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Year 2 Medicine > Chemicals in the Brain > Flashcards

Chemicals in the Brain Flashcards

1
Q

Synaptic Vesicle release and recycling

  • Pool of vesicles above the active zone is anchored to the cytoskeleton by …
  • AP to presynaptic terminal, voltage gated Ca2+ channels open, Ca2+ flows into cytoplasm
  • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates …. P-… can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • …* complex at active zone docks vesicles to the plasma membrane
A
  • Pool of vesicles above the active zone is anchored to the cytoskeleton by synapsin
  • AP to presynaptic terminal, voltage gated Ca2+ channels open, Ca2+ flows into cytoplasm
  • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • SNARE* complex at active zone docks vesicles to the plasma membrane
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2
Q

Synaptic Vesicle release and recycling

  • Pool of vesicles above the active zone is anchored to the cytoskeleton by synapsin
  • AP to presynaptic terminal, voltage gated …+ channels open, …+ flows into cytoplasm
  • …+ activates … … activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • SNARE* complex at active zone docks vesicles to the plasma membrane
A
  • Pool of vesicles above the active zone is anchored to the cytoskeleton by synapsin
  • AP to presynaptic terminal, voltage gated Ca2+ channels open, Ca2+ flows into cytoplasm
  • Ca2+ activates Calcium calmodulin activated kinase II (CaMKII) which phosphorylates synapsin. P-synapsin can no longer bind to the cytoskeleton, vesicles dock to the active zone
  • SNARE* complex at active zone docks vesicles to the plasma membrane
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3
Q

Mechanisms of exocytosis during NT release

  • … and … on pre-synaptic vesicle
  • Syntaxin and SNAP-25 on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - … complex forms to pull membranes together
  • Entering calcium ions binds to synaptotagmin
  • Calcium bound synaptotagmin catalyses membrane fusion by binding to … and the plasma membrane
A
  • Synaptobrevin and Synaptotagmin on pre-synaptic vesicle
  • Syntaxin and SNAP-25 on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - SNARE complex forms to pull membranes together
  • Entering calcium ions binds to synaptotagmin
  • Calcium bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
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4
Q

Mechanisms of exocytosis during NT release

  • Synaptobrevin and Synaptotagmin on pre-synaptic vesicle
  • … and SNAP-… on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - SNARE complex forms to pull membranes together
  • Entering … ions binds to synaptotagmin
  • … bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
A
  • Synaptobrevin and Synaptotagmin on pre-synaptic vesicle
  • Syntaxin and SNAP-25 on post-synaptic vesicle
  • AP arrives - calcium channel open, higher locally in area - SNARE complex forms to pull membranes together
  • Entering calcium ions binds to synaptotagmin
  • Calcium bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
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5
Q

Synaptic vesicle release and recycling

  • After the exocytosis, vesicle membrane is rapidly recovered via …, new vesicles bud off and are refilled with transmitter
  • whole process takes … …
A
  • After the exocytosis, vesicle membrane is rapidly recovered via endocytosis, new vesicles bud off and are refilled with transmitter
  • whole process = 1 minute
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6
Q

Cleavage of SNARE proteins by clostridial toxins

  • SNARE proteins important for NT to function
    • … toxin - affects transmission of Ach
    • … toxin - acts on interneurons as spinal cord (inhibitory) affect release of GABA and Gly - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
A
  • SNARE proteins important for NT to function
    • Botulinum toxin - affects transmission of Ach
    • Tetanus toxin - acts on interneurons as spinal cord (inhibitory) affect release of GABA and Gly - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
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7
Q

Cleavage of SNARE proteins by clostridial toxins

  • SNARE proteins important for NT to function
    • Botulinum toxin - affects transmission of …
    • … toxin - acts on interneurons as spinal cord (inhibitory) affect release of … and … - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
A
  • SNARE proteins important for NT to function
    • Botulinum toxin - affects transmission of Ach
    • Tetanus toxin - acts on interneurons as spinal cord (inhibitory) affect release of GABA and Gly - 2 inhibitory NT
  • Little boxes - sites of SNARE proteins
  • BoTX and TeTX can act here
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8
Q

