3.6.2 NERVOUS COORDINATION

• Nervous impulses are the electrical charges transmitted along a neurone.

  Created by the movement of sodium and potassium ions.
• The resting membrane potential -

  • In a neurone’s resting state (when it’s not being stimulated), the outside of the membrane is positively charged compared to the inside - more positive ions outside cell than inside. 
  • So membrane is polarised — difference in charge (called potential difference/voltage) across it.
  • Resting potential = the voltage/potential difference across the membrane when it’s at rest - about –70 mV (millivolts).
• The resting potential is created and maintained by sodium-potassium pumps and potassium ion channels in a neurone’s membrane. 

  • Sodium-potassium pumps use active transport to move three sodium ions (Na+) out of the neurone for every two potassium ions (K+) moved in. ATP is needed to do this.
  • Potassium ion channels allow facilitated diffusion of potassium ions (K+) out of the neurone, down their concentration gradient.
• Resting Potential Process -

  • Sodium-potassium pumps move sodium ions out of the neurone. Membrane not permeable to sodium ions, so can’t diffuse back in.
  • Creates a sodium ion electrochemical gradient (more positive sodium ions outside cell than inside).
  • The sod-pot pumps also move potassium ions into the neurone.
  • Cell at rest - most potassium ion channels open. Means membrane is permeable to potassium ions, so some diffuse back out through potassium ion channels.

  Overall more positive ions move out than in. Makes outside of the cell positively charged compared to inside.
• Action potentials -

  When a neurone is stimulated, sodium ion channels in the cell membrane open.

  If the stimulus is big enough, it’ll trigger a rapid change in potential difference.

  This causes the cell membrane to become depolarised (no longer polarised). 
• Action Potential Process 1

  • Stimulus — excites the neurone cell membrane, causing Na ion channels to open. Membrane more permeable to Na, so Na ions diffuse into neurone down Na ion electrochemical gradient. Makes inside of neurone less negative.
  • Depolarisation — if p.d reaches threshold (around –55 mV), more Na ion channels open. More Na ions diffuse into neurone.
  • Repolarisation — at p.d of around +30 mV Na ion channels close and K ion channels open. Membrane more permeable to K so K ions diffuse out of neurone down K ion conc grad. Starts to return membrane to its resting potential.
• Action Potential Process 2

  • Hyperpolarisation — K ion channels slow to close so slight ‘overshoot’ where too many K ions diffuse out of neurone. P.d becomes more negative than resting potential (less than –70 mV).
  • Resting potential — ion channels reset. The sodium-potassium pump returns membrane to resting potential by pumping Na ions out and K ions in, and maintains the resting potential until the membrane’s excited by another stimulus.
• The refractory period -

  After an action potential, the neurone cell membrane can’t be excited again immediately. Because ion channels recovering and can’t be made to open — Na ion channels closed during repolarisation and K ion channels closed during hyperpolarisation.

  Recovery called the refractory period.

  • Acts as a time delay between action potentials - makes sure they don’t overlap - pass along as separate (discrete) impulses. 
  • Means a limit to frequency at which nerve impulses can be transmitted, and that action potentials are unidirectional.
• Waves of depolarisation -

  When an action potential happens, some of the sodium ions that enter the neurone diffuse sideways. This causes sodium ion channels in the next region 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.
• All or Nothing Principle (of action potentials)

  • 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.
• 3 factors affect the speed of conduction of action potentials:

  • myelination
  • axon diameter
  • temperature
• Speed of conduction - myelination

  • Some neurones, including many motor neurones, are myelinated - have a myelin sheath, an electrical insulator.
  • In the peripheral nervous system, the sheath is made of Schwann cells.
  • Between the Schwann cells are the nodes of Ranvier - patches of bare membrane. Sodium ion channels are concentrated at the nodes of Ranvier.
  • Increase speed through saltatory conduction.
• Saltatory conduction

  • In a myelinated neurone, depolarisation only happens at the nodes of Ranvier (where sodium ions can get through the membrane). The neurone’s cytoplasm conducts enough electrical charge to depolarise the next node, so the impulse ‘jumps’ from node to node. Called saltatory conduction and is really fast. 
  • 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. This is slower than saltatory conduction.
• Speed of conduction - 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.
• Speed of conduction - temperature

  • Speed of conduction increases as temperature increases, as ions diffuse faster.
  • Only increases up to around 40 °C — after that the proteins begin to denature and the speed decreases.
• Synapse = the junction between 2 neurones, or between a neurone and an effector cell, e.g. a muscle cell. 

