Lecture 5 + 6: Neurotransmitters Flashcards
(161 cards)
1
Q
Why study neurotransmitters?
A
Becuase neurotransmitter systems are central building blocks of theories linking brain activity to cognition and behavior. Therefore, they are key to understand effects of disorders and psychoactive drugs on cognition and behavior.
2
Q
What criteria must molecule fullfill to be called neurotransmitter?
A
-> must be synthesized and stored in presynaptic neuron
-> must be released by presynaptic axon terminal upon stimulation
-> when experimentally applied, must produce response in postsynaptic cell that mimicks the response produced by release of neurotransmitter
3
Q
What are methods used to classify neurotransmitters?
A
immunocytochemistry - using labeled antibodies to identify location of molecules within cells
in situ hybridization - localizing mRNA transcripts for proteins
4
Q
immunocytochemistry
A
neurotransmitter candidate is injected into bloodstream of animal, causing immune response of antibodies
then blood is withdrawn from animal and analysed
antibodies are extracted and applied to the brain tissue
those antibodies are used as labels for cells containing neurotransmitter candidates
therefore, it can be used to localize any molecule for which specific antibody can be generated
5
Q
in situ hybridization
A
strands of mRNA consist of nucleotides arranged in specific sequence
each nucleotide with bind with specific nucleotide
therefore, it is possible to construct a probe (complementary strand) to mRNA strands
this probe will bind to mRNA (hybridization)
therefore, it is possible to examine whether mRNA for particular peptide is localized in the neuron
6
Q
How to study transmitter release?
A
1) using alive brain slices and bathing them with high K+ concentration and presence of Ca -> this causes membrane depolarization and trigger transmitter release
2) optogenetics
7
Q
Which criterium is hardest to satisfy in CNS neurotransmitter research?
A
2nd: must be released by presynaptic axon terminal upon stimulation
we are unsure whether molecules were released from axon terminals or are consequence of secondary synaptic activation
8
Q
How to study synaptic mimicry? (criterium 3rd: when experimentally applied, must produce response in postsynaptic cell that mimicks the response produced by release of neurotransmitter)
A
microiontophoresis -> pipette is used to inject small amounts of electrical current and neurotransmitter candidate
microelectrode is used to check if neurotransmitter is producing effects
9
Q
How to study receptors?
A
1) neuropharmacological analysis of synaptic transmission
2) ligand-binding methods
3) molecular analysis of receptor proteins
10
Q
neuropharmacological analysis of synaptic transmission
A
different receptors can be distinguished by actions of different drugs
example: acetylcholine
nicotininc Ach receptor: agonist in skeletal muscles, but no effect on heart
muscarinic Ach receptor: no effect on skeletal muscles, but agonist in heart
——————————————————
different drugs can be distinguished depending to which glutamate receptor they bind: AMPA vs NMDA vs kainate
11
Q
ligand-binding methods
A
RQ: how opiates affect the brain?
testing: radioactively labelling opiates and applying them in small quantities to neuronal membranes
results: radioactive drugs labelled specific sites on membrane
12
Q
Dale’s principle
A
idea that neuron has only one neurotransmitter
refuted: many peptide-containing neurons violate it, also there may be many co-transmitters released from one nerve terminal
13
Q
ligand
A
any molecule that binds to receptor
14
Q
what are characteristics of amino acid gated channels?
A
fastest synaptic transmission in CNS
-> pharmacology of binding sites describes how transmitters affect them
-> kinetics -> transmitter binding and channel gating determine duration of their effect
-> selectivity -> excitation vs inhibition
-> conductance -> determines magnitude of their effects
15
Q
What are 2 types of glutamate gated channels?
A
AMPA and NMDA
16
Q
AMPA receptors
A
fast excitatory transmission, permeable to both Na and K, most non permeable to Ca, enable rapid depolarization
17
Q
NMDA receptors
A
fast excitatory transmission, admit excess of Na into cell causing depolarization, may also cause widespread and lasting changes due to Ca permeability
at resting potential get blocked by magnesium
18
Q
How NMDA and AMPA receptors differ?
A
1) NMDA-gated channels are permeable to Ca
2) inward ioninc current through NMDA-gated channels is voltage dependent
19
Q
What mediates most synaptic inhibition?
A
In CNS -> GABA
everywhere else -> glycine
20
Q
How does binding of drugs to GABA receptors occur?
