8/ synapses and neurotransmitters Flashcards
how many synapses does your brain have compared to neurons?
100 trillion synapses, 100 billion neurons - 1000 synapses per neuron
what series of experiments showed neurons were distinct with synapses rather than a continuous net?
- golgi (thought continuous net) stain (cajal, late 1800s)
- physiological evidence from study of reflexes
- final evidence from electron microscopy (1950s)
why do we have synapses
- to allow for more specialisation and flexibility of response for context dependent cues and internal state
what are electrical synapses formed of
gap junctions that allow current to pass directly between neurons
note on lessening depolarisation and hyper polarisation between gap junctions. how big are gap junctions?
- more cells depolarisation is passed on to the weaker it can be
- hyperpolarisation can also pass through gap junction
- 1-2 nm in diameter
3 ways to tell if neurons are connected by gap junctions?
- stimulate one neuron and record from another - if they are connecetd signal can be recorded from the other
- dyes - see if dyes can diffuse between neurons
- genetic techniques - knock out connexin (gap junction protein). If no hyperpolarisation/depolarisation, gap junction is responsible
what are electrical synapses good for
- fast communication
- synchronising neurons
1st evidence for chemical synapses
- stimulate vagus nerve, HR slows
- added vagus fluid to a heart w/o vagus nerve and HR slowed
- chemical in vagus nerve causes HR to slow
typical components of a chemical synapse
- pre ST has lots of mitochondria
- synaptic vesicles
- secretory granules - larger than vesicles, contain neurotransmitter of a dif kind
what do motor and autonomic neurons stimulate
- motor - skeletal muscle
- autonomic - hormonal gland, smooth muscle, heart
steps in chemical synaptic transmission
- ntms in vesicles
- AP arrives, voltage gated Ca2+ channels open
- influx of Ca2+, vesicles fuse w memb and release ntm
- ntm diffuse across cleft and activate receptors
- ntms removed from cleft
synaptic vesicles vs dense core secretory granules
- synaptic: clear/small 40-50 nm.
- small molecule ntms (GABA, glutamate, acetylcholine)
- recycled by endocytosis
- Secretory granules: dense/large 100nm
- peptide ntms (opioids, endorphins)
- created and filled by ER/golgi secretory apparatus
- one and done - cant be reabsorbed
how do vesicles fuse?
- SNAREs
- synaptotagmin is a protein able to bind to calcium
- then shape change which induces shape change in V and T SNAREs - zips them together and allows vesicle to be opened and its contents released
what toxins target SNAREs
- botulinum toxin
- tetanus toxin
- cuts SNARE proteins
- muscle paralysis
ionotrophic vs metabotrophic receptors
- ionotrophic are ligan gated ion channels - directly depolarise/hyperpolarise the postsynaptic cell
- meta are g protein coupled receptors - more complex cascade
notes on removal of ntms
- diffuse away slowly
- actively taken up by transporters for recycling into presynaptic neuron or glia
- destroyed in synaptic cleft by enzymes
electrical vs chemical synapses
- electrical: signals pass both directions, signals pass directly, fast - less that 0.3ms
- chemical: signals one direction, signals can be radically transformed, slower - 0.3-5ms, more common
- both: plastic (modifiable - esp chemical), allow summing up of inputs by the post SN
NMJ
- fast and reliable neurotransmission
- motor neuron AP always cause muscle cell AP
- acetylcholine
how do NMJs achieve such efficient transmission
- very large synapse
- large number of active zones (ntm released from) in pre SN
- Post SN contains junctional folds densely filled w receptors
- active zones and junctional folds precisely aligned
how did we figure out ntm released from vesicles
- potential increased in set intervals
types of CNS synapses
- one pre SN wraps around post - high chance of post firing (NMJ)
- several pre feed onto 1 post - want each synapse individually to have low chance of causing AP
