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Neuroscience > Week 4: Neurotransmitters & Pharmacology > Flashcards

Week 4: Neurotransmitters & Pharmacology Flashcards

1
Q

The synapse

A

The junction between the terminal button of an axon & the membrane of another neurone

Allows information to be passed (transmitted) from one neuron to the other
 Information travels in one direction (during sleep, there is a point where an AP may go ‘backwards’ resetting the neurone)

- Mitochondria in presynaptic neurone - provides energy for the vesicle movement Replace resting potential via sodium-potassium pump, requiring energy
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2
Q

Structure of synapse

A

Presynaptic axon
 Terminal containing neurotransmitters , mitochondria, vesicles and other organelles

Postsynaptic ending
 Receptor sites for neurotransmitters

Synaptic cleft - where diffusion of NTs takes place

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2
Q

Summation

A
  • Need more than 1 synapse (summation) for the threshold potential to be reached, and forming an action potential
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3
Q

Synaptic transmission process: (6 steps)

A
  1. Action potential arrives at axon terminal triggering Ca2+ ions to move into cell
  2. Ca2+ ions cause the migration of vesicles (which contain NTs) to the pre-synaptic membrane
  3. The vesicles fuse to pre-synaptic membrane and break open emptying their neurotransmitters into the synaptic cleft (exocytosis)
  4. Neurotransmitters diffuse across the synaptic cleft towards the post-synaptic membrane
  5. Neurotransmitters bind to receptor sites on the post-synaptic membrane with ‘lock and key’ specificity – specific NT binds to specific receptors (NT’s trigger the opening of calcium channels = vesicle movement)
  6. This binding opens NT-dependent ion channels which change the excitability of the post-synaptic cell
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4
Q

Postsynaptic receptors (2 types)

A

Direct receptor (ionotropic)
* Binding site for a NT
* Ion channel opens when NT molecule binds

Indirect receptor (metabotropic)
* Only a binding site for a NT
* Activates enzyme
* Ion channel opens elsewhere

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5
Q

Postsynaptic potential

A

 Postsynaptic potential = ions move across post synaptic membrane and alter the membrane potential
 Depolarising (excitatory) = increased likelihood of AP (influx of sodium)
 Hyperpolarising (inhibitory) = decreased likelihood of AP (outflux of potassium)
 Depolarisation > threshold (-55mV) triggers AP

Chemical –> Electrical

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6
Q

Depolarisation vs hyperpolarisation

A

 Depends on which type of ion channel in the postsynaptic membrane is opened by the neurotransmitters

Sodium - Na+
Potassium - K+ Chloride - Cl-
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7
Q

Sodium channels

A

 Produce excitatory postsynaptic potentials
- Depolarises neurone from -70mv to -55mv (threshold) to -30mv

Move in (Think salty banana - there’s more NA+ on outside)

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7
Q
A
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8
Q

Potassium channels

A

Produce inhibitory postsynaptic potentials
- Through diffusion, K+ moves out of neurone
- Leads to repolarisation -> hyperpolarisation
Stops another AP forming during refractory period = inhibitory

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9
Q

Chloride channels

A

Cl- channels opens at rest = nothing happens (everything balanced)

Cl- channels open when neuron depolarised = Cl- ENTERS neuron = stabilisation - decreases the AP likelihood - hyperpolarised

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10
Q

Neurotransmitters (6)

A
  1. Acetylcholine (often abbreviated ACh)
    1. Dopamine
    2. Serotonin
    3. Norepinephrine (aka Noradrenaline)
    4. Glutamate
    5. GABA (gamma-aminobutyric acid) & Endorphins
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10
Q

Excitatory vs inhibitory

A

Excitatory - help propagate AP (e.g. glutamate)

Inhibitory - Reduce AP likelihood (e.g. GABA)

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11
Q

Acetylcholine (ACh)

A
  • excitatory
  • In PNS & CNS
  • In ANS, release = regulate HR, blood pressure & gut motility PNS: neurons controlling muscle contraction, excretion of certain hormones
    - Plays a role in muscle contractions, memory, motivation, sexual desire, sleep and learning. CNS: widespread - role in REM sleep, activating cerebral cortex, learning, memory

 Alzheimer’s disease is associated with a lack of ACh in certain brain regions

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12
Q

Dopamine (monoamines)

A

Excitatory or inhibitory

 Neuron cell bodies in midbrain 

▪ Reward system including feeling pleasure, heightened arousal, and learning.

