8. synapses Flashcards

1
Q

How does transmission across an intracellular gap occur? 5

A
  1. all cells are surrounded by an electrically insulating membrane - high resistance
  2. ions can only cross when ion channels open
  3. extracellular fluid has very low resistance to electrical currents, full of charged ions
  4. if ions at the end move into extracellular fluid, charge dissipates
  5. electrical signal can’t just jump due to insulation, so mixture of jumping signal and chemical gradients
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2
Q

What do we mean when we say the direction of transmission of an AP is rectifying? 1

A
  1. one way
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3
Q

What are electrical synapses? 6

A
  1. gap junction - cytoplasmic bridges between cells where charged ions can flow
  2. direct transfer of ions and small molecules
  3. a lot of the signal can be lost but it is still transmitted
  4. bidirectional/non-rectifying/symmetrical - current can pass in both directions
  5. Fast transmission – no synaptic delay
  6. Found in all multicellular animals, common in humans
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4
Q

What is the structure of a gap junction? 5

A
  1. made up of many gap junction channels
  2. each made of two connexons
  3. each comnexon made of 6 connexin subunits
  4. pores are 1-2 nm wide and in the centre
  5. membranes are very close where channels are, 2-3nm apart
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5
Q

What are the properties of electrical synapses? 6

A
  1. reliable due to one to one transmission
  2. more common in developing than adults, transmit growth signals during development and can exchange/transmit other chemicals
  3. used by invertebrates, lower vertebrates and mammals
  4. less common than chemical synapses
  5. used in fast pathways, life or death eg. escape and defense in many animals
  6. promote synchronous activity within a network, connection by electrical synapse means when one fires all others fire
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6
Q

Describe the plasticity of electrical synapses. 3

A
  1. limited, contrast to chemical synapses
  2. synaptic plasticity controls strength of synapse
  3. SP underlies learning and memory processes
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7
Q

Describe the giant fibers of drosophila. 6

A
  1. flies escape from danger in response to visual stimulation eg. shadows
  2. brain is the integration of sensory input and is connected to giant fibers (axons of giant interneurons) for fast transmission
  3. giant fibres synapse directly onto leg motoneurons
  4. inject dye into giant fiber soma in brain and it crosses gap juntions via dye coupling
  5. every electrical synapse in the pathway saves 2ms
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8
Q

Describe the gap junction drosophila mutant. 4

A
  1. if the electrical synapses don’t work, fly doesn’t show escape response eg, shaking b2 mutant
  2. shaking b2 is for the innexin (like connexin) protein
  3. no electrical synapses formed
  4. injected dye restricted to giant fiber axon
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9
Q

Describe the discovery of chemical synapses. 4

A
  1. Electrical leads to chemical leads to electrical was first demonstrated by Otto Loeui at the nmj of a frog heart
  2. ACH released from vagus nerve onto muscle to slow heart rate
  3. synaptic delay - 0.5-2ms
  4. chemical approach generally accepted from early 20thC
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10
Q

Describe Otto’s experiments. 4

A
  1. remove frog heart and vagus nerve
  2. electrical stimulation of vagus nerve slows heartbeat
  3. otto thought nerve endings released chemical
  4. pumped fluid surrounding heart into vessel with a second heart, which also slowed
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11
Q

describe chemical synaptic transmission. 5

A
  1. ap arrives and depolarizes membrane
  2. voltage gated ion channels in nerve terminal open and allow ca2+ in down gradient
  3. sudden influx of calcium causes release of vesicles containing nets into synaptic cleft
  4. nets diffuse and bind to transmembrane receptors, opening ion channels eg. ACh opens na+
  5. na+ move in whcih causes PSP
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12
Q

What adaptations do axon terminals have? 2

A
  1. Lots of mitochondria to make nets, package vesicles and dock and release vesicles
  2. Have active zones where synapse activity happens
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13
Q

What is the morphological classification of chemical synapses? 5

A
  1. Axon synapsing onto dendrite is axodendritic
  2. Location has impact on efficiency, tip vs body
  3. Axon synapsing onto the soma is axosomatic, can be seen using em
  4. Axon to axon is axoaxonic. Synapses just before synapse of another cell and influenced effectiveness of second synapse
  5. Three cells interacting to transmit and process info
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14
Q

What are the morphological types of synapses? 4

A
  1. Gray type one synapses are excitatory and usually contact dendrites
  2. Gray type two are usually inhibitory and may contact soma
  3. Asymmetrical have a thicker membrane on postsynaptic neurone
  4. Symmetrical have same thickness of membrane on both side of synapse with flattened vesicles
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15
Q

What poisonous tool are used while studying synapses? 5

A
  1. Omega conotoxin comes from marine cons hell, which injects it into prey
  2. Blocks voltage hated calcium channels so no net release, incl at nmj so no muscle contraction leads to paralysis
  3. Botulinum toxin from botulinum bacteria prevents fusion of vesicles with membrane so no net release
  4. Alpha bungaratoxin from snake venom binds ach receptors on post synaptic membrane
  5. Cues paralysis as no epsp generated and no sodium enters muscle membrane
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16
Q

What is the vesicles hypothesises? 5

A
  1. Nets are occasionally released in absence of extracellular calcium or ap
  2. Leads to miniature psp
  3. Due to accidental, spontaneous vesicles release
  4. Thought to be due to one of two things, gradual trickle of net from vesicles into cytoplasm and then membrane transport or exocytosis
  5. It’s exocytosis, nets are released in packages
17
Q

What are minute psps/minis? 6

A
  1. Have amplitudes that are multiples of quintal unit
  2. 1 quantum is release of net from one vesicle
  3. So, psps that are mini are due to release of one or more quanta
  4. Quintal analysis of ap - evoked psps shows they involve release of 200 max quanta per ap
  5. Each quantum contains several thousand molecules of net
18
Q

How are nets released by exocytosis? 4

A
  1. Docking of vesicles, vesicle held against membrane. This is calcium dependent
  2. Influx of calcium into cell
  3. Membranes of cell and vesicles fuse
  4. Vesicle is recycled and refilled, incl membrane
19
Q

What are SNARE proteins? 5

A
  1. T and v SNARE proteins anchor vesicle to membrane - docking. V in vesicle membrane, t in cell membrane
  2. Calcium moves in through voltage gated channels
    3 this disrupts synaptotagmin, which triggers a change in conformation of SNARE proteins
  3. This allows so vesicle to fuse with terminal membrane
  4. Botox disrupts the formation of snare complex
20
Q

What is botulinum toxin/Botox? 6

A
  1. Produced by clostridium botulinum and responsible for fatal cases of food poisoning
  2. Destroys SNARE proteins which blocks nmj which leads to paralysis, so used as experimental tool
  3. Used cosmetically to reduce facial wrinkles
  4. Used to treat muscle spasticity associated with upper motoneuron syndrome/cerebral palsy and stroke
  5. In these conditions,muscles show loss of reciprocal inhibition
  6. Also to treat excessive sweating, strabismus (eye misalignment) and chronic migraine
21
Q

How are synaptic vesicles recycled? 5

A
  1. Proteins and lipids synthesised in cell soma ands transported to synaptic terminal
  2. Synaptic vesicles assembles and loaded with non peptide nets in the terminals
  3. Exocytosis increases the area of plasma membrane so membrane must be internalised
  4. Vesicle membranes ungergo exocytosis several times and then are returned to soma for degradation
  5. Recycling prevents massive growth of membrane
22
Q

What is clatherin? 2

A
  1. Protein used to build intracellular, membrane bound vesicles
  2. Crates coated pit around vesicle and provides structure within which vesicle can form