Botox and Tetanus - Prevent … release

A

Botox and Tetanus - Prevent transmitter release

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9
Q

Botox and Tetanus

  • Botox and Tetanus - Prevent … release
  • Botulinium and tetanus toxin - from bacteria Clostridium Botulinum and Tetani respectively
  • Botox acts directly at the … … - the muscles lose all input and so become permanently … (treatment of muscle …)
  • Tetanus toxin inhibits the release of .. and .. at inhibitory neurons, resulting in dis-inhibition of … neurons, which causes permanent muscle …
A
  • Botox and Tetanus - Prevent transmitter release
  • Botulinium and tetanus toxin - from bacteria Clostridium Botulinum and Tetani respectively
  • Botox acts directly at the NT junction - the muscles lose all input and so become permanently relaxed (treatment of muscle spasms)
  • Tetanus toxin inhibits the release of Glycine and GABA at inhibitory neurons, resulting in dis-inhibition of cholinergic neurons, which causes permanent muscle contraction
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10
Q

Diseases that affect the presynaptic terminal

  • Congenital … syndromes - impaired vesicle recycling
  • Another type of … - LEMS - attacks presynaptic Ca2+ channels
  • … disorders - impair transsynaptic signalling
  • …toxin - triggers vesicle fusion (black widow spider poison)
  • Botulinum and tetanus toxins - … proteins affected involved in vesicle fusion
A
  • Congenital myasthenic syndromes - impaired vesicle recycling
  • Another type of myasthenia - LEMS - attacks presynaptic Ca2+ channels
  • Cognitive disorders - impair transsynaptic signalling
  • Latrotoxin - triggers vesicle fusion (black widow spider poison)
  • Botulinum and tetanus toxins - SNARE proteins affected involved in vesicle fusion
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11
Q

Membrane transporters - amino acids, amines and Ach

  • Bringing back NT from synaptic cleft to presynaptic neuron - reload into vesicles
  • Vesicular transporters powered by … gradient:
    • … proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by … gradient
    • Na+ higher outside, K+ higher inside
    • … co-transported with 2 Na+
A
  • Bringing back NT from synaptic cleft to presynaptic neuron - reload into vesicles
  • Vesicular transporters powered by proton gradient:
    • ATPase proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • Na+ higher outside, K+ higher inside
    • Glutamate co-transported with 2 Na+
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12
Q

Membrane transporters - amino acids, amines and Ach

  • Bringing back NT from … cleft to … neuron - reload into vesicles
  • Vesicular transporters powered by proton gradient:
    • ATPase proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • …+ higher outside, …+ higher inside
    • Glutamate co-transported with … Na+
A
  • Bringing back NT from synaptic cleft to presynaptic neuron - reload into vesicles
  • Vesicular transporters powered by proton gradient:
    • ATPase proton pump loads up vesicles with H+ making vesicles acidic (pH 5.5) compared to neutral pH of cytoplasm (pH7.2) e.g. 1 glutamate traded for 1 H+ (counter-transport mechanism)
  • Plasma membrane transporters powered by electrochemical gradient
    • Na+ higher outside, K+ higher inside
    • Glutamate co-transported with 2 Na+
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13
Q

Glia

  • Majority of cells of brain >…%
  • Can release NT themselves and respond to them
  • Involve in many diseases - brain cancer, HIV, dementia
  • Very important - crucial for correct functioning of … but not enough known about them
A
  • Majority of cells of brain >80%
  • Can release NT themselves and respond to them
  • Involve in many diseases - brain cancer, HIV, dementia
  • Very important - crucial for correct functioning of synapses but not enough known about them
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14
Q

Categories of Neurotransmitters:

  • Amino acids , Monoamines , Acetylcholine
    • Synthesized locally in … terminal
    • Stored in … vesicles
    • Released in response to local increase in …+
  • Neuropeptides
    • Synthesized in the cell … and transported to the terminal
    • Stored in … granules
    • Released in response to global increase in …+
A
  • Amino acids , Monoamines , Acetylcholine
    • Synthesized locally in presynaptic terminal
    • Stored in synaptic vesicles
    • Released in response to local increase in Ca2+
  • Neuropeptides
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory granules
    • Released in response to global increase in Ca2+
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15
Q

Categories of Neurotransmitters:

  • Amino acids , … , …
    • Synthesized locally in presynaptic terminal
    • Stored in synaptic vesicles
    • Released in response to … increase in Ca2+
  • …peptides
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory …
    • Released in response to … increase in Ca2+
A
  • Amino acids , Monoamines , Acetylcholine
    • Synthesized locally in presynaptic terminal
    • Stored in synaptic vesicles
    • Released in response to local increase in Ca2+
  • Neuropeptides
    • Synthesized in the cell soma and transported to the terminal
    • Stored in secretory granules
    • Released in response to global increase in Ca2+
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16
Q

