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Introduction to Neuroscience > Neurotransmitters 1 > Flashcards

Neurotransmitters 1 Flashcards

1
Q

Size of the Neurotransmitters ;

A

Aminoacids < Amines < Peptides
Size of the neurotransmitters matter because of the crossing of the blood brain barrier (dopamine cannot cross it but L-dopa can)

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2
Q

Concentration of the Neurotransmitters in the brain ;

A

Aminoacids > Amines > Peptides

Aminoacids are the most abundant and peptides are the least abundant.

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3
Q

Synthesis and Inactivation of Aminoacids and Amines ;

A

Enzymes to make neurotransmitters are synthesized in the cell body (because there is no protein on axon and axon terminal) but the neurotransmitters are synthesized in the synapse..
Inactivation through ; reuptake : active mechanisms getting rid of them within the synaptic cleft.

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4
Q

Cytoskeleton

A

Cytoskeleton is found within every cell inside cytoplasm (everything in a cell except the nucleus)
Cytoskeleton helps the cell to maintain its structure and transportation of proteins from soma to synaptic terminal and the other way around.
Cytoskeleton consists of microtubules, neurofilaments and microfilaments.

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5
Q

Microtubules :

A
  • Cytoskeleton component.
  • It is the thickest one.
  • It is formed from polymerization of the tubulin protein.
  • Tubulin withholds the cell body and the axon hillock open.
  • Microtubules are anchored to one another and other parts of the neuron by microtubule-associated proteins / I guess it is also called microtubilin binding protein).
  • Tau protein is a type of microtubule-associated protein.
  • It is the transport mechanism from cell body to the synapse.
  • Tau protein is found in axon and pathological changes in tau protein accompanies Alzheimer’s disease.
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6
Q

Microfilaments :

A
  • Cytoskeleton component.
  • Polymerized from actin protein.
  • Actin protein plays a role in changing cell shape for instance in muscle contraction.
  • It is the thinest cytoskeleton component..
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7
Q

All components of cytoskeleton system :

A
  • Microtubules (from tubulin protein) , thickest
  • Neurofilaments
  • Microfilaments (from Actin protein) , thinest
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8
Q

Anterograde Transportation

A

From soma to synapse

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9
Q

Retrograde Transportation

A

From synapse to soma

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10
Q

Anterograde Staining Substances

A
  1. Horse radish Peroxidase (HRP).

2. Phaseolus vulgaris-leuocoagglutinin (PHA-L)

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11
Q

Retrograde Staining Substances

A
  1. Fluro-Gold (FG)
  2. Cholera Toxin (CT)
  3. Fast Blue (FB)
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12
Q

Neurophysiology terms for anterograde and retrograde transport

A

Anterograde (Neuroanatomy) : Orthodroom

Retrograde (Neuroanatomy) : Antidroom

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13
Q

Immunohistochemistry and Immunofluorescence

A

You find the location of ‘already synthesized proteins’ for instance neurotransmitters or staining methods such as fluro-gold (then these staining methods are proteins)
- Immunohistochemistry :
1. You make a primary antibody for a particular protein.
2. You label it with a secondary antibody.
3. Everywhere where the staining is you get DAB (black staining).
so you know the location of the particular protein.
- Immunofluroscence :
1. Make a primary antibody for a particular protein.
2. Fluroscent Tag on the primary antibody.
3. Wherever the protein is, it radiates light.
The way its explained in the book :
1. You have a protein of interest , inject it into blood, it will generate antibodies.
2. Withdrawl blood from the animal, isolate antibodies and label them.
3. Apply antibodies to brain tissue and you will find the localization of the proteins.

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14
Q

Fluorescent in-situ hybridization

A
  • You check whether the cell is ‘ able to make a protein’. You check whether the cell has the RNA to make the protein of interest.
  • You know the nucleic acid of protein so mRNA strand of protein.
  • You make a complementary one and label it with fluorescence.
  • Check to which cell the complementary mRNA goes to because it means at this location there are cells that have the mRNA to make, synthezise certain protein.
  • So the cell has the ‘machinery make the protein’ , but whether it actually does it we don’t know.
  • ‘Possibility to make a protein’
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15
Q

Clarity Method

A

It is a technique to make the brain transparent.
You make the brain transparent , by removing the lipid layers (fats) without disrupting the cell structure via hydrogel to keep the rest of the components in place.
You can see the excitatory, inhibitory neurons, neurotransmitters etc.. in a great detail and resolution.
You can label lots of molecules in the whole brain.

