Simple Reflexes

• Rapid automatic response to a stimulus which is not under conscious control. Usually have a survival value.
• Advantages of Simple Reflexes:

  • fast - short pathway with few neurones and synapses
  • protect us from harmful stimuli
  • involuntary - leaving the brain free to carry out more complex responses
  • innate - they don't have to be learned so are immediately protecting the organism from birth.
• Resting Potential:

  • occurs when the neurone is at rest
  • a condition where the outside of the membrane is more positively charged compared to the inside which is more negatively charged.
  • neurone is said to be polarised.
  • neurone has a voltage difference of ~-70mV.
  • it is the membrane which is polarised.
• How is the resting potential maintained?


  • At rest, the sodium ion channels are closed.
  • Membrane is 100 times more permeable to K+ ions causing some to diffuse out.
  • The "sodium-potassium" pump pumps 2K+ ions in for 3Na+ ions pumped out. This further creates a charge difference.
  • This causes outside of the membrane to be more positively charged compared to inside. The inside of the membrane is more negative compared to the outside.
  • An electrochemical gradient is established.
• Depolarisation in an action potential:

  • prior to depolarisation, the stimulus causes sodium ion channels to open and sodium ions diffuse in. If enough diffuse in then the charge in pd across the membrane causes all of the voltage gated sodium ion channels to open. This is an example of positive feedback.
• When the neurone is excited past it's "threshold" the following events occurs:

  • sodium ions diffuse quickly into the axon as the voltage gated sodium ion channels open.
  • the inside of the axon becomes temporarily positive while the outside becomes temporarily negative. This is known as "depolarisation".
  • Adjacent voltage gated sodium ion channels open to continue the depolarisation
• Repolarisation:

  • This is the restoring of + charge on the outside of the axon membrane and more negative on the inside.
  • Voltage gated K+ channels open and K+ flood out.
  • This progressively makes the outside of the membrane more positive.
  • Voltage gated Na+ channels close.
  • The Na+/K+ pump, pumps Na+ out of the cell.
• Hyperpolarisation

  During repolarisation, the potential difference across the membrane decreases to below the original. This is because, the voltage gates K+ channels are slow to close so the K+ keep diffusing out of the axon. They finally do close and the Na+/K+ pump restores the original resting potential to the neurone.
• Refractory Period:

  • Brief period of time between the end of depolarisation when the VG Na+ channels close and when they are ready to reopen again.
  • No new action potentials can be created during this time.

  It ensures:

  • unidirectionality
  • the action potentials are discrete
  • to not overload the brain.
• All or None Response:

  If an axon is stimulated above it's threshold it will trigger an action potential which will always result.

  A bigger stimulus won't cause a bigger action potential but it will cause a higher frequency of action potentials.
• Factors which increase the transmission of an impulse:

  1. Increased temperature - increases speed of transmission as the ions can diffuse across the membrane faster.
  2. Myelination - transmission across a myelinated axon is faster as depolarisation only occurs at the Nodes of Ranvier as the impulse 'jumps' between the nodes - saltatory conduction. With an unmyelinated axon, the whole length of the axon's membrane needs to be depolarised so the action potential needs to travel the whole length.
  3. Axon diameter - wider axons transmit impulses faster as there is less resistance to flow of ions.
• The cholinergic synapse - this is an excitatory synapse where the neurotransmitter is acetylcholine
• Synapses (Part 1):

  1. Action potential arrives as the presynaptic neurone's synaptic knob ; its membrane is depolarised
  2. This causes VG Ca2+ channels to open, and the Ca2+ to diffuse into the knob.
  3. This causes the synaptic vesicles to move to the presynaptic neurone membrane and fuse with it. Neurotransmitters (ACh) are exocytosed into the synaptic cleft.
• Synapses (Part 2):

  1. They diffuse across and bind to receptors on the postsynaptic neurone membrane. This causes Na+ channels to open and diffuse into the axon and if threshold is reached, then depolarisation is created in the postsynaptic neurone.
  2. In cholinergic synapses, the enzyme acetylcholinesterase hydrolyses the ACh bound to the receptors back into the presynaptic neurone, and the vesicles are reassembled.
• Synapses ensure unidirectionality because:

  • the receptors are only on the postsynaptic neurone membrane
  • the synaptic vesicles are only in the presynaptic neurone knob
• Inhibitory Synapses:

  In inhibitory synapses, the neurotransmitter e.g. GABA, causes K+ channels to open and K+ to diffuse out of the axon and/or Cl- channels to open and Cl- to diffuse in.

  Both of these things make the axon more negative (hyperpolarisation) and therefore prevent threshold being reached. There is no depolarisation of the postsynaptic neurone membrane therefore and so the action potential doesn't continue.
• Temporal summination:

  This is when more than one action potential arrives at the synaptic knob of the presynaptic neurone in quick succession. The neurotransmitters from all of these impulses bind to the receptors at the same time making it more likely for the threshold to e reached and depolarisation to result.
• Spatial Summation:

  This is when more than one presynaptic neurone submits its neurotransmitters into their synaptic clefts at the same time.

  If all of these synapses are excitatory then threshold is more likely to be reached as more Na+ channels open and more Na+ diffuse in leading to more depolarisation.

  If there is a mix of excitatory and inhibitory synapses, then it is the sum of their effects on the membrane which dictates whether or not the threshold is reached and an action potential results on the postsynaptic neurone side.
• Drugs (Part 1)

  1. Some drugs bind to the receptors on the postsynaptic neurone membrane, preventing the normal neurotransmitters from doing this e.g. curare.
  2. Some drugs bind to these receptors and mimic the same effects as the neurotransmitter in the absence of them e.g. nicotine.
  3. Some drugs inhibit the enzymes designed to hydrolyse the neurotransmitters i.e. non-competitive inhibition.
• Drugs (Part 2)

  1. Some drugs cause the synaptic vesicles to fuse to the presynaptic membrane.
  2. Some drugs block the voltage gated Ca2+ channels.
  3. Some drugs prevent the re-uptake of neurotransmitters back into the vesicles so the receptors continue to be stimulated.