A
drugs by themselves do not open the channel, but they change the effect that GABA has when it binds to the channel at the same time as the drug
benzodiazepines -> increase frequency of channel opening
barbiturates -> increase duration of channel opening
21
Q
Why synaptic inhibition must be tightly controlled in the brain?
A
too little inhibition -> seizure
too much inhibition -> coma
22
Q
What is the basic structure of G-protein-coupled receptor?
A
7-membrane spanning alpha helices, transmitter binding side (extracellular) and G-protein binding side (intracellular)
23
Q
What is the basic modus operandi of G-protein-coupled receptors?
A
1) transmitter binds to receptor
2) G proteins get activated
3) G protein complexes get released and travel to activate different effector proteins
24
Q
What is the shortcut pathway? How does it relate to G-protein-coupled receptors?
A
- many neurotransmitters use shortcut pathway from receptor to G-protein to ion channel
- example: muscarininc receptors in the heart (Ach recptors)
-> G-proteins in heart muscles get activated by binding of ACh to muscarininc receptors
-> activated g protein complexes DIRECTLY cause potassium channels to open
25
What are second messenger cascades?
G-proteins can also exert their effects by directly activating certain enzymes
push and pull method - one stimulates biochemical processes, the other inhibits them
26
What are protein kinases?
kinase which selectively modifies other proteins by covalently adding phosphates to them
phosphorylation of ion channels → effect on whether they will open or close
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What are protein phosphates?
remove phosphates from proteins
why? because proteins may become quickly saturated with phosphates
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What is function of singal cascade? (G protein)
synaptic transmission G-protein-coupled receptors is complex and slow -> however, due to long chain of command you obtain signal amplification! (activation of many ion channels)
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divergence
ability of one transmitter to activate more than one subtype of receptor
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convergence
multiple neurotransmitters can converge to influence the same effector system
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When equilibrium potential and reversal portential are equivalent to each other?
in single ion system
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equilibrium potential
net ion flux at voltage is zero (outward and inward rates are the same = EQUILIBRIUM)
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reversal potential
perturbation of membrane potential on either side of the equilibrium potential reverses the net direction of ion flux
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What are types of neurotransmitters?
aminoacids
amines
peptides
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What are characteristics of aminoacids?
small
huge concentration
made in synaps with help of enzymes made in cell body
inactivated largely through reuptake - recycling
short activity
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What are characteristics of amines?
small
huge concentration
made in synaps with help of enzymes made in cell body
inactivated largely through reuptake
- recycling
short activity
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What are characteristics of peptides?
short chains of 2 or more amino acids
low concentration
they are build in cell body and need to be transported to synapse (due to size)
no reuptake = longer duration
inactivated by breakdown and diffusion
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What is cytoskeleton?
skaffolding within the neuron = so it doesn't collapse
also within dendrites and axons
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What is green staining on the neuron?
tubulin -> cell body, dendrites, proximal axon
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What is red staining on the neuron?
tau - microtubulin binding protein -> distal axon
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How does transport within neuron occur?
transport via cytoskeleton => through microtubuli
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What is anterograde transport?
from cell body (soma) to synaps = orthodrome -> can be traced with HRP, PHL
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What is retrograde transport?
from synaps to cell body (soma) - needed for long-term potentiation = antidrome -> can be traced with FG, CT, FB
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How to study systems by injection to PFC?
Inject retrograde tracer into prefrontal cortex. Look to what areas cells project to. You can also inject anterograde injections to those sites. Examples: locus coeruleus and dorsal rape (reciprocal connections with PFC).
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What are reciprocal connections?
connections sending signals both ways
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How anterograde injection in ventrolateral prefrontal cortex enables you to study areas on the other hemisphere?
because there are connections between two hemispheres via corpus callosum
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How tracing was used in attention research in rat brain?
Retrograde injection was made into prefrontal cortex. PFC is connected with basal forebrain (acetylcholine), ventral tegmentum (dopamine), dorsal raphe (serotonin), locus coerulues (noradrenaline) etc. With specific tracers you can unconver which areas are using which neurotransmitters.
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How does indirect immunhistochemistry work?
Identify proteins in the tissue you want to stain. Then, inject primary antibody against the protein -> this antibody will always attach to your protein of interest (you can have nice visualization). Secondary antibody with HRPO can be then used to color areas where you find protein.