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16
Q

Synthesis and Inactivation of Neuropeptides

A
  • Neuropeptides (neurotransmitter) are synthesized in the soma / cell body.
  • Neuropeptides (as being a neurotransmitter) are transported to the synapse.
  • So the make up of the peptides are made in the cell body and no change of make up in the synapse.
  • Inactivation of neuropeptides through ; breakdown and diffusion.
  • So there are no active re-uptake.
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17
Q

Working mechanisms of neuropeptides vs. working mechanisms of amino acids and amines ;

A
  • Neuropeptides have a broader and longer spectrum of activity than aminoacids and amines because there is no active re-uptake mechanisms for neuropeptides.
    Whereas aminoacids and amines are actively taken up by re-uptake machanisms.
  • Actions of aminoacids and amines is very short whereas actions of neuropeptides are relatively long because they have to diffuse or broken down.
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18
Q

Acetylcholine

A
  • It is class of its own.
  • It is also a modulator.
  • Normally modulators cannot excite or inhibit cells by themselves but ACh does.
  • ACh have very diffuse pattern of activation.
  • Most of the brain gets information from the ACh producing cells in the basal forebrain.
  • It is excitatory neurotransmitter.
  • It is the major neurotransmitter in muscles.
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19
Q

Where do the ACh producing cells located ?

A
  • Basal Forebrain : Basal nucleus of Meynert, Medial Septal Nuclei. ACh cells in these regions produce ACh for the entire brain.
  • When basal forebrain is active it modulates the activity within the entire cortex.
    More specifically synthesis in :
    1. Medial Septum
    2. Nucleus of the diagonal band of Broca
    3.Caudate Putamen (interneurons) - interneurons only connects the same region so only the Caudate whereas normal neurons connects vast majority of regions. (Entire cortical area)
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20
Q

AcetylCholine Synapse

A
  1. ACh is packed into the vesicles in the synapse.
  2. Vesicles are put in the synaptic cleft.
  3. ‘Acetylcholinesterase’ (AChE) break downs ACh into Acetic Acid and Choline.
  4. Choline is taken up.
  5. We have Acetyl CoA in the cell body and ‘choline acetyltransferase’ (ChAT) combines Acetyl CoA with Choline.
    Reuptake through ; Acetylcholinesterase(AChE)
    ACh synthesis through ;
    Choline acetyltransferase (ChAT)

Organophosphates blocks Acetylcholinesterase (so blocks reuptake) : at first you have muscle spasm and then muscle paralyses.

21
Q

Orghanophosphates

A

block acetylcholine esterase. So at first you have too much ACh : muscle spasm but then because choline cannot taken-up and use to synthesize new ACh , you have depletion of ACh : neuromuscular paralysis.
Novichok is a type of organophosphates.

22
Q

ACh receptors on the post-membrane :

A
  1. Ionotropic Receptors
    - They have a central pore.
    - Nicotine ACh receptor (nAChR) is a type of it and consists of 5 sub-units(proteins).
    They have fast and short opening and closings.
  2. Metabotropic Receptors :
    Muscarinic Receptors
    - Consists of 7 sub-units.
    - Coupled with G-protein
    - They have no pore.
    - G-proteins change the opening and closing profiles of iontropic receptors.
    - Slow and long-lasting action.
    - Most of the dopamine, noradrenaline, serotonin receptors are metabotropic receptors, so they have long-lasting modulating effect.
23
Q

Ligand-Gated vs. Metabotropic Receptors

A

Ligand-Gated Receptors / Ionotropic Receptors
- Fast action.
- Fast opening and closing of the pore.
Metabotropic Receptors :
- Slow and long-lasting action, by changing the opening and closing profiles of ionotropic receptors.

24
Q

Function of ACh :

A

ACh projections from basal forebrain ;
- Enhance long-term potentiation & learning and memory.
- Enhance selective attention.
- Involved in the generation of neuronal oscillations.
- ACh is a transmitter at neuromuscular junctions.
- ACh is a transmitter of the parasympathetic nervous system. It is involved in the ‘rest and digest’ function.
Noradrenalin is involved in the fight and flight function.