Neurotransmitters in the CNS

  • Fast e.g. … …
  • Slow e.g. …
A
  • Fast e.g. amino acids (GLUTAMATE/GABA)
  • Slow e.g. neuropeptides (Oxytocin,noradrenaline)
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17
Q

Amino acid NT - fast

  • …:
    • slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) - CNS
  • …:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • GABA - brain
    • Glycine (Gly) - spinal cord and brain stem
A
  • Excitatory:
    • slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) - CNS
  • Inhibitory:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • GABA - brain
    • Glycine (Gly) spinal cord and brain stem
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18
Q

… neurotransmitters - slightly hyperpolarises the postsynaptic cell’s membrane

A

Inhibitory neurotransmitters - slightly hyperpolarises the postsynaptic cell’s membrane

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19
Q

Amino acid NT - fast

  • Excitatory:
    • slightly depolarises the postsynaptic cell’s membrane
    • … (…) - CNS
  • Inhibitory:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • … - brain
    • … (…) - spinal cord and brain stem
A
  • Excitatory:
    • slightly depolarises the postsynaptic cell’s membrane
    • Glutamate (Glu) - CNS
  • Inhibitory:
    • slightly hyperpolarises the postsynaptic cell’s membrane
    • GABA - brain
    • Glycine (Gly) spinal cord and brain stem
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20
Q

… neurotransmitters - slightly depolarises the postsynaptic cell’s membrane

A

Excitatory neurotransmitters - slightly depolarises the postsynaptic cell’s membrane

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21
Q

GABA (brain) and glycline (spinal cord and brain stem) are both what type of neurotransmitter?

A

Inhibitory - slightly hyperpolarises the postsynaptic cell’s membrane

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22
Q

Glutamate (Glu) - CNS is what type of neurotransmitter?

A

Excitatory - slightly depolarises the postsynaptic cell’s membrane

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23
Q

Diffuse modulatory systems e.g. the Serotonergic system

  • Function in: m…, sleep, p…, emotion, a..
  • Common principles : core
    • small set of neurons. most arise from … …
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
A
  • Function in: mood, sleep, pain, emotion, appetite
  • Common principles : core
    • small set of neurons. most arise from brain stem
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
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24
Q

Diffuse modulatory systems e.g. the Serotonergic system

  • Function in: mood, …, pain, …, appetite
  • Common principles : core
    • small set of neurons. most arise from … ….
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
A
  • Function in: mood, sleep, pain, emotion, appetite
  • Common principles : core
    • small set of neurons. most arise from brain stem
    • 1 -> 100,000 (Each neuron can affect many others, because each one has an axon that may contact more than 100,000 postsynaptic neurons spread widely across the brain.)
25
Q

Why have more NT’s?

A
  • 6 different layers of neuro-cortex - Different inputs and outputs
    • E.g top layers - feedback connections with other parts of cortex
    • 3 and 4 - mainly thalamus
    • 5 and 6 - cortical structure
  • Complexity in terms of wiring and inputs and outputs
26
Q

Glutamate - excitatory

  • Synthesized in presynaptic terminal from 2 sources
    • From glucose via the … cycle
    • From glutamine converted by glutaminase into glutamate
  • Loaded and … in vesicles by vesicular glutamate … (VGLUTs)
  • … by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell and surrounding glia
  • Glial cells convert Glu to glutamine and this is transported from the glia back to nerve terminals where it is converted back into glutamate
A
  • Synthesized in presynaptic terminal from 2 sources
    • From glucose via the Krebs cycle
    • From glutamine converted by glutaminase into glutamate
  • Loaded and stored in vesicles by vesicular glutamate transporters (VGLUTs)
  • Reuptake by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell and surrounding glia
  • Glial cells convert Glu to glutamine and this is transported from the glia back to nerve terminals where it is converted back into glutamate
27
Q

GABA (y-aminobutyric acid) - inhibitory

  • Synthesized from … (…) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • Loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by … using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than …
A
  • Synthesized from glutamate (Glu) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • Loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than recycling
    *
28
Q

GABA (y-aminobutyric acid) - inhibitory

  • Synthesized from glutamate (Glu) in a reaction catalyzed by … … … (GAD)
  • Loaded and stored into vesicles by a … … transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than recycling
A
  • Synthesized from glutamate (Glu) in a reaction catalyzed by glutamic acid decarboxylase (GAD)
  • Loaded and stored into vesicles by a vesicular GABA transporter, GAT (Gly uses the same transporter)
  • Cleared from synapse by reuptake using transporters on glia and neurons including non-GABAergic neurons
  • Higher proportion of GABA is made de novo to refill vesicles rather than recycling
    *
29
Q