  Synaptic Cleft = the gap between the cells at a synapse. 
• Presynaptic neurone (one before synapse) has a swelling called a synaptic knob, containing synaptic vesicles filled with chemicals called neurotransmitters.

  • Many different neurotransmitters. One called acetylcholine (ACh), binds to cholinergic receptors. Synapses that use acetylcholine are cholinergic synapses.
• • When an action potential reaches the end of a neurone it causes neurotransmitters to be released into the synaptic cleft. 
  • They diffuse across to the postsynaptic membrane (one after the synapse) and bind to specific receptors. 
  • When neurotransmitters bind to receptors they might trigger an action potential (in a neurone), cause muscle contraction (in a muscle cell), or cause a hormone to be secreted (from a gland cell).
• • Because the receptors are only on the postsynaptic membranes, synapses make sure impulses are unidirectional.
  • Neurotransmitters are removed from the synaptic cleft so the response doesn’t keep happening, e.g. they’re taken back into the presynaptic neurone or broken down by enzymes (and products taken into the neurone).
• Cholinergic synapses - ACh binds to cholinergic receptors to cause an action potential in the postsynaptic membrane.
• Nerve impulse transmission across a cholinergic synapse 1:

  • Action potential arrives at synaptic knob of presynaptic neurone.
  • Stimulates voltage-gated Ca ion channels in presynaptic neurone to open.
  • Ca ions (Ca2+) diffuse into synaptic knob. (Pumped out afterwards by active transport.)
  • Causes the synaptic vesicles to fuse with the presynaptic membrane.
  • Vesicles release the neurotransmitter acetylcholine (ACh) into the synaptic cleft by exocytosis.
• Nerve impulse transmission across a cholinergic synapse 2:

  • ACh diffuses across synaptic cleft + binds to specific cholinergic receptors on the postsynaptic membrane.
  • Causes Na ion channels in postsynaptic neurone to open.
  • Influx of Na ions into postsynaptic membrane causes depolarisation. An action potential on postsynaptic membrane generated if threshold reached. 
  • ACh removed from synaptic cleft so response doesn’t keep happening. Broken down by acetylcholinesterase (AChE) and the products are re-absorbed by the presynaptic neurone and used to make more ACh.
• Neurotransmitters can be excitatory, inhibitory or both.

  • Excitatory neurotransmitters depolarise the postsynaptic membrane, making it fire an action potential if the threshold is reached.
  • Acetylcholine is an excitatory neurotransmitter at cholinergic synapses in the CNS and at neuromuscular junctions
  • Inhibitory neurotransmitters hyperpolarise the postsynaptic membrane (make the potential difference more negative), preventing it from firing an action potential. Called inhibitory synapse. 
• Summation at synapses -

  • If a stimulus is weak, only a small amount of neurotransmitter will be released from a neurone into the synaptic cleft.
  • 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 (or 1 neurone stimulated a lot in a short period of time) is added together. Means synapses accurately process information. 
  • 2 types of summation: spatial, temporal
• Spatial summation -

  2 or more presynaptic neurones release their neurotransmitters at the same time onto the same postsynaptic neurone.

  The small amount of neurotransmitter released from each of these neurones can be enough altogether to reach the threshold in the postsynaptic neurone and trigger an action potential.

  If some neurones release an inhibitory neurotransmitter then the total effect of all the neurotransmitters might be no action potential.
• Temporal summation -

  • 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 junction - a specialised cholinergic synapse between a motor neurone and a muscle cell.

  Use the neurotransmitter acetylcholine (ACh), which binds to cholinergic receptors called nicotinic cholinergic receptors.
• Neuromuscular junctions work in basically the same way as cholinergic synapses.

  In both types of synapse, ACh is broken down in the synaptic cleft by acetylcholinesterase (AChE). 

  Differences:

  At a neuromuscular junction:

  • The postsynaptic membrane has lots of folds that form clefts which store AChE.
  • The postsynaptic membrane has more receptors than other synapses.
  • ACh is always excitatory, so when a motor neurone fires an action potential, it normally triggers a response in a muscle cell. This isn’t always the case for a synapse between two neurones.
• Drugs can affect synaptic transmission in various ways:

  • Some (agonists) are the same shape as neurotransmitters so mimic their action at receptors. More receptors activated.
  • Some (antagonists) block receptors so can’t be activated by neurotransmitters. Fewer receptors (if any) can be activated.
  • Some inhibit the enzyme that breaks down neurotransmitters. So more neurotransmitters in the synaptic cleft to bind to receptors and they’re there for longer.
  • Some stimulate/inhibit release of neurotransmitter from presynaptic neurone so more/fewer receptors activated.