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Theme 1: Fundamental Neuroscience and the Brain > Chemicals in the brain > Flashcards

Chemicals in the brain Flashcards

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1
Q

Synaptic vesicle release and recycling

A

Pool of vesicles anchored to cytoskeleton by synapsin

AP causes voltage gated Ca2+ channels to open so influx

Ca2+ activates CaMKII which phosphorylates synapsin

P-synapsin no longer binds to cytoskeleton so vesicles dock to active zone

SNARE complex at active zone docks vesicles to plasma membrane

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2
Q

Mechanisms of exoctyosis during neurotransmitter release

A
  1. Vesicle docks
  2. SNARE complexes form to pull membranes together
  3. Entering Ca2+ binds to synaptotagmin
  4. Ca2+ bound synaptotagmin catalyses membrane fusion by binding to SNAREs and the plasma membrane
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3
Q

Synaptic recycling

A

Vesicle membrane rapidly recovered via endocytosis

New vesicles bud off and are refilled with transmitter

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4
Q

Cleavage of SNARE proteins by clostridial toxins

A

Sites of proteolysis that blocks neurotransmitter release

Botulinum toxin reduces neuromuscular transmission ACh

Tatanus toxin reduces interneurones at spinal cord GABA Gly

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5
Q

Botox and tetanus

A

Prevent transmitter release

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6
Q

Botulinum and tetanus toxins

A

From bacteroa Clostridium botulinum and tetani

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7
Q

Botox

A

Acts directly at the neuromuscular junction

Muscle lose all input and so become permanently relaxed

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8
Q

Tetanus toxin

A

Inhibits release of glycine and GABA at inhibitory neurones

Results in dis-inhibition of cholinergic neurones which causes permanent muscle contraction

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9
Q

Diseases that affect presynaptic terminal

A

Congenital myasthenic syndromes result in impaired vesicle recycling

Latrotoxin triggers vesicle fusion

Botulinum and tetanus affect SNARE protein in fusion

Cognitive disorders impair transsynaptic signaling

LEMS attack presynaptic Ca2+ channels

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10
Q

Vesicular transporters powered by proton gradient

A

ATPase proton pump loads up vesicles with H+

Makes vesicle acidic compared to neutral pH of cytoplasm

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11
Q

Plasma membrane transporters powered by electrochemical gradient

A

Na+ higher outside, K+ higher inside

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12
Q

Glia

A

Astrocytes have extensions that wrap around synapses

One neurone signals to another by releasing neurotransmitters

These transmitters also taken up by astrocyte

Once activated, astrocytes experience increase in intracellular Ca2+ and release own transmitters into synapse

Transmitters enhance or inhibit synaptic activity

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13
Q

Categories of neurotransmitters

A

Amino acids: synthesised locally in presynaptic vesicle

Monamines: stored in synaptic vesicle

Acetylcholine: released in response to local increase in Ca2+

Neuropeptides: synthesised in cell some and transported to terminal; stored in secretory granules; released in response to global increase in Ca2+

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14
Q

Fast transmitters

A

Stored in synaptic vesicles

Close to voltage gated calcium channels in membrane of nerve terminal

Released in short bursts when membrane is depolarised

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15
Q

Slow transmitters

A

Stored in separate vesicles further from the membrane

Must first migrate to the membrane and occurs only when Ca2+ builds up sufficiently

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16
Q

Excitatory NT in the CNS

A

Slightly depolarises the PostS membrane

Glutamate (CSNS)

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17
Q

Inhibitory NT in the CNS

A

Slightly hyperpolarises the PostS membrane

GABA (brain)

Glycine (spinal cord and brain stem)

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18
Q

Diffuse modulatory systems

A

Function in:

  • mood
  • sleep
  • pain
  • emotion
  • appetite
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19
Q

Synthesis of glutamate

A
  1. From glucose via the Krebs cycle

2. From glutamine converted to glutaminase into glutamate

20
Q

Glutamate

A

Loaded and stored in vesicle by VGLUTs

Reuptake by excitatory amino acid transporters in plasma membrane of PreS cell and surrounding glia

Glial cells convert GLut to glutamine then transported back to nerve terminals back to glutamate

