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Brain and Behaviour > Neurotransmission and Neuromodulation > Flashcards

Neurotransmission and Neuromodulation Flashcards

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1
Q

What is the neuron made up of?

A

Dendrites
Soma
Axon
Terminal boutons

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2
Q

What are dendrites?

A

Receive info from other neurons

Has a large receptive field

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3
Q

What are dendritic spines?

A

This is the part that protrudes from the dendrite, it contains lots of excitatory receptors + how communication takes place

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4
Q

What is a soma?

A

The cell body of the neuron

Contains the machinery = controls processing in the cell + integrates info

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5
Q

What is an axon?

A

Carries info (action potential) from the some to the terminal boutons + to other cells.

Axons can branch to contact multiple neurons

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6
Q

What are terminal boutons?

A

Found at the end of the axon, location of the synapse, communication point w/ other neuron

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7
Q

What is in the neuronal membrane?

A

Boundary of soma, dendrites, axon and terminal boutons.

Separates the extracellular environment from the intracellular environment

Membrane = lipid bilayer (5nm)

Proteins structures = detect substances outside of the cell, allow access of certain substances into the cell (gated: chemical or electrical)

Cytoskeltal

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8
Q

What is an electrical synapse?

A

Very rare int he adult mammalian neurons e.g. found in the retina

Junction between neurons = very small (3nm gap junction)

Gap = spanned by proteins (connexions) - used to communicate between neurons (ions move freely)

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9
Q

What are chemical synapses?

A

Common in adult mammalian neurons

Junction between neurons (synaptic cleft) = 20-50nm

Chemicals (neurotransmitters) = released from presynaptic neuron to communicate w. postsynaptic neurons

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10
Q

What is some early evidence for chemical transmission?

A

Loewi (1920s) = applying fluid after vagus nerve simulation slowed down heart rate.

Substance = ‘sufficient’ to change heart activity

Acceptance = primary means of communication of brain in 60s

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11
Q

Where is the axondendritic synapses located?

A

Majority

Axon on the dendrite

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12
Q

Where is Axiomatic synapses located?

A

some inhibitory neurons do this

Soma on soma

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13
Q

Where is Axoaxonix synapse located?

A

Axon on axon impinging on it = controls info flow through this way

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14
Q

How does chemical transmission happen?

A
  1. Neurotransmitter (NT) synthesis, transport and storage
  2. Depolarisation (action potential)
  3. Open voltage-gated Ca2+ channel
  4. Ca2+ influx
  5. Movement + docking of vesicles
  6. Exocytosis-diffusion

7-8. Interact w/ receptors at the post-synaptic neuron in/ deactivation of NTs

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15
Q

What are Neurotransmitters?

A

Chemical= used to transmit info from the presynaptic neuron to the postsynaptic neuron

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16
Q

What is the criteria for neurotransmitters?

A
  1. Chemical synthesized presynaptically.
  2. Electrical stimulation = release of the chemical.
  3. Chemical = physiological effect (excite/ inhibit a neuron)
  4. Terminate activity
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17
Q

What happens between the neurotransmitter and postsynaptic action?

A

Neurotransmitter binds to receptors on the postsynaptic membrane = affects the activity of the postsynaptic cell.

Configuration of the receptors = spec. for diff. neurotransmitters.

Opening of an ionic channel (typically) = Ionotropic receptor

Activates an internal 2nd messenger
systems = affect the functioning of the postsynaptic cells = Metabotropic receptor

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18
Q

How are receptors pharmacology different?

A

Varies in their pharmacology = what transmitter binds to the receptor + how drugs interact

Agonist = a drug (or or endogenous ligand/neurotransmitter) = can combine w/ a receptor on a cell to produce a cellular reaction (full activation)

Antagonist = a drug that reduces/ inhibits the activity of the agonist/ endogenous ligand - no cellular effect after interacting with receptor

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19
Q

How are receptors different in other ways?