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How can you use viruses in your studies?
Virus is able to quickly infect multiple cells. As the infection spreads, you can have map of the whole system.
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What is fluorescent in situ hybridization?
laboratory technique used to detect and locate a specific DNA sequence on a chromosome
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How does in fluorescent in situ hybridization work?
In this technique, the full set of chromosomes from an individual is affixed to a glass slide and then exposed to a “probe”—a small piece of purified DNA tagged with a fluorescent dye. The fluorescently labeled probe finds and then binds to its matching sequence within the set of chromosomes. With the use of a special microscope, the chromosome and sub-chromosomal location where the fluorescent probe bound can be seen.
52
What is CLARITY technique?
New technique which enables to make the whole brain transparent by removing lipids blocking the view. Molecular markers can be added to highlight specific structures.
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How is cerebral cortex organized?
layer 2: send information to other cortical areas (ipsilateral)
layer 3: send information to other cortical areas, opposite hemisphere
layer 5: connected to sub-cortical structures (striatum, superior colliculus)
layer 6: connected to thalamus = sending information to layer 4 and receiving them back
54
What happens if you inject retrograde tracer in nucleus accumbens?
You can examine which layers of prefrontal cortex are connected to it. Layer 5! because it connects to subcortical areas (also layers 2 and 3 - because connections are within the same hemisphere and across hemispheres)
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What areas are targeting nucleus accumbens?
On the basis of retrograde injection in NA:
- prefrontal cortex
- thalamus
- ventral tegmental area
- amygdala
- ventral hippocampus
- dorsal raphe
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Why there are no drugs which target glutamate?
Because glutamate is used by all cortical areas. Too much of it would lead to overstimulation (epilepsy), blocking it would lead to death.
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To what system acetylcholine belongs?
cholinergic system
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What is good marker for cells using acetylcholine?
ChAT = specific enzyme required in acetylcholine synthesis
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What does ChAT do?
transfers acetyl group from acetyl CoA to choline
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What limits how much acetylcholine can be synthesized?
availability of choline
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What degrades acetylcholine in synaptic cleft?
AChE - degrades acetylcholine into choline and acetic acid
(choline is recycled)
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What receptors have acetylcholine?
nicotinic receptors
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What are characteristics of acetylcholine?
- medium - sized neurotransmitter
- similar to monoamines
- class of its own
- part of diffuse modulatory systems
- production depends on 2 enzymes: choline acetyltransferase - making
acetylcholine esterase - recycling
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How acetylcholine relates to Navalny poisioning?
Poison used blocked acetylcholine esterase - so transmitter could not be broken down. Therefore, there was too much acetylcholine in the system -> overactivation of muscles (spasms), then paralysis.
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Why is calcium important in vesicle packaging?
because it causes depolarization, enabling fusion with membrane
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What is role of synapsin in vesicle packaging?
connects the pool of vesicles
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What is the role of CaMKII in vesicle packaging?
dissociates synapsin from vesicles
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What are the roles of SNAPS and SNARES in vesicle packaging?
priming and docking (fusing) with the membrane
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How does fusing of vesicle with membrane occur?
1) SNARES enable to dock vesicle in membrane
2) synaptotagmin binds SNARE complex
3) entrence of calcum enables curvature in plasma membrane
4) fusion of vesicle with membrane -> exocytosis release of neurotransmitter
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How is vesicle recovered?
1) first, proteins attach clathrin to memrame
2) clathrin triskelia assemble into coat, curving embrane to form coated pit
3) assembled clathrin cage constricts lipid stalk connecting two membranes
4) dynamin ring forms and pinches off the lipid stalk
5) coated vesicle is translocated by actin filaments
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Where most of acetylcholine is made?
medial septal nuclei, basal nucleus of Meynert
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How acetylcholine projects to other brain areas?
via basal forebrain to cerebral cortex
vis ponto-mesencephalo-tegmental complex to thalamus
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What two types of receptors acetylcholine has?
1) nicotinic = fast, short lasting action, gate flips open due to conformational change
2) muscarinic = slower, long lasting action, G-protein subunits cause intracellular messenging
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What type of receptors are nicotininc channels?
they are ligand-gated receptors: binding to them makes them open
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What type of receptors are muscarinic channels?
metabotropic receptors - they don't open, but have G-coupled proteins binded to them = activation of G-coupled proteins contributes to intracellular messenging and ion channels opening
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What central acetylcholine projections from basal forebrain do?
