6B: Nervous Coordination

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  • Created by: DBaruch
  • Created on: 07-11-16 19:29

The resting membrane potential

  • In a neurones resting state, the outside of the cell is positively charged compared to the inside this is because there are more positive ions on the outside compared to inside, this causes the membrane to be polarised as there is a difference in charge. The voltage across the membrane when its at rest is called resting potential and is about 70millivolts
  • The resting potential is maintained by sodium-potassium pumps and potassium ion channels in a neurones membrane. Sodium-potassium pumps use active transport to move 3 sodium ions out of the neurone for every 2 potassium ions moved in ATP is needed to do this. Potassium ion channels allow facilitated diffusion of potassium ions out of the neurone, down their concentration gradient.
  • The sodium-potassium pump move sodium ions out of the neurone, but the membrane isn't permeable to sodium ions so they can't diffuse back in. This creates a sodium ion electrochemical gradient because there are more positive sodium outside the cell. The sodium-potassium pumps also move potassium ions in to the neurone. When the cell's at rest, most potassium ion channels are open. This means that the membrane is permeable to potassium ions so some diffuse back out through potassium ion channels.
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Action Potentials

  • 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 sodium ion electrochemical gradient. This makes the inside of the neurone less negative
  • Depolaristation- if the potential difference reaches the threshold, more sodium ion channels open. More sodium ions diffuse into the neurone.
  • Repolarisation- at a potential difference of around +30mV the sodium channels close and potassium channels open. The membrane is more permeable to potassium so potassium ions diffuse out of the neurone down the potassium ion concentration gradient.
  • Hyperpolarisation- potassium ion channels are slow to close so there's a slight "overshoot" where too many potassium ions diffuse out of the neurone. The resting potential becomes more negative than the resting potential
  • Resting potential- the ion channels are reset. The sodium-potassium pump returns the membrane to its resting potential by pumping sodium ions out and potassium ions in, this maintains the resting potential until another stimulus excites the membrane
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The refractory period and waves of depolarisation

  • After an action potential, the neurone cannot be excited straight away. This is because the ion channels are recovering and they can't be made to open. Sodium channels are closed during repolarisation and potassium ion channels are closed during hyperpolarisation. The refractory period acts as a time delay between 1 action potential and the next. This makes sure that action potentials don't overlap but pass along as separate impulses.
  • When an action potential occurs, some of the sodium ions that enter the neurone difuse sideways. This causes the sodium ion channels in the next of the neurone to open and sodium ions diffuse into that part. This causes a wave of depolarisation to travel along the neurone. The wave moves away from the parts of the membrane in the refractory period because these parts can't fire an action potential.
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All or nothing principle

  • Once the threshold is reached, an action potential will always fire with the same change in voltage, no matter how big the stimulus is. If the threshold isn't reached, an action potential won't fire. A bigger stimulus won't cause a bigger action potential but it will cause them to fire more frequently
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Speed of conduction

  • Myelination- some neurones are myelinated meaning that they have a myelin sheath which is an electrical insulator. In the peripheral nervous system, the sheath is made of a type of cell called a schwann cell. Between the schwann cells are tiny patches of bare membrane called nodes of ranvier. Sodium ion channels are concentrated at the nodes of ranvier.
  • Saltatory conduction- in a myelinated neurone, depolaristation only happens at the nodes of ranvier. The neurones cytoplasm conducts enough electricity to depolarise the next node, so the impulse "jumps" from node to node. In a non-myelinated neurone, the impulse travels as a wave along the whole length of the axon membrane, so you get depolarisation along the whole length of the membrane.
  • Axon diameter- action potentials are conducted quicker along axons with bigger diameters because there is less resistance to the flow of ions than in the cytoplasm of a smaller axon, with less resistance, depolaristation reaches other parts of the neurone cell membrane quicker
  • Temperature- the speed of conduction only increases up to around 40 oC as ion diffusion is faster, after 40 oC proteins begin to denature.
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Synapses and neurotransmitters

