
  3. Sarcoplasmic reticulum = A network of internal membranes which stores & release calcium ions required for muscle contraction
  4. Muscle fibres have lots of mitochondria & are multinucleate (contain many nuclei)
  5. Fibres are made of long organelles called myofibrils. They're made of proteins & specialised for contraction

  
• Myofibrils Structure:

  1. Thick myofilaments are made of myosin, Thin by Actin
  2. Dark bands contain thick myosin filaments overlapped with some thin actin filaments (A Bands)
  3. Light bands contain only thin actin filaments (I Band)
  4. A myofibril is made of short units called sarcomeres, the end of which is a Z Line
  5. The M line is in the middle of the sarcomere in the middle of a myosin filament
  6. The H Zone is the central area which only contains myosin filaments

  
• Sliding Filament Theory:

  1. Myosin & Actin filaments slide over each other to make sarcomeres contract - the myofilaments themselves don't contract
  2. The simultaneous contraction of lots of sarcomeres means the myofibrils & muscle fibres contract
  3. Sarcomeres return to their original length as the muscle relaxes.

  The A band stays the same length, but the I Band & H Zone get shorter, so the overall sarcomere gets shorter

  
• Muscle Contraction:

  1. Myosin filaments have globular heads that are hinged
  2. Each myosin head has a binding site for actin & for ATP
  3. Actin filaments have binding sites for myosin heads called actin-myosin binding sites
  4. Another protein called tropomyosin is found in between actin filaments. It helps myofilaments move past each other.
  5. In resting muscle the tropomyosin blocks the actin-myosin binding sight - thus the myofilaments can't slide past each other

  
• How is Muscle Contraction Triggered (1)?

  1. The action potential stimulates the muscle cell, depolarising the sarcolemma, spreading down to the sarcoplasmic reticulum
  2. Sarcoplasmic reticulum releases calcium ions into the sarcoplasm
  3. Calcium ions bind to protein attached to tropomyosin, changing its shape & pushing the tropomyosin out the binding site
  4. Binding site is exposed, allowing myosin head to bind to the actin with the bond being called an actin-myosin cross bridge
  5. Calcium ions also activate the enzyme ATP hydrolyse which hydrolyses ATP to provide energy

  
• How is Muscle Contraction Triggered (2)?

  1. The energy released causes the myosin head to bend, pulling the actin filament along
  2. Another ATP molecule breaks the actin-myosin cross bridge so it detaches
  3. It reattaches at a different binding site further along the actin filament
  4. Many cross bridges from & break rapidly, pulling the actin along & causing contraction
  5. Cycle continues as long as calcium ions present

  
• When Excitation stops, Calcium ions leave:

  1. When the muscle stops being stimulated, calcium ions leave their binding sites & are moved by active transport into the sarcoplasmic reticulum (requires ATP)
  2. Tropomyosin molecules move back, blocking the actin-myosin binding site
  3. Myosin heads detach so muscles don't contract
  4. Actin filaments slide back to their relaxed position, lengthening the sarcomere

  
• Energy provided for Muscle Contraction (Aerobic Respiration):

  • Most ATP generated via oxidative phosphorylation in the cell's mitochondria
  • Aerobic respiration only works with an oxygen supply so it's good for long period of low-intensity exercise
• Energy provided for Muscle Contraction (Anaerobic Respiration):

  • ATP made rapidly in glycolysis
  • End product of glycolysis is pyruvate, which is converted to lactate by lactate fermentation
  • Lactate can quickly build up in the muscles & cause muscle fatigue
  • Anaerobic respiration is good for short periods of hard exercise (e.g. 400m sprint)
• Energy provided for Muscle Contraction (ATP-Phosphocreatine (PCr) System):

  • ATP is made by phosphorylating ADP with a phosphate group from PCr
  • PCr is stored inside cells & the ATP-PCr system generates ATP very quickly
  • PCr runs out after a few seconds so works best during short bursts of vigorous exercise (e.g. a tennis serve)
  • The ATP-PCr system is anaerobic (no oxygen) & alactic (doesn't form lactate)

  
• Slow Twitch Muscle Fibres:

  • Contract Slowly
  • Muscles used for posture
  • Good for endurance activities e.g. maintaining posture in a long-distance running
  • Can work long times without tiring
  • Energy released through aerobic respiration. Contains lots of mitochondria & blood vessels to supply muscles with oxygen
  • Red in colour as they're rich in myoglobin - red protein that stores oxygen
• Fast Twitch Muscle Fibres:

  • Contract quickly
  • Muscles used for fast movement
  • Good for short bursts of speed & power e.g. eye movement or sprinting
  • Tires quickly
  • Energy's released quickly through anaerobic respiration using glycogen (stored glucose). Few mitochondria or blood vessels
  • White in colour as they don't contain much myoglobin (can't store much oxygen)