- enhance long term potentiation, learning, selective attention
- involved in neuronal oscillations
- transmitter at neuromuscular junction
- parasympathetic nervous system = rest and digest function
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How is acetylcholine involved in Alzheimer's disease?
- cholinergic recpeptors are gone
- memory impairments
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What is medication used in Alzheimer's disease? How does it relate to acetylcholine?
- acetylcholine esterase blockers = acetylcholine stays in synapse (works when some acetylcholine in system is left)
- NMDA blocade = prevent over excitation of glutamate by which cell die (so it prevents death of acetylcholine cells)
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What is myastenia gravis?
autoimmune disease
eats your nicotine receptors
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What are MEPP?
muscular end plate potentials = every time muscle twiches, there is activation of MEPP
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How is MEPP affected in myastenia gravis?
amplitude goes down - so muscle activation is still there, just limited
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What is the medication for myastenia gravis?
- cholinesterase inhibitors = enhance communciation between nerves and muscles
- corticosteroids, immunosuppressants = limit immune system and antibody production, so they don't eat your receptors
83
What is patch-clamp technique? What related to acetycholine can be studied by it?
Suction is used to attach a micropipette filled with electrolyte solution to the cell membrane. This forms a seal, isolating a patch of the membrane to enable the flow of currents across this section of the membrane to be measured.
You can use it to study one single acetycholine receptor or identify it (by increasing amount of acetylcholine in the system and checking which channel will open)
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To what can reversible nicotinic acetylcholine receptors inhibitors be used?
in anesthesia!
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What happens if you put muscarininc acetylcholine receptor AGONIST in the system?
heart rate and blood pressure drops
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What happens if you put muscarininc acetylcholine receptor ANTAGONIST in the system?
pupil dilation; can be used in resuscitation
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What do catecholaminergic neurons?
regulate movement, mood, attention, visceral function
all contain enzyme tyrosine hydroxylase - which catalyses conversion of tyrosine into compound dopa
examples: dopamine, norepinephrine, epinephrine (adrenaline)
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What is a difference between norepinephrine and epinephrine (adrenaline)?
Epinephrine and norepinephrine are very similar neurotransmitters and hormones (=fight or flight). Epinephrine has slightly more of an effect on your heart, while norepinephrine has more of an effect on your blood vessels.
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What role compound dopa plays in Parkinson's disease?
In Parkinson's disease, dopaminergic neurons in brain degenerate and die. Dopa administration enables increase in dopamine in the system.
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What are serotonergic neurons?
serotonin! 5-HT
neurons relatively few in number, but play important role - regulate mood, emotions and sleep
synthesis: tryptohan -> 5-HTP -> 5-HT
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What are amino acidergic neurons?
glutamate and GABA
serve as neurotransmitters at most CNS synapses
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How are glutamate and glycine synthesized?
synthesized from glucose and other precursors by enzymes
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How is GABA synthesized?
only synthesized by neurons which use it as neurotransmitter (why? because it is not one of 20 amino acids used to construct proteins)
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What are GABA ergic neurons?
major source of synaptic inhibition in the nervous system
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What happens in glutamate at synapse?
1) glutamine gets transformed into glutamate
2) then glutamate is transported with help of VGLUT protein (vesicle) and released in the synapse
3) afterwards, glutamate is recycled and converted into glutamine again via glutamine synthase
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What are 3 types of glia cells?
1) astrocytes
2) oligodendrocytes
3) microglial cells
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What are characteristics of astrocytes?
- star-like
- maintain appropriate chemical environment for neuronal signaling
- most numerous type
- fill spaces between neurons
- influence neurite growth
- regulate chemical context of extracellular space
- reuptake of transmitters
- endfeed on blood vessels
- may be involved in learning memory
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What happens to mouse with extra human astrocytes?
learns quicker, because astrocytes provide it with more energy => upgraded learning, making less errors in the Barnes Maze
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What are AMPA receptors?
glutamate-gated ion channels
mediate fast excitatory synaptic transmission
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Whar are NMDA receptors?
glutamate channels
at first they are blocked -> only depolarization of AMPA and binding of glutamate causes them to open
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What is the difference between AMPA and NMDA glutamate gated channels?