  • A synapse is the junction between a neurone and another neurone, or between a neurone and an effector cell for example a muscle or gland cell. The tiny gap between the cells as a synapse is called the synaptic cleft. The presynaptic neurone has a swelling called a synaptic knob, this cotains the vesicles filled with neurotransmitters.
  • When an action potential reaches the end of the neurone it causes neurotransmitters to be released into the cleft. They diffuse across to the postsynaptic membrane and bind to specific receptors. When neurotransmitters bind to receptors they might trigger an action potential. Because the receptors are only on the postsynaptic membranes, synapses make sure impulses are unidirectional. Neurotransmitters are removed from the cleft so the response doesn't keep happening they are taken back into the presynaptic neurone or they are broken down by enzymes.
  • Acetylcholine (ACh), binds to cholinergic receptors. Synapses that use ACh are called cholinergic synapses.
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Cholinergic synapses

  • Arrival of an action potential- an action potential arrives at the synaptic knob of the presynaptic neurone. The action potential stimulates voltage-gated calcium ion channels in the presynaptic neurone to open. Calcium ions diffuse into the synaptic knob.
  • Fusion of the vesicles- the influx of calcium ions into the synaptic knob causes the synaptic vesicles to fuse with the presynaptic membrane. The vesicles release the neurotransmitter ACh into the synaptic cleft by exocytosis( the process by which a vesicle inside a cell moves to the cell-surface membrane, fuses with the membrane and releases its contents outside the cell)
  • Diffusion of ACh- ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the postsynaptic membrane. This causes sodium ion channels in the postsynaptic neurone to open. The influc of sodium ions into the postsynaptic membrane causes depolarisation. An action potential on the postsynaptic membrane is generated if the threshold is reached. ACh is removed from the synpatic cleft so the response doesn't keep happening. It is broken down by acetylcholinesterase (AChE) and the products are reabsorbed by the presynaptic neurone and used to make more ACh
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Excitatory and inhibitory neurotransmitters

  • Neurotransmitters can be excitatory, inhibitory or both. Excitatory neurotransmitters depolarise the postsynaptic membrane, making it fire an action potential if the threshold is reached. Inhibitory neurotransmitters hyperpolarise the postsynaptic membrane, preventing it from firing and action potential.
  • For example Acetylcholine is an inhibtory neurotransmitter at cholinergic synapses in the heart. When it binds to receptors here, it can causes potassium ion channels to open on the post synaptic membrane, hyper polarising. ACh is also an excitatory neurotransmitter as it binds to cholingeric receptors to cause an action poteintial in the postsynaptic membrane at cholingeric synapses in the CNS and neuromuscular junctions.
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Summation

  • If a stimulus is weak, only a small amount of neurotransmitter will be released from a neurone into the synaptic cleft. This might not be enough to excite the postsynaptic membrane to the threshold level and stimulate an action potential. Summation is where the effect of neurotransmitters released from many neurones is added together.
  • Spatial summation- spatial summation is where 2 or more postsynaptic neurones release their neurotransmitters at the same time onto the same postsynaptic neurone. The small amount of neurotransmitter relased from each of these neurones can be enough altogether to reach a threshold and trigger an action potential
  • 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 relased into the synaptic cleft.
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Neuromuscular junctions

  • A neuromuscular junction is a specialised cholingeric synapse between a motor neurone and a muscle cell. Neuromuscular junctions use the neurotransmitter ACh, which binds to cholinergic receptors called nicotinic cholinergic receptors. Neuromuscular junctions release ACh from vesicles in the presynaptic membrane, ACh then diffuses across the synaptic cleft and binds to cholinergic receptors on the postsynaptic membrane. In both types of synapses, ACh is broken down in the synaptic cleft by the enzyme acetylcholinesterase (AChE).
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Neuromuscular junctions

