CTR - 8 - Synapses

Question 1

What is a benefit and negative of electrical synapses?

Answer 1

Very rapid response

Cannot be modulated easily (cannot be timed well)

Question 2

What are the two types of synapses?

Answer 2

Chemical and electrical

Question 3

Channels at the axon terminal of the pre-synaptic neuron are _________ gated.

Answer 3

Voltage

Question 4

Channels at the dendrite of the post-synaptic neuron are _________ gated.

Answer 4

Ligand / chemically

Question 5

What is the role of Ca2+ in a synapse?

Answer 5

Causes vesicles to release their contents via exocytosis into the synaptic cleft

Question 6

How can a neurotransmitter response be terminated?

Answer 6

Diffusion away from the synapse

Enzymatic degradation

Re-uptake through transport proteins

Question 7

How do anti-depressants work

Answer 7

Block re-uptake of neurotransmitter at a synapse

Question 8

During exocytosis in a synapse, what happens?

Answer 8

v-SNARE proteins on vesicle surface bind with t-SNARE proteins on surface –> open a pore –> vesicle releases contents to exterior

Question 9

What can block exocytosis? What effect does this have?

Answer 9

Botulin and tetanus toxins

Cut the proteins (t-snare and v-snare) so that exocytosis cannot occur.

Therefore, no NT released even with AP reaching the synapse

No muscle contraction –> muscles relax

Question 10

What determines how much neurotransmitter is released?

How doe this affect GP size?

Answer 10

Frequency of AP
= high freq –> more calcium released –> more vesicles released –> more neurotransmitter released

Amount of neurotransmitter in vesicles

Increased amount of NT –> opens more Na+ channels on postsynaptic neurone –> increased GP size

Question 11

What are EPSPs and IPSPs? What ions are involved?

Answer 11

Excitatory post-synaptic potentials

• NT binding increases chance of postsynaptic neuron generating AP
• Na+ into cell
• More positive inside = depolarisation

Inhibitory post-synaptic potentials

• Nt binding decreases chance of postsynaptic neuron generating AP
• K+ out, Cl- into cell
• More negative inside = hyperpolarisation

Question 12

What is an example of divergence in the same pathway?

Answer 12

Walking (leg curl = hamstring) - in the same muscle group

Question 13

What is an example of divergence in multiple pathways?

Answer 13

Walking (swing arms and legs) - different muscle groups

Question 14

What is an example of convergence from multiple sources?

Answer 14

Appetite (smell and look nice)

Question 15

What is an example of a reverberating circuit?

Answer 15

repetetive / rhythmic activities (sleep wake, breathing)

Question 16

What is released at the neuromuscular junction? What does it cause?

Answer 16

ACh. Generates GP (if threshold) –> AP –> causes Ca2+ to flow in –> initiate protein filaments to contract

Question 17

What does acetylcholine-esterase do at the NMJ? Purpose?

Answer 17

Breaks down excess ACh in synaptic cleft./

Which stops contraction of muscle (otherwise, ACh would stay there –> continous APs)

Question 18

What is an agonist at the NMJ?

Answer 18

Nicotine - causes same effect when binding to NMJ.

Question 19

What is the cause of myasthenia gravis? Symptoms? Treatment?

Answer 19

Auto-immune = antibodies destroy ACh receptors (less ACh receptors at NMJ)

Symptoms: diminished motor response at NMJ (muscle weakness, fatigue)

Treatment : ACh esterase inhibitors limit breakdown of ACh - more ACh available (maximises effect on remaining receptors)

Question 20

What are the effects of the curare toxin? Treatment

Answer 20

ACh competitive antognist - occupies ACh receptor (prevents ACh binding postsynaptically –> no opening of ion channels –> no AP –> paralysis of skeletal muscle)

ACh inhibitors - limit breakdown of released ACh - leaving more available for the available receptors.

Question 21

What do organophosphates do? Treatment

Answer 21

Inactivates ACh-esterase –> ACh not broken down –> high levels of ACh in synaptic cleft –> desensitise ACh receptors –> ACh receptor-channels close even in presence of ACh –> neuromuscular transmission fails

Treatment - atropine - ACh receptor blocker in parasymapthethic NS
Also - acetylcholine esterase reactivator

Question 22

What causes botulism? Treatment?

Answer 22

Botulin - prevents ACh release (by cutting t-snares and v-snares) –> no binding of ACh –> ion channels remains closed –> no depolarisation –> no AP –> muscle remains relaxed

Treatment –> ventilator, surgery, stomach pump

Question 23

What is learning?

Answer 23

Process by which knowledge is acquired about the world

Question 24

What is memory?

Answer 24

Process by which knowledge is encoded, stored and later retrieved

Question 25

What is consolidation? How long does it take?

Answer 25

Process of converting short term memory to long term memory (takes seconds to minutes)

Question 26

What is declarative memory. One location. HM

Answer 26

Storage abut facts and events (places, people, objects)

- medial temporal lobe (HM had this removed)

Question 27

What is non declarative memory?

Answer 27

Procedural, automatic, skills, habits, emotional responses

Question 28

What is habituation. A form of _________

Answer 28

Learning to ignore meaningless stimuli

Form of non-assosciative learning

Question 29

What happens to neurons during habituation?

Answer 29

GP becomes smaller and smaller

Presynaptic votage-gated channels become progressively and persistently less effective when opened repetitively

Therefore, not producing an AP