A

Kinetic = rate of transmitter binding + channel gating - determine duration of effects

Selectivity = what ions are fluxed (Na+, Cl-, K+ and/or Ca2+)

Conductance = the rate of flux

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20
Q

How are receptors different in other ways?

A

Kinetic = rate of transmitter binding + channel gating - determine duration of effects

Selectivity = what ions are fluxed (Na+, Cl-, K+ and/or Ca2+)

Conductance = the rate of flux

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21
Q

What are inotropic receptors?

A

Fast transmission = ion movement = immediate change in the postsynaptic cell

Excitatory fast transmission:
- Ion channel opens
- Movement of pos. ions into neurone (Na+) (e.g. Glutamate receptors)
- Depolarisation
- Excitatory post synaptic potential (EPSP)

Inhibitory fast transmission:
- Ion channel opens
- Movement of neg. ions into neuron (Cl-) (e.g. GABAA receptors)
- Hyperpolarisation
- Inhibitory post synaptic potential (IPSP)

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22
Q

What are metabotropic receptor?

A

G-protein coupled receptor: gets activated

  1. Neurotransmitter binds to receptor + activates the G-protein (exchange GDP for GTP)
  2. G protein splits + activates other enzymes
  3. Breakdown of GTP turns off G protein activity
  4. Series of chemical reactions = amplification of the signal – second messenger system
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23
Q

What is the amplification of G-protein coupled receptors activation?

A

Slow but bigger effects:
- transmitter activates receptor
- receptor activates G-protein
- G- protein stimulated adenylyl cyclase to covert ATP to cAMP
- cAMP activates protein kinase A
- Protein kinase A phosphorylates potassium channels

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24
Q

What is neurotransmitter deactivation?

A

Neurotransmitter must be inactivated after use to remove them from the synaptic cleft

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25
Q

How is neurotransmitter reaction done?

A
  1. Neuron has transporters (a vacuum cleaner) = re-uptake them neurotransmitter molecules back up to the neuron
  2. Deactivating enzyme = breaks down excessive neurotransmitters + gets rid of it.
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26
Q

What is another way of regulating synaptic transmission?

A

Autoreceptors = found on the presynaptic terminal

Responds to neurotransmitters in the synaptic cleft + generally G-protein coupled (don’t directly open ion channels)
Terminal autoreceptor example = THC

Regulates internal process controlling the synthesis + release of neurotransmitters.

Neg. feedback mechanism = slow down neuronal transmission. AUTORECEPTORS ARE NOT THE SAME AS REUPTAKE SITES

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26
Q

What is another way of regulating synaptic transmission?

A

Autoreceptors = found on the presynaptic terminal

Responds to neurotransmitters in the synaptic cleft + generally G-protein coupled (don’t directly open ion channels)
Terminal autoreceptor example = THC

Regulates internal process controlling the synthesis + release of neurotransmitters.

Neg. feedback mechanism = slow down neuronal transmission. AUTORECEPTORS ARE NOT THE SAME AS REUPTAKE SITES

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27
Q

What are some examples of classical neurotransmitters?

A

Examples:
1. Amino acids = fast transmission e.g GABA, glutamate
2. Monoamines e.g dopamine, serotonin,
3. Acetylcholine

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28
Q

What are classical neurotransmitters?

A

Synthesised locally in the presynaptic terminal

Stored = synaptic vesicles

Released in response to local increase in Ca2+ (calcium)

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29
Q

What are neuropeptides as a type of neurotransmitter?

A

E.g endorphins for pain relief

Synthesised in the cell some + transported to the terminal

Stored = secretory granules

Released in response to global increase in Ca2+ (calcium)

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30
Q

Are there other types of neurotransmitters?

A

Yes = other small molecule transmitters e.g nitric oxide

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31
Q

How does fast synaptic transmission occur?

A

Glutamate inotropic receptors in general flux NA+ (sodium) = EXCITATORY post synaptic potential) EPSP + depolarising the post synaptic neuron

GABA inotropic receptors flux Cl- (chlorine) = IPSP (INHIBITORY Post Synaptic Potential) hyper polarising the postsynaptic neuron

Acetylcholine, serotonin + ATP activate inotropic receptors

32
Q

What is the importance of glutamate?

