Nervous co-ordination

1) The process starts in the SAN which is in the walls of the right atrium.

2) The SAN acts as a pacemaker by sending out waves of electrical activity to the atrial walls to set the rhythm of the heartbeat.

3) This causes the right and left atria to contract at the same time.

4) A band of non-conducting collagen tissue prevents the waves from being passed directly from the atria to the ventricles.

5) The waves are instead transferred from the SAN to the AVN.

6) The AVN passes the waves to the bundle of His, but theres a slight delay to allow the atria to empty

7) The bundle of His is a group of muscle fibres that conduct the waves between the ventricles and the ape. The bundle splits into the Purkyne tissue.

8) The Purkyne tissue carries the waves into the muscular wall of the ventricles causing them to contract simultaneously from the bottom up.

High blood pressure - Baroreceptors detect it - Impulses are sent to the medulla which send impulses along parasympathetic neurones. These secret acetylcholine which binds to receptors on SAN - Heart rate slows down and blood pressure returms back to normal.

Low blood pressure- Baroreceptors detect it - Impulses are sent to the medulla which sends impulses along sympathetic neurones, they secrete noradrenaline which binds to receptors on SAN- Heart rate increases to increase blood pressure back to normal.

High blood O2, low CO2 or high pH levels - Chemoreceptors detect it - Impulses sent to the medulla. sends impulses along parasympathetic neurones, they secrete acetycholine which binds to receptors on SAN- Heart rate decreses to return chemical levels back to normal.

Low blood O2, high blood CO2 or low pH- Chemoreceptors detect it- Impulses sent to medulla, sends impulses along symapthetic neurones which secrete noradrenaline which binds to receptors on SAN- Heart rate increases to turn chemical levels back to normal.

1) Stimulus - this excites the neurone cell membrane causing sodium ion channels to open. The membrane becomes more permeable to sodium, so sodium ions diffuse into the neurone down the chemical gradient making the inside of the neurone less negative

2) Depolarisation- if the potential difference reaches the threshold (around -55mV) more sodium ion channels open so more sodium ions diffuse rapidly into the neurone.

3) Repolarisation- at a potential difference of around +30mV the sodium ion channels close and the potassium ion channels open. The membrane is now more permeable to potassium ions so they diffuse out of the neurone down their conc gradient. This starts to get the membrane back to its resting potential.

4) Hyperpolarisation- potassium ion channels are slow to close so theres a slight overshoot where too many potassium ion diffuse out of the neurone. The potential difference becomes more negative than the resting potential.

5) Resting potential- the ion channels are reset. The sodium potassium pump returns the membrane to its resting potential and maintains it until the membrane is excited again.

6) Refractory period- neurone can't be excited straight away

1) Myelination- allows saltatory conduction, where the impulse can jump along the nodes of ranvier which increases the speed of conduction.

2) Axon diameter- action potentials are conducted quicker along axons with bigger diameters because there's less resistance to the flow of ions than in the cytoplasm of a smaller axon. With less resistance, depolarisation reaches other parts of the neurone cell membrane quicker.

3) Temperature- the speed of conduction increases as temperature increases, because ions diffuse faster. Speed only increases up to around 40 degrees- after that the proteins denature and the speed decreases.

Spatial summation- when many neurones connect to one neurone. The small amount of neurotransmitter released from each of these neurones can be enough altogether to reach the threshold and trigger an action potential.

Temporal summation- where two or more nerve impulses arrive in quick succession from the same presynaptic neurone. This makes an action potential more likely because more neurotransmitter is releases into the synaptic cleft.

- Skeletal muscles are attached to bones by tendons.

- Ligaments attach bones to other bones to keep them together.

- Pairs of skeletal muscles contract and relax to move bones at a joint. The bones of the skeleton are incompressible so they can act as levers, giving the muscles something to pull against.

- Muscles that work together to move a bone are called antagonistic pairs. The contracting muscle is called the agonist and the relaxing muscle is called the antagonist.

- Skeletal muscle is made up of large bundles of long cells called muscle fibres.

- The cell membrane of muscle fibre cells is called the sarcolemma.

- Bits of the sarcolemma fold inwards across the muscle fibre and stick into the sarcoplasm. These fold are T tubules and they help spread electrical impulses throughout the sarcoplasm.

- The sarcoplasmic reticulum stores and releases calcium ions that are needed for muscle contraction.

- Muscle fibres have lots of mitochondria to provide the ATP thats needed for muscle contraction.

- Myofibrils contain bundles of thick and thin myofilaments that move past each other to make the muscles contract.

- Thick myofilaments are made of the protein myosin.

- Thin myofilaments are made of the protein actin.

1) Myosin and actin filaments slide over one another to make the sarcomeres contract - the myofilaments themselves don't contract

2) The simultaneous contraction of lots of sarcomeres means the myofibrils and muscle fibres contract.

3) Sarcomeres return to their original lenght as the muscles relax

1) An action potential stimulates a muscle cell and depolarises the sarcolemma, depolarisation spreads down T tubules to sarcoplasmic reticulum causing Ca2+ ions to be released.

2) The Ca2+ ions bind to tropomyosin causing it to change shape, pulling it out of the binding site on the actin filament.

3) This exposes the binding site allowing the myosin head to bind. The bond formed when the head binds = actin-myosin cross bridge.

4) Calcium ions also activate ATP hydrolase which breaks down ATP to providing the energy needed for muscle contraction.

5) The energy released causes the myosin head to bend which pulls the actin filament along in a rowing action

6) Another ATP molecule provides the energy to break the cross bridge so the head detaches.

7) The head reattaches to a different binding site further along the filament, the cycle is repeated causing the muscle to contract.