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Neurotransmission and Neuromodulation Flashcards

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
How is neurotransmitter reaction done?
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.
26
What is another way of regulating synaptic transmission?
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
26
What is another way of regulating synaptic transmission?
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
27
What are some examples of classical neurotransmitters?
Examples: 1. Amino acids = fast transmission e.g GABA, glutamate 2. Monoamines e.g dopamine, serotonin, 3. Acetylcholine
28
What are classical neurotransmitters?
Synthesised locally in the presynaptic terminal Stored = synaptic vesicles Released in response to local increase in Ca2+ (calcium)
29
What are neuropeptides as a type of neurotransmitter?
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)
30
Are there other types of neurotransmitters?
Yes = other small molecule transmitters e.g nitric oxide
31
How does fast synaptic transmission occur?
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
What is the importance of glutamate?
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
How is glutamate synthesis stored, released and reuptaked?
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
How do receptors respond to glutamate?
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
How does the AMPA receptor work?
Iontropic receptor Binding of glutamate = opening of Na+ (sodium) channel (slight K+, Potassium), causes depolarisation Selective agonists: AMPA Antagonists: CNQX, DNQX
36
How does the NMDA receptor work?
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
What is a summary of selectivity and conductance of glutamate receptors?
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
What happens in the dysregulation of NMDA receports?
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
What is glutamate excitotoxicity?
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
What is the GABA inhibitory transmitter?
Gamma aminobutyric acid = fast major inhibitory neurotransmitter Activates an ionotropic receptor (GABAA receptor) = opens a chloride channel (Cl-) leading to hyperpolarisation (IPSP).
41
What is the GABA inhibitory transmitter?
Gamma aminobutyric acid = fast major inhibitory neurotransmitter Activates an ionotropic receptor (GABAA receptor) = opens a chloride channel (Cl-) leading to hyperpolarisation (IPSP).
42
How is GABA synthesised, stored, released and re-uptaked?
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
How are GABA receptors different?
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
Why is GABA important?
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
How can you die from alcohol?
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
How does GABAa receptors work as drugs (pharmacology?
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
What is an example of how GABAa working as drugs?
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
How do drugs increasing GABA activity, reduce anxiety?
Agonists = Alcohol, barbiturates Indirect agonists = Benzodiazepines (BDZ) = anti-convulsant
49
How do drugs decreasing GABA activity increase anxiety (anxiogenic)?
Antagonist = flumazenil (also for reversing sedation bc BDZ overdose) These drugs all act at GABAa inotropic receptor
50
How do drugs at the GABAa receptor when th ekinetics are changed?
GABA + barbiturate = agonist strong affect GABA + benzodiazepine (indirect agonist) = effect GABA + flumazenil (antagonist) = no effect They said that using barbiturates is recommended
51
What are the problems of barbiturates?
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
What is Benzodiazepines?
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
What are the strengths and weaknesses of using Benzodiazepines?
Strengths: - good, fast acting anxiolytics - large therapeutic window Disadvantages: - May cause dependance - Effects amplified by alcohol
54
What is the difference between neurotransmission and neuromodulation?
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
What are the diffuse modulatory systems?
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
Where is dopamine located in the brain?
Cell bodies in the midbrain (substantial nigra) + project in the forebrain (neostriatum)
57
What is Nigrostriatal system in the dopaminergic system?
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
What does the mesolimbic system in dopaminergic system?
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
What does the mesocortical system in dopaminergic system?
Ventral tegmental area (VTA) projections to prefrontal cortex = role in functions e.g WM + planning Dysfunction = SZ
60
How is dopamine synthesised?
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
How is dopamine stored?
Catecholamine storage = loaded in vesicles
62
How do we know that drugs affect dopamine synthesis + storage and modulate bhvr?
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
What other drugs affect dopamine storage?
AMPT = inactivates TH (not used in treatment) Role + importance of neurotransmitter systems in bhvr revealed by drugs.
64
How is dopamine released?
Depolarization of presynaptic membrane Influx of Ca2+ through voltage gated Ca2+ channels Ca2+ dependent vesicle docking + release (Ca2+ dependent exocytosis)
65
How does dopamine reuptake/ metabolism work?
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
Can drugs of abuse affect dopamine release + reuptake, modulate bhvr?
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
Where is serotonin located in the brain?
Nine raphe nuclei (in hte brain stem) w/ diffuse projections = each projects to diff. part of the brain.
68
How does the serotnonergic system work?
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
How is serotonin made?
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
how is serotonin stored, released and re-uptaked/ metabolised?
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
What drugs affect serotonin release and reuptake, modulating bhvr?
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
Where is the cholinergic system found?
In the periphery Acetylcholine (ACh) at neuromuscular junction (NMJ) + synapses in the autonomic ganglia
73
How does the cholinergic system work?
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
Describe the acetylcholine system
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
What drugs affect acetylcholine release, storage and degradation in modulating bhvr/ neurological function?
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
What drugs affect vesicle docking and release?
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
What drugs affect vesicle docking and release?
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
What are disorders caused by dysfunctioning cholinergic system?
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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