A

Major fast excitatory neurotransmitter in the CNS

Very widespread through the CNS = every neuron has a glutamate receptor

Activates different types of receptors: mGluR, NMDA, AMPA, Kainate

33
Q

How is glutamate synthesis stored, released and reuptaked?

A
  1. Synthesized in nerve terminals from glucose or glutamine
  2. Loaded + stored in vesicles by vesicular glutamate transporters
  3. Released by exocytosis (Ca2+ dependent mechanism)
  4. Acts at Glutamate receptors on postsynaptic membrane
  5. Reuptake by excitatory amino acid transporters (EAATs) in the plasma membrane of presynaptic cell + surrounding glia
34
Q

How do receptors respond to glutamate?

A

Based on their pharmacology, three types of ionotropic receptor have
been described that respond to glutamate
1. NMDA:
- Agonist = NMDA
- Antagonist = APV
2. AMPA:
- Agonist = AMPA
- Antagonist = CNQX
3. Kainate:
- Agonist = Kainic acid
- Antagonist = CNQX

Named based on the agonists selective for them

35
Q

How does the AMPA receptor work?

A

Iontropic receptor

Binding of glutamate = opening of Na+ (sodium) channel (slight K+, Potassium), causes depolarisation

Selective agonists: AMPA
Antagonists: CNQX, DNQX

36
Q

How does the NMDA receptor work?

A

Ionotropic receptor

Permeable to Na+, K+ and Ca2+
Binding of glutamate – nothing happens

Voltage dependent blockade:
At Resting membrane potential (-65mV):
- glutamate binds
- channel opens
- blocked by Mg2+

Depolarised membrane (-30mV):
- Mg2+ pushed out of pore
- channel is open
- ion movement
- further depolarisation

Different ‘kinetics’ from AMPA receptor (open much longer)

Glycine = very improtant

37
Q

What is a summary of selectivity and conductance of glutamate receptors?

A

AMPA (+ kainate) receptors = Fast opening channels permeable to Na+ and K+

NMDA receptors:
1) Slow opening channels – permeable to Ca2+ as well as Na+ and K+
2) Requires glycine as a cofactor = no glycine, no activation
3) Gated by membrane voltage

NMDA receptors = only activated in an already depolarized membrane + in presence of glutamate

38
Q

What happens in the dysregulation of NMDA receports?

A

NMDA reports = blocked by phencyclidine (PCP) + MK801 which bind in the open pore.

Blockade of NMDA receptors = symps. resembling hallucinations assoc. w/ Sz (reduced NMDAR function)

Certain antipsychotic drugs = enhance current flow through NMDA channels + relieve Sz symps.

39
Q

What is glutamate excitotoxicity?

A

Excessive CA2+ (calcium) influence into the cell = activates calcium dependent proteases + phospholipase that damage cell

This kind of cell damage = after stroke + chronic stress

40
Q

What is the GABA inhibitory transmitter?

A

Gamma aminobutyric acid = fast major inhibitory neurotransmitter

Activates an ionotropic receptor
(GABAA receptor) = opens a
chloride channel (Cl-) leading to
hyperpolarisation (IPSP).

41
Q

What is the GABA inhibitory transmitter?

A

Gamma aminobutyric acid = fast major inhibitory neurotransmitter

Activates an ionotropic receptor
(GABAA receptor) = opens a
chloride channel (Cl-) leading to
hyperpolarisation (IPSP).

42
Q

How is GABA synthesised, stored, released and re-uptaked?

A
  1. Synthesized from glutamate
  2. Loaded + stored into synapses by a vesicular GABA transporter
  3. GABA released by exocytosis (Ca2+ dependent mechanism)
  4. GABA acts at ionotropic GABAA + metabotropic GABAB receptors on postsynaptic membrane
  5. GABA cleared from synapse by reuptake using transporters on glia
    + neurons including non-GABAergic neurons
43
Q

How are GABA receptors different?