  • A neuromuscular junction is a specialised cholingeric synapse between a motor neurone and a muscle cell. Neuromuscular junctions use the neurotransmitter ACh, which binds to cholinergic receptors called nicotinic cholinergic receptors. Neuromuscular junctions release ACh from vesicles in the presynaptic membrane, ACh then diffuses across the synaptic cleft and binds to cholinergic receptors on the postsynaptic membrane. In both types of synapses, ACh is broken down in the synaptic cleft by the enzyme acetylcholinesterase (AChE). Thepostsynaptic membrane has lots of folds that form clefts. These clefts store AChE.The postsynaptic membrane has more receptorsthan other synpases. ACh is always excitatory, so when motor neurone fires an action potential, it normally triggers a reponse in a muscle cell. This isn't always the case for a synapse between 2 neurones.
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Drugs at synapses

  • Drugs can affect synaptic tranmission. for example drugs are the same shape as neurotransmitters so they mimic their action at receptors these drugs are called agonists this means that more receptors are activated. For example nicotine mimics acetylcholine so binds to nicotinic cholinergic receptors in the brain.
  • Some drugs block receptors so they can't be activated by neurotransmitters these drugs are called antagonists. This means fewer receptors can be activated for example curare blocks the effects of ACh by blocking nicotinic cholinergic recepotrs at neuromusculer junctions, so muscle cells can't be stimulated, this results in muscle paralysis.
  • Some drugs inhibit the enzyme that breaks down neurotransmitters. This means there are more neurotransmitters in the synaptic cleft to bind to receptors and they are there for longer for example nerve gases stop ACh from being broken down in the synpatic cleft. This can lead to loss of muscle control.
  • Some drugs stimulate the release of the neurotransmitter from the presynaptic neurone so more receptors are activated for example ampheteamines force a neurotransmitter called dopamine out of the synaptic vesicles and into the synaptic cleft.
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Types of muscle and muscle structure

  • Smooth muslce- contracts without conscious control. It's found in walls of internal organs.
  • Cardiac muscle- contracts without conscious control but its only found in the heart
  • Skeletal muscle- is the type of muscle you use to move.
  • Skeletal muscles are attached to bones by tendons. Ligaments attach bones to other bones. Pairs of skeletal muscles contract and relax to move bones at a joint.
  • Antagonistic pairs are muscles that work together.The contracting muscle is called the agonist and the relaxing muscle is called antagonist. For example biceps and triceps.
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Structure of skeletal muscle

  • Skeletal muscles are made up of large bundles oflong cells, called muscle fibres. The cell membrane of muscle fibre cells is called sarcolemma. Bits of sarcolemma fold inwards across the muscle fibre and stick into the sarcoplams. These folds are called transverse tubules and they help to send electrical impulses thoughout the sarcoplasm so they reach all parts of the muscle fibre. A network of internal membranes called the sarcoplasmic reticulum runs thoughout the sarcoplasm. The sarcoplasmic reticulum stores and releases calcium ions that are need for muscle contraction. Muscle fibres have lots of mitochondira to provide ATP that is needed for muscle contraction. They multinucleate and have lots of long cylindrical organelles called myofibrils.
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Myofibrils

  • Myofibrils contain bundles of thick and thin myofilaments that move past each other to make muscles contact. The myofilaments are made of the protein myosin and the thin myofilaments are made made of the protein actin. Looking at a myofibril under an electron microscope shows there are a pattern of alternating dark and light bands. Dark bands contain thick myosin filaments and some overlapping actin filaments and they are called A-bands. Light bands contain actin only and these are called I-bands. A myofibril is made up of many short units called sarcomeres. The ends of each sarcomere are marked with a Z-line. In the middle of each sarcomere is an M-line. It is the middle of the myosin filaments, around the M-line is the H-zone which contains only myosin filaments
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Myofibril image