Regulation of amino acid transmitter release

  • Too much …/ too little … - hyper-excitability - epilepsy –> excitotoxicity
  • Too much … - sedation/coma
A
  • Too much Glu/ too little GABA - hyper-excitability - epilepsy –> excitotoxicity
  • Too much GABA - sedation/coma
30
Q

Cerebral ischemia - too much GLU

  • The metabolic events that retain the electrochemical gradient are abolished
  • Reversal of the Na+/K+ gradient
  • Transporters release … from cells by reverse operation
  • … -> cell death (large increase of Ca2+ -> enzymes -> digestion of overexcited cells - death)
A

Cerebral ischemia - too much GLU

  • The metabolic events that retain the electrochemical gradient are abolished
  • Reversal of the Na+/K+ gradient
  • Transporters release glutamate from cells by reverse operation
  • Excitotoxic -> cell death (large increase of Ca2+ -> enzymes -> digestion of overexcited cells - death)
31
Q

Cerebral ischemia - too much …

A

Cerebral ischemia - too much GLU

32
Q

GHB y-hydroxybutyrate (date rape drug) - too much …

A

GHB y-hydroxybutyrate (date rape drug) - too much GABA

33
Q

GHB y-hydroxybutyrate (date rape drug) - too much GABA

  • A GABA metabolite that can be converted back to GABA
  • Increases amount of available GABA
  • Too much = … and …
A
  • A GABA metabolite that can be converted back to GABA
  • Increases amount of available GABA
  • Too much = unconsciousness and coma
34
Q

The monoamines

  • … - dopamine, epinephrine, norepinephrine
  • … - serotonin
A
  • Catecholamines - dopamine, epinephrine, norepinephrine
  • Indolamines - serotonin
35
Q

The monoamines

  • Catecholamines - …, epinephrine, …
  • Indolamines - …
A
  • Catecholamines - dopamine, epinephrine, norepinephrine
  • Indolamines - serotonin
36
Q

Catecholamine synthesis I

  • Dopamine synthesis occurs in … steps
A
  • Dopamine synthesis occurs in 2 steps
37
Q

Catecholamine synthesis II

A
  • DBH located in synaptic vesicles only, and NE is the only transmitter synthesised within vesicles
38
Q

Administration of levodopa for treating what disease?

A

Parkinson’s disease (Levodopa - converted to dopamine in brain - can cross blood brain barrier)

39
Q

Levodopa - converted to dopamine in brain - can cross blood… …

A

Levodopa - converted to dopamine in brain - can cross blood brain barrier

40
Q

Catecholamine storage

  • Loaded into vesicles by Vesicular … … (VMATs) (proton gradient like Glu and GABA transporters)
  • Modulation of catecholamine synthesis by drugs:
    • L-DOPA - Levodopa - precursor of …, is used as a treatment for Parkinson’s. Dopa decarboxylase converts it into … increasing the pool of releasable transmitter
A
  • Loaded into vesicles by Vesicular monoamine transporters (VMATs) (proton gradient like Glu and GABA transporters)
  • Modulation of catecholamine synthesis by drugs:
    • L-DOPA - Levodopa - precursor of dopamine, is used as a treatment for Parkinson’s. Dopa decarboxylase converts it into dopamine increasing the pool of releasable transmitter
41
Q

Catecholamine release and reuptake

  • Released by Ca2+ dependant …
  • Binds and activates …
  • Signal terminated by … into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • … back into vesicles
    • Enzymatically degraded by … oxidases MAOs OR
    • Inactivated by catechol-O-methyl-transferase COMT
A
  • Released by Ca2+ dependant exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • Reloaded back into vesicles
    • Enzymatically degraded by monoamine oxidases MAOs OR
    • Inactivated by catechol-O-methyl-transferase COMT
42
Q

Catecholamine release and reuptake

  • Released by Ca2+ dependant exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • Reloaded back into vesicles
    • Enzymatically degraded by … OR
    • Inactivated by …
A
  • Released by Ca2+ dependant exocytosis
  • Binds and activates receptor
  • Signal terminated by reuptake into the axon terminal by transporters powered by electrochemical gradient (Dopamine transporters DATs, Norepinephrine transporters (NETs) etc)
  • In the cytoplasm -
    • Reloaded back into vesicles
    • Enzymatically degraded by monoamine oxidases MAOs OR
    • Inactivated by catechol-O-methyl-transferase COMT
43
Q