Whereas NMDA receptors gate channels with slow kinetics, responsible primarily for generating long-term synaptic potentiation and depression, AMPARs are the main fast transduction elements at synapses and are critical for the expression of plasticity.
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glutamate system
glutamate mediates fast excitatory transmission in CNS - super dangerous to modulate
NMDA receptors = important in feedback processing, short term memory, brain plasticity
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What happens if you put blockage on NMDA receptors?
dissociative anesthesia, hallucinations and other psychosis like symptoms
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Why is NMDA called molecular coincidence detector?
Only when both Neuron A and Neuron B are activated does the NMDA receptor become activated: magnesium unblocks the channel and glutamate opens the channel. In this way, the NMDA receptor acts as a “coincidence detector” that detects the simultaneous activation of both Neuron A and Neuron B
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What is important for long-term potentiation?
coexisting activity of AMPA and NMDA receptors; calcium (if you block calcium, LTP impossible)
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What is low frequency synaptic transmission?
1) glutamate binds to AMPA and NMDA
2) AMPA activated
3) NMDA blocked (magnesium)
4) EPSP mediated by AMPA
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What is high frequency synaptic transmission?
1) glutamate binds to AMPA and NMDA
2) STRONG DEPOLARIZATION
3) magnesium blockage of NMDA is lifted (due to voltage)
4) calcium enters cells
5) long term potentiation
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What is Morris water maze?
There is a water pool in which mouse swims. The task is to find platform in the pool. After long time, mouse is able to identify it (also it is shown where platform is). If you block NMDA, there is no long term potentiation - performance of mouse drops, because it cannot learn.
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What is main role of NMDA in long term potentiation?
adding trigger = initiation
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What is long term depression?
activity-dependent reduction in the efficacy of neuronal synapses
happens when you remove AMPA receptors
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What happens in long term depression?
prolonged low frequency stimulation
there is small and slow rise in calcium
loss of synaptic AMPA receptors
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neurogenesis
growth of new neurons and contacts from stem cells
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synaptic plasticity
more efficient communication between neurons = neurons that fire together, wire together
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What structures can grow new cells?
hippocampus, caudate nucleus -> so learning can occur in old people!
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What happens to rats in enriched environment?
brain is bigger and has more connections; cells have bigger dendritic trees, animals have better cognition and motor skills; also holds for offspring of mothers raised in enriched environment
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What happens in excessive glutamatergic excitation?
brain damage => ischemic stroke (lack of oxygen, no glutamate reuptake, continous depolarization, excessive Ca influx, cell death)
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What does GAD?
transforms glutamate to GABA
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What is shunting inhibition?
GABA channels are inhibitory - permeable to chloride. Influx of chloride makes ion super negative making it impossible for postsynaptic neuron to fire.
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What are benzodiazapines?
GABA agonists -> used as tranquillizers in the anxiety disorder treatments - they have modulatory effect (enhancement of GABA effect)
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What is ATP?
key molecule in cellular metabolism
neurotransmitter
concentrated in all synaptic vesicles in CNS and PNS
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What are endocannabinoids?
small lipid molecules -> released from postsynaptic neurons and act on presynaptic terminals (RETROGRADE) - important for feedback system
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What are examples of diffuse modulatory systems?
1) Acetylcholine - basal forebrain
2) Serotonin - raphe nuclei
3) Dopamine - ventral tegmentum
4) Norepinephrine - locus coeruleus
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Emotions in brain circuits
1) detection of environmental stimuli -> senses, thalamus
2) interpretation of signals -> hippocampus, amygdala
3) evaluation -> prefrontal cortex, nucleus accumbens, dopamine
4) action preparation -> motor cortex, hypothalamus, brain stem
end: visible behavior
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How to treat ADHD?
We need modulators which enable fine tuning activation of the system. For example:
- noradrenergic (norepinephrine) = lowering impulsivity
- serotonergic
- dopamine reuptake inhibitors = with depression treatment
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What is main problem in ADHD?
significantly smaller prefrontal cortex => therefore modulators should be used
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How nicotine relates to ADHD?
sort of self-medication; nicotine binds to acetylcholine receptors - getting control over PFC
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What is neostriatum?
part of the basal ganglia that includes - the caudate nucleus (voluntary movement),
- putamen (learning, motor control),
- nucleus accumbens (reward),
but NOT globus pallidus
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What is paleostriatum?