▪ Dopamine also facilitates focus, concentration, memory, sleep, mood and motivation.

▪ Dysfunctions of the dopamine system include Parkinson’s disease, schizophrenia, bipolar disease, restless legs syndrome and attention deficit hyperactivity disorder (ADHD)

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13
Q

Norepinephrine (monoamines)

A

▪ Epinephrine (aka adrenaline) and Norepinephrine

▪ Found in peripheral NS (autonomic NS) & CNS (pons & medulla)

▪ Also released into blood (as a hormone), causing blood vessel contraction & increased heart rate

▪ Responsible for “fight-or-flight response” to fear and stress.

▪ Stimulates body’s response by increasing heart rate, breathing, blood pressure, blood sugar, blood flow to muscles, heightened attention and focus. (Sympathetic NS)

▪ Excess epinephrine can lead to high blood pressure, diabetes, heart disease and other health problems.

▪ As a drug, epinephrine is used to treat anaphylaxis, asthma attacks, cardiac arrest and severe infections
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13
Q

Serotonin (monoamines)

A

 Excitatory or inhibitory

 Cell bodies of neurons in midbrain, pons, medulla 

 Contributes to various functions, e.g., mood, eating, sleep, arousal, pain 
Regulation, anxiety appetite

 imbalances include seasonal affective disorder, anxiety, depression, impulsivity, fibromyalgia, and chronic pain.

▪ Medications that regulate serotonin and treat these disorders include selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs)

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14
Q

Peptides

A

▪ Endorphins. pain relievers - play a role in perception of pain. “feel good” feelings.

▪ Released by hypothalamus and pituitary gland

▪ Inhibitors (opioid receptors)

▪ Low levels of endorphins may play a role in fibromyalgia and some types of headaches

14
Q

Amino Acids (Glutamate)

A
  • Glutamate
    • Most common excitatory neurotransmitter
    • Used by brain to synthesis GABA
    • Most abundant neurotransmitter in brain
    • Key role in cognitive functions like thinking, learning and Memory
  • Imbalances in glutamate levels associated with Alzheimer’s disease, dementia, Parkinson’s, Huntington’s disease and seizures
15
Q

Amino acids (Gamma-aminobutyric acid (GABA))

A
  • Gamma-aminobutryic acid (GABA).
    • Synthesised from glutamate and vitamin B6
    • The most common inhibitory neurotransmitter of the nervous system, particularly in the brain.
    • Regulates brain activity to prevent problems in the areas of anxiety, irritability, concentration, sleep, seizures and depression.
    ▪ Contributes to motor control, vision, regulation of anxiety & many other cortical functions

▪ Drugs that increase GABA in brain are used to treat epilepsy & calm trembling in Huntington’s disease

16
Q

Neurotransmitter removal from synapse

A
  1. Reuptake: NT quickly pumped back into nearby glia or the axon terminal that released it
    (via transporter protein)
    1. Deactivation: NT destroyed (inactivated) by enzymes near receptors so it’s not recognized by receptor (acetylcholinase breaks down acetylcholine)
  2. Removal: diffuses into surrounding area (e.g., blood)
17
Q

Psychopharmocology

A

Study of the effects of drugs on the nervous system and behaviour

 Important field in neuroscience  * Responsible for development of psychotherapeutic drugs to treat psychological & behavioral disorders
18
Q

What are drugs?