Modulation of catecholamine release and reuptake by drugs:

  • … - reverses transporter so pumps out transmitter and blocks reuptake (DA and NE)
  • … and Methylphenidate (Ritalin) blocks DA reuptake into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • s… - MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • … - COMT inhibitor (treatment of PD)
A
  • Amphetamine - reverses transporter so pumps out transmitter and blocks reuptake (DA and NE)
  • Cocaine and Methylphenidate (Ritalin) blocks DA reuptake into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • Selegiline - MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • Entacapone - COMT inhibitor (treatment of PD)
44
Q

Modulation of catecholamine release and reuptake by drugs:

  • Amphetamine - reverses transporter so pumps out transmitter and blocks … (DA and NE)
  • Cocaine and Methylphenidate (Ritalin) blocks DA … into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • Selegiline - … inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • Entacapone - … inhibitor (treatment of PD)
A
  • Amphetamine - reverses transporter so pumps out transmitter and blocks reuptake (DA and NE)
  • Cocaine and Methylphenidate (Ritalin) blocks DA reuptake into terminals. More DA in synaptic cleft - extend into terminals. More DA in synaptic cleft - extended action on postsynaptic neuron
  • Selegiline - MAO inhibitor found in dopaminergic nerve terminals thus preventing the degradation of DA allowing more to be released on subsequent activations (treatment of early-stage PD, depression and dementia)
  • Entacapone - COMT inhibitor (treatment of PD)
45
Q

Serotonin (5-HT)

  • Synthesis:
A
46
Q

Serotonin storage, release and reuptake

  • … in vesicles
  • Signal terminated by … by Serotonin transporters (SERTs) on presynaptic membrane
  • Destroyed by … in cytoplasm
A
  • Stored in vesicles
  • Signal terminated by reuptake by Serotonin transporters (SERTs) on presynaptic membrane
  • Destroyed by MAOs in cytoplasm
47
Q

Drugs modulating serotonin release and reuptake

  • … (…) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of depression and OCD
  • … stimulates the release of serotonin and inhibits it’s reuptake - has been used as an appetite suppressant in the treatment of obesity
  • … - methylenedioxymethamphetamine - …: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in PTSD)
A
  • Fluoxetine (Prozac) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of depression and OCD
  • Fenfluramine stimulates the release of serotonin and inhibits it’s reuptake - has been used as an appetite suppressant in the treatment of obesity
  • MDMA - methylenedioxymethamphetamine - Ecstasy: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in PTSD)
48
Q

Drugs modulating serotonin release and reuptake

  • Fluoxetine (Prozac) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of … and …
  • Fenfluramine stimulates the release of serotonin and inhibits it’s reuptake - has been used as an … suppressant in the treatment of …
  • MDMA - methylenedioxymethamphetamine - Ecstasy: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in …)
A
  • Fluoxetine (Prozac) - blocks reuptake of Serotonin - SSRI - selective serotonin reuptake inhibitor - treatment of depression and OCD
  • Fenfluramine stimulates the release of serotonin and inhibits it’s reuptake - has been used as an appetite suppressant in the treatment of obesity
  • MDMA - methylenedioxymethamphetamine - Ecstasy: causes NE and serotonin transporters to run backwards releasing NT into synapse/extracellular space (Assessed for therapeutic potential in PTSD)
    *
49
Q

Acetylcholine - Ach

  • … … (ChAT, CAT) converts choline + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by … acetylcholine … (VAChT)
  • Rapidly … in synaptic cleft by Acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
A
  • Choline Acetyltransferase (ChAT, CAT) converts choline + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by vesicular acetylcholine transporter (VAChT)
  • Rapidly degraded in synaptic clef by Acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
50
Q

Acetylcholine - Ach

  • Choline Acetyltransferase (ChAT, CAT) converts … + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by vesicular acetylcholine transporter (VAChT)
  • Rapidly degraded in synaptic cleft by … (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
A
  • Choline Acetyltransferase (ChAT, CAT) converts choline + acetyl CoA (coenzyme A) into acetylcholine
  • Packed into vesicles by vesicular acetylcholine transporter (VAChT)
  • Rapidly degraded in synaptic clef by Acetylcholinesterase (AChE)
  • Choline is transported back into the presynaptic terminal and converted to acetylcholine
51
Q