A
  1. GABAA ionotropic receptors
    • Ligand gated Cl- channel
    • Fast IPSPs
  2. GABAB metabotropic receptors
    • G protein coupled receptors
    • Indirectly coupled to K+ or Ca2+
    • channel through 2nd messengers
    • (opens K+ channel, closes Ca2+ channel)
    • Slow IPSPs
44
Q

Why is GABA important?

A

Too much GABA = sedation/coma
(At right dose, drugs increasing GABA transmission = treat epilepsy)

GHB gamma-hydroxybutyrate (date rape drug)
- GABA metabolite = converted back to GABA by transamination
- Increases amount of available GABA
- Moderate dose like alcohol, too much = unconsciousness + coma

Too much GABA in the brain

45
Q

How can you die from alcohol?

A

Quite drunk = BAC of 0.2-0.3

Death = BAC of 0.35-0.5

People usually passes out before they ingest the lethal dose, but some don’t.

46
Q

How does GABAa receptors work as drugs (pharmacology?

A

Complex receptor w/ multiple binding sites

Drugs binding @ GABA binding site:
- Muscimol – agonist
- Bicuculine, picrotoxin – antagonist

Drugs binding elsewhere on the receptor (no competition with GABA)
Benzodiazepine
Barbiturates
Ethanol
Neurosteroids
(net result more inhibitory Cl- current, stronger IPSPs and
behavioural consequences of enhanced inhibition)

47
Q

What is an example of how GABAa working as drugs?

A

Amanita muscaria = used in Siberia for1000’s years as inebriant

Eat spec. fungi in the shape of fly-agarics= become drunk worse
than on vodka, + for them = very best banquet.” - from

Kamiensky Dluzyk Diary of Muscovite Captivity published 1874 pg 382.

48
Q

How do drugs increasing GABA activity, reduce anxiety?

A

Agonists = Alcohol, barbiturates

Indirect agonists = Benzodiazepines (BDZ) = anti-convulsant

49
Q

How do drugs decreasing GABA activity increase anxiety (anxiogenic)?

A

Antagonist = flumazenil (also for reversing sedation bc BDZ overdose)

These drugs all act at GABAa inotropic receptor

50
Q

How do drugs at the GABAa receptor when th ekinetics are changed?

A

GABA + barbiturate = agonist strong affect

GABA + benzodiazepine (indirect agonist) = effect

GABA + flumazenil (antagonist) = no effect

They said that using barbiturates is recommended

51
Q

What are the problems of barbiturates?

A
  1. General (non-spec) depression of neuronal activity = includes functions e.g breathing
  2. Poor therapeutic ratio. Small diff. between therapeutic dose + overdose. High suicide risk in emotionally unstable Ps.
  3. LT treatment = dependence + withdrawal
  4. Only used for severe insomnia + seizures
52
Q

What is Benzodiazepines?

A

Discovered in 1960s

Was first chlordiazepoxide (librium)

After diazepam (valium) = became major treatment for anxiety disorders

Acts as an anxiolytic, anticonvulsant, sedative, muscle relaxant, amnestic

53
Q

What are the strengths and weaknesses of using Benzodiazepines?

A

Strengths:
- good, fast acting anxiolytics
- large therapeutic window

Disadvantages:
- May cause dependance
- Effects amplified by alcohol

54
Q

What is the difference between neurotransmission and neuromodulation?

A

Primary neurotransmitters (glutamate + GABA) = main workhorses of the brain. They directly mediate the transmission of info between neurons via activation (excitation, EPSPs0 or inactivation (inhibition, IPSPs) of post-synaptic targets

Neurotransmitters (dopamine) = affect the response properties of neurons (e.g release, excitability, how likely it will release a neurotransmitter) + don’t carry primary info themselves. They fine tune the activity of neurons

55
Q

What are the diffuse modulatory systems?