21
Q

GABA synthesis

A

From glutamate in a reaction catalysed by glutaminc acid decarboxylase

22
Q

GABA

A

Loaded and stored into vesicle by a vesicular GABA transporter

Cleared from synapse by reuptake using transporters on glia and neurones

Higher proportion of GABA is made de novo to refill vesicles rather than recycling

23
Q

Too much Glu/ too little GABA

A

Hyper-excitability

Epilepsy

Excitotoxicity

24
Q

Too much GAB

A

Sedation/ coma

25
Q

Cerebral ischaemia

A

The metabolic events retain the electrochemical gradient are abolished

Reversal of the Na+/K+ gradient

Transporters release glutamate from cells by reverse operation

Excitotoxic cell death (Ca+- enzymes- digestion)

26
Q

GHB y-hydroxybutyrate (date rape drug)

A

A GABA metabolite that can be converted back to GABA

Increases amount of available GABA

Too much leads to unconsciousness and coma

27
Q

Catecholamines

A

Dopamine

Epinephrine (adrenaline)

Norephineprhine

28
Q

Indolamines

A

Serotonin

29
Q

Catecholamine synthesis

A

Tyrosine— (TH)

L-Dihydroxy-phenylalanin— (dopa decarboxylase)

Dopamine— (DBH)

Noerepinephrine—(PNMT)

Epinephrine

30
Q

Catecholamine storage

A

Loaded into vesicles by VMATs

31
Q

VMATs

A

Vesicular monoamine transporters

32
Q

Modulation of catecholamine synthesis by drugs

A

L-DOPA

  • levodopa
  • the precursor of dopamine
  • used as treatment for Parkinson’s disease
  • dopa decarboxylase converts it into dopamine increases pool of releasable transmitter
33
Q

Catecholamine release and reuptake

A

Released by Ca2+ dependant exocytosis

Binds and activates receptor

Signal terminated by reuptake into axon terminal by transporters powered by EC gradient

In cytoplasm

  • reloaded back into vesicle
  • enzymatically degraded by monoamine oxidase
  • inactivated by Catechol-O-methyl-transferase
34
Q

Amphetamines

A

Reverses transporter so pumps out transmitter and blacks reuptake

35
Q

Cocaine and methylphenidate

A

Blocks DA reuptake into terminals

More DA in synaptic cleft

Extended action of PostS neurone

36
Q

Selegiline

A

MOA inhibitor found in dopaminergic nerve terminals

Prevents degradation of DA

More released on subsequent activations

37
Q

Entacapone

A

COMT inhibitor

Treatment of Parkinson’s

38
Q

Serotinin

A

Stored in vesicles

Signal terminated by reuptake sertonin transporters on PreS membrane

Destroyed by MAOs in cytoplasm

39
Q

Fluoextine

A

Blocks reuptake of serotonin

Treatment of

  • depression
  • OCD
40
Q

Fenfluramine

A

Stimulates release of serotonin and inhibits its reuptake

Appetite suppressant

41
Q

MDMA

A

Causes NE and serotonin transporters to run backwards

Release NT into synapse

Assessed for therapeutic potential in PTSD

42
Q

Achetylcholine

A

ChAT converts choline and acetyl-CoA to acetylcholine

Packaged into vesicles by VAChT

Rapidly degraded in cleft by AChE

43
Q

AChE inhibitors

A

Blocks breakdown of ACh

Prolongs its action in the cleft

Neostigmine (treatment of myasthenia gravis)

44
Q

Neuropeptides

A

Short polypeptide chains (3-36 aa)

Vesicle fusion and exocytosis as result of global Ca2+ influx

Neuropeptide vesicle membrane recycled by not refilled

Bind to activate receptor

Terminated by diffusion from site of release

Degraded by proteases in extracellular environment

Release is slower and signals last longer

45
Q

Soluble gases

A

NO and CO

  1. NO made in PostS neurone by NO synthase
  2. Gas not stored but rapidly diffuses between cells
  3. Activates guanylyl cyclase makes second messenger cGMP
  4. After few seconds NO is converted to biologically inactive compound
46
Q

Endocannabinoids

A

Small lipids mostly causes reduced GAB release at certain inhibitory terminals

Active component of marijuana

Theme 1: Fundamental Neuroscience and the Brain (20 decks)

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