Image result for structure of muscle

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Sliding filament theory

  • Muscle contraction is explained by the sliding filament theory. This is where myosin and actin filaments slide over one another to make sarcomeres contract- the myofilaments dont contract. The simultaneous contraction of lots of sarcomeres means the myofibrils and muscle fibres contract. Sarcomeres return to their original length as the muscle relaxes.
  • Image result for sliding filament theory (http://www.teachpe.com/images/anatomy-physiology/sliding_filament_1a.jpg)
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Myosin and actin filaments and binding sites in re

  • Myosin filaments have globular heads that are hinged, so they can move back and forth. Each myosin head has a binding site for actin and a binding site for ATP
  • Actin filaments have binding sites for myosin heads, called actin-myosin binding sites. Another protein called tropomyosin is found between actin filaments. It helps myofilaments move past each other
  • For myosin and actin filaments to slide past each other, the myosin head needs to bind to the actin-myosin binding site on the actin filaments. In a resting muscle the actin-myosin binding is blocked by tropomyosin. This means myofilaments can't slide past each other because the myosin heads can't bind to the actin filaments.
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The process of muscle contraction

  • Arrival of an action potential- when an action potential arives it depolarises the sarcolemma. The depolarisation spreads down the T-tubules to the sarcoplasmic reticulum. This causes the sarcoplasmic reticulum to relase stored calcium ions into the sarcoplasm. The increase in calcium ions triggers a muscle contraction. Calcium ions bind to a protein attached to tropomyosin causing the protein to change shape. This pulls the attached tropomyosin out of the actin-myosin binding site on the actin filament. This exposes the binding site which allows the myosin head to bind. The bond formed when a myosin head attacheds to a actin filament is called an actin-myosin cross bridge.
  • Movement of the actin filament- calcium ions also activate the enzyme ATP hydrolase, the energy released from ATP causes the myosin head to bend which pulls the actin filament along in a rowing action
  • Breaking of the cross bridge- Another ATP molevule provides the energy to break the actin-myosin cross bridge, so the myosin head detaches from the the actin filament. The myosin head then returns to its starting position and reattaches to a different binding site further along the actin filament and the cycle is repeated. Many actin-myosin cross bridges form and break rapidly, pulling the actin filament along, this shortens the sarcomere causing the muscle to contract
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Energy for muscle contraction

  • Aerobic respiration- most ATP is generated via oxidative phosphorylation in the cells mitochondria. Aerobic respiration only works when theres oxygen so its good for long periods of low intensity exercise.
  • Anaerobic respiration- ATP is made rapidly by glycolysis. The end product is pyruvate, which is converted to lactate by lactate fermentation. Lactate can quickly build up in the muscles and causes muscle fatigue. Anaerobic repisration is good for short periods of hard exercise
  • ATP-phosphocreatine system(PCr)- ATP is made by phosphorylating ADP. PCr is stored inside cells and the ATP-PCr system generates ATP very quickly. PCr runs out after short bursts of vigorous exercise. The ATP-PCr system is anaerobic and its alactic. Some of creatine gets broken down into creatinine, which is removed from the body via the kidneys. Creatinine levels can be higher in people who exercise regularly. High creatinine levels may also indicate kidney damage
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Slow and fast twitch

  • Slow twitch- they contract slowly and can work for a long time without getting fatigued. This makes them good for endurance activities. High amounts of slow twitch muscle fibres are found in the muscles used for posture. Energy is relased slowly through aerobic respiration. They have lots of of mitochondria and blood vessels to supply the muscles with oxygen. The mitochondria are found near the edge of muscle fires, so that there is a short diffusion pathway.
  • Fast twitch- they contract quickly and fatigue quickly. This makes them good for short bursts of speed and power. High proportions of fast twitch muscles are found in the legs, arms and eyes. Energy is released quickly through anaerobic respiration using glycogen in fast twitch muscle fibres they also have stores of phosphocreatine so that energy can be generated very quickly when need. They have few mitochondria or blood vessels and dont have much myoglobin so they cannot store much oxygen.
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