Synaptic transmission

• Synapses and neurotransmitters:

  • a synapse is a junction between an neurone and another neurone, or between a neurone and an effector cell e.g. muscle or gland cell
  • the tiny gaps between the cells at a synapse is called the synaptic cleft
  • the presynaptic neurone (before the synapse) has a swelling called a synaptic knob
  • this contains synaptic vesicles filled with chemicals called neurotransmitters
• Effect of an action potential:

  • 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 mambrane 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 - the impulse can only travel in one direction
  • neurotransmitters are removed from the cleft so the response doesn't keep happening e.g. they are taken back into the presynaptic neurone or are broken down by enzymes (and the products are taken into the neurone)
• Acetylcholine:

  • ACh
  • binds to cholinergic receptors
  • synapses that use acetylcholine are called cholinergic synapses
• Cholinergic synapses: - how a nerve impulse is transmitted across:

  1. arrival of an action potential
  2. fusion of the vesicle
  3. diffusion of ACh
• 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 (Ca2+) diffuse into the synaptic knob
  • (pumped out afterwards by active transport)
• voltage-gated ion channels are channels that only open when the potential difference across a membrane reaches a certain voltage
• 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 acetylcholine ACh into the synaptic cleft by exocytosis
• the influx of calcium ions means that the calcium ions have flowed into the synaptic knob
• exocytosis is the process by which a vesicle inside a cell moves to the cell-surface membrane, fuses with the membrane and releases its content outside the cell
• Diffusion of ACh:

  • ACh diffuses across the synaptic cleft and binds to specific cholinergic receptors on the postsynaptic membane
  • this causes sodium ion cannels in the postsynaptic neurone to open
  • the influx 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 synaptic cleft so the response doesn't keep happening
• • ACh is broken down by an enzyme called acetylcholinerase (AChE)
  • products re-absorbed by the presynaptic neurone and used to make more ACh
• Excitatory and inhibitory neurotransmitters:

  • NTs can be excitatory or inhibitory
• Excitatory neurotransmitters depolarise the postsynaptic membrane, making it fire an action potential if the threshold is reached

  e.g. acetylcholine is an excitatory neurotransmitter (it binds to cholinergic receptors to cause an action potential in the post synaptic membrane) at cholinergic synapses in the CNS and at the neuromuscular junctions
• Inhibitory neurotransmitters hyperpolarise the postsynaptic membrane (make the potential difference more negative) preventing it from firing and action potential
• E.g. inhibitory:

  • GABA is an inhibitory neurotransmitter - when it binds to its receptors it causes potassium ion channels to open on the postsynaptic membrane, hyperpolarising the neurone
  • acetylcholine is an inhibitory NT at cholinergic synapses in the heart - when it binds to receptors here, it can cause potassium ion channels to open on the postsynaptic membrane, hyperpolarising it
• a synapse where inhibitory NTs are released from the presynaptic membrane following an action potential is called an inhibitory synapse
• depolarise - means making the potential difference across the neurone membrane more positive
• hyperpolarise - means making the potential difference across the membrane more negative
• Summation at synapses:

  • if a stimulus is weak - only a small amount of NT 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 (or one neurone that is stimulated a lot in a short period of time) is added together
  • it means that synapses accurately process info, finely tuning the response
• There are 2 types of summation:

  1. spatial summation
  2. temporal summation
• spatial summation:

  • where 2 or more presynaptic neurones release their NTs at the same onto the same postsynaptic neurone
  • the small amount of NT released from each of these neurones can be enogh altogether to reach the threshold in the postsynaptic neurone and trigger an action potential
  • if some neurones release an inhib NT then the total effect of all NTs might be no action potential
• only excitatory NTs can trigger an action potential
• summation is where the sum total of lots of smaller impulses triggers an action potential
• temporal summation:

  • where 2 or more nerve impulses arrive in quick succession from the same presynaptic neurone
  • this makes an action potential more likely bc more NT is released into the synaptic cleft
• impulses have to follow each other very quickly, otherwise the NT will be removed from the cleft before it has reached a level higher enough to trigger an action potential
• Neuromuscular junctions:

  • a specialised cholinergic synapse between a motor neurone and a muscle cell
  • NMJs use the NT ACh, whic binds to cholinergic receptors called cholinergic receptors
• postsynaptic membrane - also called motor end plate
• NMJs work in basically the same way as cholinergic synapses i.e.

  • they both release ACh from vesicles in the presynaptic membrane
  • ACh then diffuses across the synaptic cleft and binds to cholinergic receptors on the postsynaptic membrane, and this triggers an action potential if the threshold is reached
  • in both types of synapse, ACh is broken down in the synaptic cleft by the enzyme acetylcholinesterase (AChE)
• Differences between the 2 types of synapse - at a NMJ:

  • the postsynaptic membrane has lots of folds that form clefts - these clefts 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 - not always the case for a synapse between 2 neurones
• Drugs at synapses:

  • drugs can affect synaptic transmission
  • they can do this in various ways
  • e.g. some drugs are the same shape as NTs so they mimic their action at receptors (agonists)
  • this means more receptors are activated
• e.g. nicotine mimics acetylcholine so binds to nicotine cholinergic receptors in the brain
• • some drugs block receptors so they can't be activated by NTs (antagonists)
  • means fewer receptors is any can be activated
  • e.g. curare blocks the effects of ACh by clocking nicotine cholinergic receptors at NMJs - so muscle cells can't be stimulated - results in the muscle being paralysed
• • some drugs inhibit the enzyme that breaks down NTs (stop it from working)
  • means that there are more NTs in the synaptic cleft to bind to receptors and they are there for longer
  • e.g. nerve gases stop ACh from being broken down in the synaptic cleft - lead to loss of muscle control
• • some drugs stimulate the release of NT from the postsynaptic neurone so more receptors are activated
  • e.g. amphetamines force dopamine out of synaptic vesicles and into the synaptic cleft - increases the effect of dopamine e.g. increases alertness
• • some drugs inhibit the release of NTs from the presynaptic neurone so fewer receptors are activated
  • opioids block calcium ion channels in the presynaptic neurone - this means that fewer vesicles fuse with the presynaptic membrane so less NT is released
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