A

Spec. pops. of neurons = project diffusely + modulate the activity of glutamate + GABA neurons in their target areas

A lot of these neurons originate from the primitive brain
- Dopa. = brain stem mid brain
- Serot. = all over brain stem
- Noradren = brain stem area
- Acetylcholine = all brain stem area

56
Q

Where is dopamine located in the brain?

A

Cell bodies in the midbrain (substantial nigra) + project in the forebrain (neostriatum)

57
Q

What is Nigrostriatal system in the dopaminergic system?

A

Substantia nigra projections to neostriatum (caudate and putamen) role in movement

If these neurons dysfunction:
- Parkinsons = destroyed DA projections from SN to basal ganglia

- Huntington's = destroyed DA target in striatum
58
Q

What does the mesolimbic system in dopaminergic system?

A

Ventral tegmental area projections to nucleus accumbens (NAcc) = role in reinforcement (reward).

A system that makes you want to do something again

Dysfunction = addiction, most drugs of abuse - enhanced DA release in the NAcc

59
Q

What does the mesocortical system in dopaminergic system?

A

Ventral tegmental area (VTA) projections to prefrontal cortex = role in functions e.g WM + planning

Dysfunction = SZ

60
Q

How is dopamine synthesised?

A

Tyrosine (essential amino acid get through diet)

Catalysed by tyrosine hydroxylate (TH) = rate limiting step (slowest step)

L-Dopa

Catalysed by dopa decarboxylase

Dopamine

61
Q

How is dopamine stored?

A

Catecholamine storage = loaded in vesicles

62
Q

How do we know that drugs affect dopamine synthesis + storage and modulate bhvr?

A

Reserpine = impairs storage of monoaminesin synaptic vesicles. (The vesicles remain empty resulting in no transmitter release upon activation). Caused depression when removing dopamine.

L-DOPA = the precursor of dopamine - used as a treatment for Parkinson’s
disease. (Bypasses rate-limiting TH step – Dopa decarboxylase converts it into
dopamine increases the pool of releasable transmitter

63
Q

What other drugs affect dopamine storage?

A

AMPT = inactivates TH (not used in treatment)

Role + importance of neurotransmitter systems in bhvr revealed by drugs.

64
Q

How is dopamine released?

A

Depolarization of presynaptic membrane

Influx of Ca2+ through voltage gated Ca2+ channels

Ca2+ dependent vesicle docking +
release (Ca2+ dependent exocytosis)

65
Q

How does dopamine reuptake/ metabolism work?

A

Signal terminated by reuptake into the axon terminal by transporters powered
by electrochemical gradient (Dopamine transporters (DATs))

In the cytoplasm dopamine is:
- reloaded back into vesicles
- enzymatically degraded by Monoamine oxidases (MAOs) or
Catechol-O-methyl-transferase (COMT)

66
Q

Can drugs of abuse affect dopamine release + reuptake, modulate bhvr?

A

Cocaine, Amphetamine + Methylphenidate (Ritalin) = psychostimulants
- They block the reuptake of monoamines (e.g dopamine transporter) into terminals. More dopamine in synaptic cleft
- Extended action of dopamine on postsynaptic neuron.(Amphetamine reverses transporter so pumps out transmitter - uncontrolled release)

Prevents the degeneration of dopamine:
- Selegiline = Monoamine oxidase B inhibitor
- Entacapone = COMT inhibitor
- prevent the breakdown of catecholamines,
- increases the releasable pool

Drugs = antidepressant activity + be used for treating Parkinson’s

67
Q

Where is serotonin located in the brain?

A

Nine raphe nuclei (in hte brain stem) w/ diffuse projections = each projects to diff. part of the brain.

68
Q

How does the serotnonergic system work?

A

Descending projections to cerebellum and spinal cord (pain)

Ascending projections (reticular activating system (with Locus Coeruleus))

Dorsal + medial raphe
project throughout the cerebral cortex

Raphe neurons
- fire tonically during wakefulness
- quiet during sleep

Function in:
- mood
- sleep
- pain
- emotion
- appetite

69
Q

How is serotonin made?