globus pallidus (movement control): externa and interna
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What are sub-sections of substantia nigra?
pars compacta - densely packed dopamine neruons
pars reticulata - inhibitory GABA neurons
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subthalamic nucleus
mostly excitatory glutamate neurons that project to internal globus pallidus
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Where is dopamine synthesized in the brain?
substantia nigra, ventral tegmental area
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What are functions of dopamine in nigro-striatal system?
modulates cortical motor control and action selection
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What are functions of dopamine in meso (VTA)-cortical/limbic system?
reward processing, motivation, modulation of cognitive (executive) control
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What are dopamine projection areas?
nucleus accumbens - medial shell (dopamine + GABA), laterall shell, core (dopamine)
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What is characteristic for dopamine receptors?
all are metabotropic and G-protein-coupled
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How activation/disinhibition of cortex progresses?
1) substantia nigra send excitatory signal (dopamine)
2) dorsal striatum sends inhibitory signal
3) globus pallidus gets inhibited
4) thalamus can send excitatory signal to cortex (glutamate)
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What happens in Parkinson's disease?
substantia nigra are gone -> therefore globus pallidus keeps inhibiting thalamus -> no dopamine in the system -> no/slow-movement
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early stage of Parkinson
reduced arm swing, smaller steps, slower speed, postural changes
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mid-moderate Parkinson
60-70% dopamine cells gone, no arm swing, small, shuffling steps, stooped posture
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advanced Parkinson
reduced step length, bradykinesa, reduced postural control and stability, defragmentation of turns, freezing of gait (freezing in the middle of movement), very hard to both walk and turn
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severe Parkinson
very huge inhibition of movement may translate to being bed-ridden
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to what refers OFF stage in Parkinson?
stage without medication
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how to help Parkinson's patients?
visual cueing - lines on the floor, rhythmic auditory cueing - playing music
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to what refers ON stage in Parkinson?
on medication
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What role dopamine plays in reward/motivation?
central role in valuation of actions and stimuli
valuation translates to optimal decision making
specifically, dopamine is crucial for learning (reinforcement)
neurons signal reward prediction error -> system tends to be suprised when expected reward is not presented = over-activation
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Olds and Millner (50s)
rat self-stimulated itself to death by stimulating medial forebrain bundle (dopamine study)
147
How deep brain stimulation can help with severe depression?
stimulation is applied to medial forebrain bundle (or areas connected to it like thalamus, internal capsule, cingulate gyrus)
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remote controlled rat
stimulation of whisker system = sensorimotor system used by animals such as rodents to collect environmental information -> if rat turns into desired direction, it gets rewarded
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How dopamine relates to working memory?
There is a hungry rat placed in the maze that needs to find food. If you increase amount of dopamine -> rat makes more errors! If you decrease amount of dopamine -> rat makes more errors. Inverted U response!
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What are risks correlated with Parkinson's disease?
1) pesticides
2) skin cancer
3) infections
4) traumatic brain injury
5) milk ? - pesticides
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What are things which can help avoid Parkinson?
caffeine, red staff in pepper and tomatoes, green leaves, exercise, smoking
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Where is norepineprine synthesized?
locus coeruleus
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Where is norepinephrine projected over the brain?
all over the place! reuptake via norepinephrine transporter
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What are functions of norepinephrine?
released by adrenal medulla into blood stream as hormone (mediates stress and fight-or-flight responses)
neurotransmitter in sympathetic NS
major neuromodulator in CNS - regulates arousal
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What are functions of norepinephrine and their projections?
facilicate sensory processing
enhance cognitive flexibility, executive function
promote offline memory consolidation
sleep-wake cycle
feeding behavior
arousal
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What are characteristics of norepinephrine receptors?
all are metabotropic and g-protein coupled
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To what are norepinephrine injections used?
to help with heart attack = instant arousal
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What do antidepressants?
block reuptake of norepinephrine = promote arousal
MAO-blockers: prevent break down
tricyclic: block reuptake
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What characterizes attention deficit/hyperactivity disorder medication?
block reuptake od norepinephrine
in ADHD - there is deficiency of norepinephrine
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Is dopamine BY ITSELF able to activate neuron?
No, because it has modulatory effects
its release alone does not change spontaneous activity of PFC neurons
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What happens if you activate both dopamine and hippocampus?
inverted U shape respone
PFC neurons activated BUT they have their optimal range
