3.6.2.2 - SYNAPTIC TRANSMISSION Flashcards
it is important that a neurotransmitter such as serotonin is transported back out of synapse.
explain why (2)
- if not removed, it will keep binding to receptors
- keeps causing action potentials/depolaisation in post-synaptic membrane
cannabinoids receptors are found in the pre-synaptic membrane of the neuromuscular junctions.
when a cannabinoids binds to its receptor, it closes calcium ion channels.
suggest how cannabinoids could prevent muscle contraction (4)
- prevents influx of calcium ions into pre-synaptic membrane
- synaptic vesicles don’t fuse with membrane / vesicles do not release neurotransmitter
- neurotransmitter does not diffuse across synaptic cleft / does not bind to receptors on post-synaptic membrane
- no action potential / depolarisation of post-synaptic membrane / sodium ion channels do not open
cannabinoids include substances found in cannabis that can enter brain tissue.
scientists are developing artificial cannabinoids that can enter neurotransmitter junctions but cannot enter brain tissue.
suggest why these artificial cannabinoids would be better to use than cannabis when treating someone with multiple sclerosis (2)
- they won’t affect synapses in the brain
- they won’t cause problems with the brain’s function / won’t damage the brain
- so only the neurotransmitter junctions will be affected
when a nerve impulse arrives at a synapse. it causes the release of a neurotransmitter from vesicles in the presynaptic knob.
describe how (3)
- nerve impulse/depolarisation of membrane causes calcium ion channels to open
- calcium ions enter by facilitated diffusion
- caused synaptic vesicles to fuse with presynaptic membrane
dopamine is a neurotransmitter released in some synapses in the brain.
the transmission of dopamine is similar to that of acetylcholine.
dopamine stimulates the production of nerve impulses in post synaptic neurones.
describe how (3)
- dopamine diffuses across synapse
- attaches to receptors on postsynaptic membrane
- stimulates entry of sodium ions and depolarisation/action potential
GABA is a neurotransmitter released in some inhibitory synapses in the brain.
GABA causes negatively charged chloride ions to enter postsynaptic neurones.
explain how this inhibits postsynaptic neurones (3)
- inside of postsynaptic neurones becomes more negative
- more sodium ions required to reach the threshold OR not enough sodium ions to reach the threshold
- for action potential/depolarisation
describe the sequence of events involved in transmission across a cholinergic synapse. (5)
do not include details on the breakdown of acetylcholine
- depolarisation of presynaptic membrane
- calcium channels open and calcium ions enter synaptic knob
- calcium ions cause synaptic vesicles to move to/fuse with the presynaptic membrane and release acetylcholine
- acetylcholine diffuses across synaptic cleft
- acetylcholine attaches to receptors on postsynaptic membrane
- sodium ions enter postsynaptic neurone leading to depolarisation
describe the role of calcium ions and ATP in the contraction of a myofibril (5)
- calcium ions diffuse into myofibrils from sarcoplasmic reticulum
- calcium ions cause movement of tropomyosin on actin
- which causes exposure of binding sites on the actin
- myosin heads attach to binding sites on actin
- hydrolysis of ATP con myosin heads causes the heads to bend
- bending/pulling actin molecules
- attachment of a new ATP molecule to ech myosin head causes myosin heads to detach from actin sites
give two reasons why transmission across a cholinergic synapse is unidirectional (2)
- only presynaptic membrane releases/has acetylcholine/neurotransmitte
- only the postsynaptic membrane has receptors
MG is an autoimmune disease caused when antibodies bind to the sarcolemma (postsynaptic membrane) of neuromuscular junctions. this can weaken contraction of muscles.
suggest and explain how MG can weaken contraction of muscles (2)
don’t include myofibril or muscle contraction in answer
- less acetylcholine binds to receptors
- less/no depolarisation/action potentials
MG is an autoimmune disease caused when antibodies bind to the sarcolemma (postsynaptic membrane) of neuromuscular junctions. this can weaken contraction of muscles.
mestinon is a drug that inhibits the enzyme acetylcholinesterase.
mestinon can help in the treatment of MG. explain how. (3)
- less acetylcholine broken down
- so more acetylcholine attaches to receptors
- depolarisation of sarcolemma occurs OR action potential produced
dopamine has a role in numerous processes in the brain including pain relief. the release of dopamine can be stimulated by chemicals called endorphins produced in the brain.
endorphins attach to opioid receptors on presynaptic neurones that release dopamine.
morphine is a drug that has a similar structure to endorphins and can provide pain relief. explain how (2)
- morphine attaches to opioid receptors
- more dopamine released to provide pain relief
dopamine has a role in numerous processes in the brain including pain relief. the release of dopamine can be stimulated by chemicals called endorphins produced in the brain.
endorphins attach to opioid receptors on presynaptic neurones that release dopamine.
morphine is a drug that has a similar structure to endorphins and can provide pain relief. explain how (2)
- morphine attaches to opioid receptors
- more dopamine released to provide pain relief
GABA is a neurotransmitter released in some inhibitory synapses in the brain. GABA causes negatively charged chloride ions to enter postsynaptic neurones.
explain how this inhibits postsynaptic neurones (3)
- inside of postsynaptic neurone becomes more negative/hyper-polarisation
- so more sodium ions required to reach the threshold
- for depolarisation/action potential
acetylcholine is a neurotransmitter which binds to postsynaptic membranes and stimulates the production of nerve impulses. GABA is another neurotransmitter. it is produced by certain neurones in the brain and spinal cord. GABA binds to postsynaptic membranes and inhibits the production of nerve impulses.
describe the sequence of events leading to the release of acetylcholine and its binding to the postsynaptic membrane (4)
- AP arrives/depolarisation occurs
- calcium ions enter synaptic knob
- vesicles fuse with membrane
- acetylcholine diffuses across synaptic cleft
- binds to receptors