pharmacology at the synapse- lecture 5

Question 1

from axon to synapse stages

Answer 1

1. synthesis and storage
2. recieving the action potential
3. the effects of depolarisation
4. the release of neurotransmitters into the cleft

Question 2

1. synthesis and storage

Answer 2

neurotransmitters are synthesised by golgi apparatus, neurotransmitters are stored in spherical packets called synaptic vesicles, these are passed down microtubules to presynaptic button

Question 3

2. recieving the action potential

Answer 3

synaptic vesicles float around waiting for an action potential o arrive, the action potential is recieved by the presynaptic membrane causing depolarisation (membrane becomes more positive)

Question 4

3. the effects of depolarisation

Answer 4

depolarisation causes vesicles to dock on the pre-synaptic membrane, depolarisation causes calcium channels to open and influx of calcium enters pre-synaptic terminal

Question 5

4. release of neurotransmitters into cleft

Answer 5

some calcium ions attach to the dock causing the vesicle to fuse with the membrane, this creates fusion pores, the vesicles release the neurotransmitters into the synaptic cleft through fusion pores

this is called exocytosis and lasts around 1-2 milliseconds

Question 6

from synaptic cleft to post synaptic membrane

Answer 6

attachment and activation- when the neurotransmitter attaches to the post-synaptic membrane it changes its membrane potential, neurotransmitters only attach to specific binding sites/recptors, neurotransmitter that attach to specific binding sites are called ligands

Question 7

stopping info flow stages

Answer 7

1. deactivation
2. reuptake
3. enzymatic breakdown

Question 8

1. deactivation

Answer 8

activation does not continue forever (axons and synapses would become over-stimulated), so once the message is recieved synaptic transmission is terminated in 2 ways- reuptake, enzymatic breakdown

Question 9

2. reuptake

Answer 9

neurotransmitters detach from receptors and are taken back into the presynaptic membrane (they can then be reused)

Question 10

3. enzymatic breakdown

Answer 10

specific enzymes destroy the neurotransmitters preventing further activation

Question 11

neurotransmitters

Answer 11

• chemicals that communicate between neurons
• some cause depolarisation at post synaptic membrane causing an excitatory post synaptic potential
• some cause hyperpolarisation causing an inhibitory post-synaptic potential
• some are inhibitory, some are excitatory and some are both (depends on their receptors)

Question 12

neurotransmitter action

Answer 12

• some are excitatory (they turn things up)
• some are inhibitory (they slow things down)

Question 13

neuropeptides

Answer 13

• the most common neuropeptides are endogenous opiods (enkephalins/endorphins)
• slows firing rate of neurons carrying pain signals
• natural pain relief and pleasure
• e.g. morphine exactly replicate effects of our naturally occuring opiods

Question 14

glutamate

Answer 14

• glutamate is excitatory (it increases/speeds things up)
• produces EPSPs
• synapses that use glutamate are glutamatergic synapses
• glutamate increases activation by
  1. causing depolarisation= excitatory post synaptic potentials (EPSPs)
  2. lowering the threshold required for excitation= increasing firing rate in neurons

Question 15

gaba

Answer 15

• it is inhibitory (it decreases/slows)
• produces IPSPs
• synapses that use gaba are gabaergic synapses
• gaba prevents the brain from becoming excessively aroused by:
  1. causing hyperpolarisation= inhibitory post synaptic potentials (IPSPs)
  2. increasing the threshold required for excitation= decreasing firing rate in neurons

Question 16

glutamate and gaba

Answer 16

both abundant in CNS

Question 17

breakdown and reuptake of monoamines

Answer 17

• monoamines are broken down by an enzyme called monoamine oxidase (MAO), this converts excess monoamines into inactive substances
• drugs that prevent the action of MAO are called monoamine oxidase inhibitors, these increase levels of monoamines

Question 18

acetylcholine

Answer 18

• acetylcholine is synthesised from choline and acetate
• synsapses that use acetylcholine are called cholinergic synapses, they are generally excitatory
• there are 2 types of cholinogeric synapses- 1. mscarinic midbrain medulla pons (slower prolonged reactions), 2. nicotinic substantia nigra locus coeruleus septum (fast acting responses)
• acetylcholine is broken down by acetylcholinesterase (AchE), this is abundant in the synaptic cleft to prevent over stimulation

Question 19

agonists

Answer 19

drugs that increase the action of neurotransmitter
e.g.
L-Dopa is given toparkinsons patients to increase release of dopamine- dopamine agonist
black widow spider venom- stimulates the release of acetylcholine- cholinogeric agonist
nicotin- mimics acetylcholine at nicotine receptors- cholinogeric agonist

Question 20

antagonist

Answer 20

drugs that decrease the action of a neurotransmitter
e.g.
resperine (calming agent and snake bite anti-venom)- makes vesicles leaky and monoamines leak out of vesicles and broken down by enzymes- monoamine antagonist
botox- prevents the release of acetylcholine/blocks acetylcholine binding- cholinogeric antagonist

Question 21

reward pathways

Answer 21

• the brain reward pathway i mostly dopaminergic (ventral tegmental area- limbic system- frontal cortex)
• it makes us feel good when we engage in behaviour necessary for survival
• not suprisingly most drugs (of use and abuse) also work along this pathway