Drugs modulating acetylcholine degradation

  • AChE (acetylcholinesterase) …
    • Blocks the breakdown of Ach, prolonging its actions in the synaptic … e.g. neostigmine (treatment of myasthenia gravis, MG)
    • Positive - helps with … of disease
A
  • AChE (acetylcholinesterase) inhibitors
    • Blocks the breakdown of Ach, prolonging its actions in the synaptic cleft e.g. neostigmine (treatment of myasthenia gravis, MG)
    • Positive - helps with symptoms of disease
52
Q

AChE (acetylcholinesterase) inhibitors

  • Blocks the breakdown of Ach, prolonging its actions in the synaptic cleft e.g. … (treatment of myasthenia gravis, MG)
  • Positive - helps with symptoms of disease
A
  • Blocks the breakdown of Ach, prolonging its actions in the synaptic cleft e.g. neostigmine (treatment of myasthenia gravis, MG)
  • Positive - helps with symptoms of disease
53
Q

Neuropeptides

  • … transmission
  • Vary in their methods of … and release from small molecule transmitters
  • … polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
A
  • Slow transmission
  • Vary in their methods of synthesis and release from small molecule transmitters
  • Short polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
54
Q

Neuropeptides

  • Slow transmission
  • Vary in their methods of synthesis and release from small molecule transmitters
  • Short polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. e…, neuropeptide Y, substance P, endogenous opioids, v…
A
  • Slow transmission
  • Vary in their methods of synthesis and release from small molecule transmitters
  • Short polypeptide chains - 3-36 amino acids
  • Over one hundred neuropeptides described
  • E.g. endorphins, neuropeptide Y, substance P, endogenous opioids, vasopressin
55
Q

Neuropeptide release and degradation

  • Follow the … pathway and NOT released in the same manner as small molecule transmitters
  • Dense core vesicle fusion and … occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane … but not refilled
  • Bind to and activate …
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by .. in the extracellular environment
  • Release is … than small molecule release and signals may be maintained for …
A
  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • Dense core vesicle fusion and exocytosis occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
  • Bind to and activate receptor
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
  • Release is slower than small molecule release and signals may be maintained for longer
56
Q

Neuropeptide release and degradation

  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • Dense core … … and exocytosis occurs as a result of global elevations of …+ (sustained or repeated depolarization or release of …+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
  • Bind to and … receptor
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the … environment
  • Release is … than small molecule release and signals may be maintained for longer
A
  • Follow the secretory pathway and NOT released in the same manner as small molecule transmitters
  • Dense core vesicle fusion and exocytosis occurs as a result of global elevations of Ca2+ (sustained or repeated depolarization or release of Ca2+ from intracellular stores)
  • Neuropeptide vesicle membrane recycled but not refilled
  • Bind to and activate receptor
  • Neuropeptides signalling is terminated by diffusion from site of release and degradation by proteases in the extracellular environment
  • Release is slower than small molecule release and signals may be maintained for longer
57
Q

Other transmitters/ retrograde signalling

  • Soluble gases - Nitric oxide and carbon monoxide
    • NO made in … neuron by Nitric oxide synthase (activated by the binding of Ca2+ and calmodulin)
    • The gas is not … but rapidly diffuses from it’s site of synthesis. Diffuses between cells (into presynaptic cell - retrograde transmitter)
    • Activates guanylyl cyclase which makes the … messenger cGMP
    • Within a few seconds of being produced NO is converted to biologically … compound (Switching off the signal)
    • Potentially useful for coordinating activities of multiple cells in a small region (tens of micrometers) how big is a neuron?
A
  • Soluble gases - Nitric oxide and carbon monoxide
    • NO made in postsynaptic neuron by Nitric oxide synthase (activated by the binding of Ca2+ and calmodulin)
    • The gas is not stored but rapidly diffuses from it’s site of synthesis. Diffuses between cells (into presynaptic cell - retrograde transmitter)
    • Activates guanylyl cyclase which makes the second messenger cGMP
    • Within a few seconds of being produced NO is converted to biologically inactive compound (Switching off the signal)
    • Potentially useful for coordinating activities of multiple cells in a small region (tens of micrometers) how big is a neuron?
58
Q

Other transmitters - retrograde signalling

  • Endocannabinoids
    • Small lipids which mostly cause reduced … release at certain inhibitory terminals
    • A cannabinoid is also the active component of …
A
  • Endocannabinoids
    • Small lipids which mostly cause reduced GABA release at certain inhibitory terminals
    • A cannabinoid is also the active component of marijuana (Cannabis sativa)

Year 2 Medicine (162 decks)

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