25
Q

Disorders of Acetylcholine Systems :

A
  • Alzheimer Disease (CNS):
    Degeneration of ACh nuclei in the basal forebrain. Basal forebrain is important for cognitive processes. While the disease progress Alzheimer patients have declining cognitive performances.
  • Myasthenia Gravis (PNS) :
    antibodies against nACh receptors at neuromuscular junctions (autoimmune disorder).
26
Q

Medication for Alzheimer’s Disease :

A
  • You can block Acetylcholine esterase so that ACh stays longer in the synaptic cleft. Temporarily beneficial for attention, concentration, speech. (for moderate forms of dementia). This is to get rid of the fast changing effect of the disease.
  • NMDA blockage : it prevents overactive glutamate activation (because cells can die). But you will have side effects.
27
Q

Myasthenia Gravis :

A
  • Autoimmune disease.
  • nACh receptors on the muscles are under attack.
  • The effect of ACh on the end plate potentials is reduced, because there is no receptors get activated.
  • You get more and more paralyzed.
28
Q

Medication for myasthenia Gravis :

A
  • Choline esterase inhibitors (so that the amount of ACh in the synaptic cleft is higher) and this enhances the communication between nerves and muscles.
  • Immunosuppressants : supression of the immunsystem but it is difficult to attack only nicotinic ACh receptors, therefore whole immune system is suppressed which increases the risk of infection , liver damage, kidney damage.
  • Corticosteroids : also inhibits the immune system and limits antibody production.
29
Q

Curare

A

It blocks nicotinic ACh receptors (ligand-gated).

It is a venom of some snakes , the moment you are bitten, you have muscle paralyses.

30
Q

Nicotonic ACh receptor inhibitors (nACh) :

A

Reversible nicotinic ACh receptors are used in anesthesia because the brain activity for a certain amount of time is lowered.

31
Q

Muscarine :

A

Muscarine is agonist of muscarinic ACh receptors.
So it increases the activity of ACh.
Since ACh is involved in rest and digest functions, muscarine will drop the heart rate and blood pressure even more.

32
Q

Atropine :

A

Atropine is antagonist of ACh.
Since ACh is involved in rest and digest functions , atropine will increase pupil dilation (more like fight or flight response).
When you have bradycardia so very low heart pressure : give atropine. Atropine working on muscarinic ACh receptor makes sense because you want to have long-lasting effect.

33
Q

AChE (Acetylcholinesterase) inhibitors :

A
  • Nerve gases inhibit AChE. At first you have massive ACh in the synaptic cleft but then depletion. (sarin effect, irreversible inhibitors).
  • Many of the medications used in Alzheimer’s disease are reversible inhibitors. (since they have degeneration of cholinergic neurons in the basal forebrain).
34
Q

Glutamate receptors :

A

Ionotropic glutamate receptor : AMPA receptors.
Glutamate excite the AMPA receptors, pore opens and Na+ ions flow in.
NMDA receptor : it is also ionotropic receptor.

35
Q

Glutamate Synapse :

A
  1. You have glutamate in synaptic cleft.
  2. Glutamate is taken up by excitatory amino acid transporters via astrocytes and transferred into ‘glutamine’.
  3. It is taken up into the cell.
  4. Glutamine is transferred into Glutamate by Glutaminase.
36
Q

Astrocytes

A

It is a type of glia.
Most numerous glia in the brain.
It fills the spaces between neurons therefore influence neuritis growth and regulates chemical content of extracellular space.
It has end feet on blood vessels which means astrocytes connects with blood vessels and take up some substances and feed them into the rest of the brain.
It maintains the appropriate chemical environment for neuronal signaling (take us glutamate).
- Most important glial cell for homeostasis of the brain.

