module 9- synapses

what is a synapse

the specialised connection point between two neurons where signals are transmitted electrically or chemically

2 types of synapses

• electrical (spark): direct ion transfer via gap junctions

• chemical (soup of chemicals surrounding the neurons): signal transmission via neurotransmitters

what is a rectifying synapse

1-way transmission of signal

what is a non-rectifying synapse

2-way transmission of signal

electrical synapse + 4 features

2 neurons have a close relationship because they’re connected by specialised proteins → forms a gap junction

1. non-rectifying

2. direct transfer of ions

3. fast transmission

4. signal often attenuated (smaller signal in postsynaptic neuron)

structure of an electrical synapse

• gap junctions formed by:

  • 2 connexons/1 in each membrane [vertebrates] → each connexon made up of 6 connexins/subunits

  • innexins (drosophila/fly escape reflex)

2 situations where electrical synapses are used

• escape situations → very fast response needed

• coordinate the activity of cells over a large area of tissue

how does the drosophila/fly escape reflex demonstrate electrical synapses

• giant fibers (axons of interneurons) form gap junctions with motor neurons via innexins

• allows for ultra-fast signal transmission for escape responses

what type of synapse is more common in vertebrate nervous system

chemical

chemical synapse + feature

electrical → chemical → electrical

• action potential triggers NT release into the synaptic cleft

• NTs bind to receptors on the postsynaptic neuron which generates a postsynaptic potential

  • adaptable/flexible/lots of plasticity

Otto Loewi experiment

• proves chemical transmission

• stimulating the vagus nerve released vagusstoff (ACh) into bathing fluid which slows the heart rate

• pump submerged in bathing fluid linked a heart with the vagus nerve in tact to a heart without vagus nerve & 2nd heart rate also slowed

vesicular release in chemical synapse

1. action potential triggers opening of voltage sensitive Ca channels

2. small changes in Ca concentration in active zone (axon terminal/presynaptic membrane) triggers release of NTs

2 ways synapses turn off signals

1. an enzyme breaks down NT in synaptic cleft

2. re-uptake system (can be for NT itself or breakdown products of NT)

why are there lots of mitochondria in the presynaptic neuron

vesicular release requires a lot of energy (30% of brains energy)

4 steps of vesicular release in chemical synapse (SNARE proteins)

1. SNARE proteins interact with each other & vesicle is drawn close to the membrane

2. action potential causes increase in Ca concentration

3. SNARE proteins go through conformational change

4. vesicle fuses with the membrane & releases its contents into the synaptic cleft

differences between spontaneous & evoked release

• spontaneous: random single-vesicle release (no calcium), lower number of vesicles fusing with the membrane, produces miniature end plate potential (MEPP)

• evoked: action potential → calcium influx → high number of vesicles fuse with the membrane (e.g., 200 quanta at neuromuscular junctions), produces EPP

Fatt & Katz experiment

• measured miniature end plate potential sizes

• miniature end plate potential sizes vary stepwise (double, triple, x4 etc)

• 1 quantum = amount of NT per vesicle

what is the quantal hypothesis

• NT release occurs in discrete, fixed-size quanta

• each quanta = the amount of NT in a single vesicle

how to calculate quantal content

full end plate potential (evoked release) / 1 quantum current

• average vesicles released per evoked response

function of clathrin

• after vesicle fuses with membrane clathrin molecules coat the vesicle & forms interactions with other clathrin molecules

• 20 hexagon & 12 pentagon structure around vesicles

• drags vesicle away from the membrane

• clathrin molecules leave the vesicle so vesicle can be reused

3 features of vesicle recycling

• constant vesicle size

• constant number of vesicles (so same number of NTs)

• constant size of nerve terminal

what toxin destroys SNARE protiens

botulinum toxin

what toxin blocks voltage gated Ca channels

omega conotoxin

tetanus

• caused by anaerobic bacteria

• tetanus toxins enters presynaptic nerve terminals in skeletal muscle neuromuscular junctions & travels back up motor neurons into the CNS

• released from dendrites of motor neurons & taken up by inhibitory neurons

• then destroys SNARE proteins

• causes muscle spasms