A

Tryptophan (essential amnio acid from diet) = rate limiting

Tryptophan hydroxylase

5-hydryoxytryptopha (5-HTP)

Acromatic amino acid decarboxylase

Serotonin (5-hydroxytryptamine, 5HT)

Tryptophan + mood:
- depletion diet: method of experimentally inducing a depressive state
- Enrichment = improving mood

70
Q

how is serotonin stored, released and re-uptaked/ metabolised?

A

Storage = loaded into vesicles

Release = Ca2+ dependent exocytosis

Reuptake/ metabolism = signal terminated by reuptake through Serotonin transporters (SERTs) on
presynaptic membrane + degraded by MAOs in the cytoplasm

71
Q

What drugs affect serotonin release and reuptake, modulating bhvr?

A

Fluoxetine (Prozac) = blocks reuptake of serotonin (SSRI – selective
serotonin reuptake inhibitor) – antidepressant / anti-anxiety

Fenfluramine = causes release of serotonin + inhibits its reuptake (used as an appetite suppressant obesity treatment)

MDMA 3,4-methylenedioxy-methamphetamine (ecstasy) = noradrenaline and serotonin
transporters (SERT) to work in reverse
releasing neurotransmitter into synapse/ extracellular space

Monoamine oxidase inhibitors (boost monoamines)

72
Q

Where is the cholinergic system found?

A

In the periphery

Acetylcholine (ACh) at neuromuscular junction (NMJ) + synapses in the autonomic ganglia

73
Q

How does the cholinergic system work?

A

In the brain:
- Basal forebrain complex
- Projections to hippocampus + cortex

Pontomesencephalotegmental complex = cholinergic link between brain stem + basal forebrain complex

cholinergic interneurons (in striatum + cortex) = each interneuron innervates 1000’s of local principal neurons + modulates their activity

74
Q

Describe the acetylcholine system

A

Synthesis = made from choline neuron (amount of choline is rate limiting step)

Storage = loaded into vesicles

Release = Ca2+ dependent exocytosis

Metabolism:
- Rapidly degraded in synaptic cleft by acetylcholinesterase
- Choline is transported back into the
presynaptic terminal + converted to
acetylcholine

(acetylcholinesterase is made by the cholinergic neuron, secreted into synaptic cleft + assoc. w/ the axonal membrane)

75
Q

What drugs affect acetylcholine release, storage and degradation in modulating bhvr/ neurological function?

A

Acetylcholinesterase inhibitors = block the breakdown of ACh - prolonging its actions in the synaptic cleft e.g. Physostigmine

Treatments for Alzheimer’s disease,
e.g Myasthenia gravis (autoimmune disorder, AchR’s destroyed)

76
Q

What drugs affect vesicle docking and release?

A

ACh release at Neuro-Muscular Junction, NMJ)

Botulinum + tetanus toxins = from bacteria Clostridium botulinum and tetani
- blocks the docking of vesicles by attacking SNAREs- no release

Botox acts directly at synapse in NMJ = muscles lose all input + become permanently relaxed.

77
Q

What drugs affect vesicle docking and release?

A

Tetanus toxin = retrogradely transported up at NMJ + works at
inhibitory (Glycine) synapses on cholinergic motor neurons of
spinal cord

-Also attacks SNARE proteins
(Inhibiting the release of Glycine at these sites “disinhibits” the cholinergic
neurons so they continuously fire resulting = permanent muscle
contraction, ‘lock jaw’

78
Q

What are disorders caused by dysfunctioning cholinergic system?

A

Peripheral (Myasthenia gravis) =
Autoimmune disease - destroys cholinergic receptors in the muscle =
muscle weakness + eventual loss of muscle activity

Brain (Alzheimer’s disease) = Loss of cholinergic neurons in the basal ganglia
- possibly underlies deficits in memory assoc. w/ the disease.
- Drugs that increase acetylcholine help (e.g. donepezil)

Addiction = nicotine addiction

Other psychiatric disorders = Sz (Comorbidity w/ smoking)

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