37
Q

NMDA receptors vs. AMPA receptors :

A
  • Both of them are glutamate receptors.
  • Both of them have pores.
  • AMPA receptors opening and closing is very fast with a strong peak of activation whereas NMDA receptors are slower and long-lasting. (associated with learning and memory).
  • NMDA receptors open only after AMPA receptors are opened. Because Mg+2 binds to NMDA receptor and it blocks NMDA receptor. Activation of AMPA gets rid of the Mg+2 then the NMDA receptor starts activating for a longer time than AMPA receptors.
38
Q

Glutamate System :

A
  • Glutamate mediates fast excitatory transmission in the CNS through AMPA receptors.
  • NMDA receptors are important for feedback processing, short-term memory and brain plasticity (learning and memory).
  • If you block NMDA receptors : ‘ dissociative anesthesia’ where you don’t remember things but your brain is still active (because AMPA receptors are working I guess).
  • If you are astrocytes are not working well, you have excessive glutamate release. It results in ischemia (oxygen deficits because the brain is excessively active, oxygen is not enough) , epilepsy
39
Q

Long-Term Potentiation

A
  • Glutamate binds to the AMPA and NMDA receptors.
  • Activation in the AMPA receptors drive membrane potential to NMDA’s threshold so NMDA receptors open.
  • Ca+ flows into the postsynaptic cell and it activates enzymes.
  • It changes the post synapse so AMPA receptors are upregulated , so when the next activation hits the AMPA receptors the activation of AMPA receptors is higher. This increases the AMPA receptors’ channel conductance which causes long-lasting increase in EPSP(excitatory postsynaptic potentials) amplitude.
  • This is a mechanism for learning and memory.
40
Q

The relationship between Oxygen Deficit in the brain and glutamate

A
  1. Glutamate reuptake via Astrocytes is an active process, that requires oxygen.
  2. When there is no oxygen, glutamate cannot be taken-up into the cell again.
  3. This results in excessive glutamate in the system - continous depolarization.
  4. Excessive Ca+ influx in the neuron through NMDA receptors.
  5. Cell death.
    So excessive glutametergic excitation produces brain damage.
41
Q

Example of excitatory and inhibitory neurotransmitters

A

Excitatory : Glutamate + ACh.
Inhibitory : GABA : when GABA receptors open Cl- flows into the postsynaptic cell : hyper polarize the cell : block the activity of the cell.

42
Q

Synthesis of GABA :

A
  1. GABA in the synaptic cleft.
  2. It is taken-up by GAT cotransporters via glial cells.
  3. When Glucose enters the brain , glutamate is broken down to GABA by glutamic acid decarboxylase.
    So in GABAergic neurons there is an additional enzyme : glutamic acid decarboxylase.
    - Glutamate cells are turned into GABA cells because they have glutamic acid decarboxylase.
43
Q

Benzodiazepines and Barbiturates :

A

Agonist of ionotropic GABA receptors.
Act as sedatives. (because GABA is an inhibitory neurotransmitter.
Benzodiazepines are used as tranquilizers and used in the treatment of anxiety disorder.

44
Q

Shunting Inhibition :

A

It is how GABA inhibits cells.
Before the activation in the dendrites reaches the cell body GABA blocks the activation. So there is no transfer of action potentials towards the cell.
So by blocking the activation before it reaches the cell body , GABA prevents the cell from producing action potentials.

45
Q

Functions of GABA system :

A
  • It creates a balance between excitation and inhibition.
  • Therefore it prevents excessive activity (epilepsy).
  • It generates neuronal oscillations through activation and deactivation of GABAergic cells. Neuronal oscillations are important for cognition.
  • Excessive GABAergic inhibition : sedation / narcosis (so no cognitive performance).
46
Q

Diazepam

A

Type of Benzodiazapine.
It is agonist of GABA receptors.
It has a modulatory effect and has no effect on its own but it enhances the effect of GABA.
Benzodiazepines increases the frequency of opening of GABAergic channels.

47
Q

Barbiturates

A

GABA agonist
Increases the opening time of GABAergic channels.
It is more dangerous than diazepam because if you do it long-enough all GABAergic channels will be open and the brain will stop functioning.

48
Q

GABA receptors in young brain vs GABA receptors in normal brain

A

In the very young brain, more Cl- concentration inside the brain than outside. Therefore when GABA receptors open instead of coming in and hyper polarizing the cell CL- goes out and the cell depolarizes.
But normally in normal brain there is low Cl- concentration in the brain so when GABA receptor opens Cl- flows in : hyperpolarization.

Introduction to Neuroscience (6 decks)

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