A

 Drugs are exogenous chemicals (not manufactured inside the body)

 Unnecessary for normal functioning 

 Alter molecular functions

 Effects are physiological or behavioural

 Natural vs artificial
19
Q

Drugs and synaptic transmission: Agonist vs antagonist

A

Agonist: Facilitate/ mimic action of a NTs

Antagonist: Inhibit action of a NTs, block postsynaptic effects

19
Q

Sites of drug action

A

 Where drug interacts with molecules
 Drugs affecting behaviour normally affect synaptic transmission

20
Q

Mechanisms of drug action: 6 stages

A
  1. synthesis
  2. storage
  3. Release
  4. receptors
  5. reuptake
  6. destruction
21
Q

Drugs 2. Storage

A
  • alter NTs storage in presynaptic neuron
  • modifies concentration in synaptic cleft
  • transporter proteins in vesicle membranes move NT from cytoplasm into vesicles
  • antagonist inactivate transporters
    —> vesicles remain empty = can’t release NTs into synaptic cleft
21
Q

Drugs: 3. Release

A

 Changes neurotransmitter release from presynaptic cell
 Modifies concentration in synaptic cleft

Modes of alteration
	1. Prevent release of NT (antagonist) 2. Trigger NT release (agonist)
22
Q

Drugs 1. synthesis

A

 Alter neurotransmitter synthesis in presynaptic neuron
 Modifies concentration in synaptic cleft
 NT produced from specific precursor molecules (see diagram)
 Enzymes required for change from precursor to NT (can act on the enzyme, may lead to no dopamine being produced)

Modes of alteration
	1. Inactivate the enzymes (antagonist)
	2. Introduce precursor molecules (mimicking) (agonist)
23
Q

Drugs 4. Receptors

A

 Act on neurotransmitter receptors
 Modify postsynaptic potentials

24
Q

Drugs: 5. reuptake

A

 Modify removal of neurotransmitters from synaptic cleft
 Change neurotransmitter concentrations in the cleft
 Agonists reduce or block reuptake

25
Q

Drugs: 6. Destruction

A

 Modify neurotransmitter destruction in synaptic cleft
 Enzymes typically inactivate neurotransmitters (agonist)
 Enzyme Acetylcholinesterase (AChE) in postsynaptic membrane deactivates Ach
 Neostigmine: inactivates AChE
 ACh remains in synaptic cleft longer
 Myasthenia Gravis

26
Q

Reading: Ligand

A

A chemical that binds with the binding site of a receptor

27
Q

Reading: binding site

A

The location on a receptor protein to which a ligand binds

Neurotransmitters are naturally occurring ligands

28
Q

Reading: Dendritic spine

A

A small bud on the surface of a dendrite, with which a terminal button of another neuron forms a synapse.

29
Q

Presence of mitochondria in terminal buttons: what does this suggest?

A

implies that the terminal button needs energy to perform its functions.

(There are also synaptic vesicles and microtubules for transport)

30
Q

Reading: synaptic vesicles

A

small, bubble-like structures made of membrane and filled with molecules. A terminal button can contain from a few hundred to nearly a million synaptic vesicles

31
Q

What causes vesicles to move?

A

Arrival of AP at presynaptic neuron = calcium released = vesicles move using energy —-> exocytosis —–> diffusion

32
Q

Reading: Process after NTs have diffused across synaptic cleft?

A

Once binding occurs, the postsynaptic receptors open neurotransmitter-dependent ion channels (sometimes called ligand-gated ion channels), which allow the passage of specific ions into or out of the cell = depolarisation.

33
Q

Direct ion-channel

A

Ion channel with its own binding site

NTs binds = ion channel opens

IONOTROPIC RECEPTOR

(E.g. ionotropic ion channels include sodium, potassium, chloride and calcium channels)

34
Q

Indirect ion-channel

A

Ligand binding to some receptors does not open ion channels directly but instead starts a chain of chemical events.

METABOTROPIC RECEPTORS

(The NTs will be the 1st messenger, but there will be a second involved)

35
Q

Reading: 2 types of postsynaptic potentials

A

EPSP’s

IPSP’s

- Determined by characteristics of the postsynaptic receptor, specifically the type of ion channel they open.
36
Q

Reading: EPSP’s

A

Excitatory (depolarising) post-synaptic potential

e.g. Influx of sodium causes depolarisation

37
Q

Reading: IPSP’s

A

Inhibitory (hyperpolarising) post-synaptic potential

e.g. efflux of potassium (K+) = hyperpolarisation. & influx of Chloride (Cl-) = hyperpolarisation

Neuroscience (22 decks)

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