WEEK 4 LECTURE + TUTORIAL Flashcards

neurotransmission and psychopharmacology (32 cards)

1
Q

Synapses

A

-Junction between the terminal button of an axon and the membrane of another neuron
-Spaces between the terminal button of one neuron and the dendritic or somatic membrane of another
-Primary means of communication between neurons is synaptic transmission
-Info travels in one direction

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2
Q

Structure of a synapse

A

-presynaptic axon: terminal containing neurotransmitters, mitochondria and other organelles.
-Postsynaptic ending: receptor sites for neurotransmitters
-Synaptic cleft, contains extracellular fluid through which the neurotransmitter diffuses
-two prominent structures are located in the cytoplasm of the terminal button: mitochondria and synaptic vesicles, small, bubble-like structures made of membranes and filled with molecules
-The presence of mitochondria implies that the terminal button needs energy to perform its functions
-A chemical that attaches to a binding site is called a ligand

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3
Q

Synaptic Transmission Process:
Part 1

A
  1. Action potential arrives at axon terminal triggering CA2+ ions to move into the cell
    1.Synaptic transmission is initiated when an action potential invades a nerve terminal, opening CA2+ at the active zone
    1.CA2+ triggers synaptic vesicle exocytosis, thereby releasing the neurotransmitters contained in the vesicles and initiating synaptic transmission
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4
Q

Synaptic Transmission Process
Part 2/3

A
  • CA2+ Ions cause the migration of vesicles (which contain NTs) to the pre-synaptic membrane
    -The vesicles fuse to the pre synaptic membrane and break open, emptying their neurotransmitters into the synaptic cleft
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5
Q

Synaptic Transmission
Part 4/5/6

A

-Neurotransmitters diffuse across the synaptic cleft towards the post-synaptic membrane, move from an area of high concentration to disperse across the synapse due to the force of diffusion
-Neurotransmitters bind to receptor cites on the post synaptic membrane with the lock and key specificity - specific NT binds to the specific receptor
-The binding opens NT-dependent ion channels which change the excitability of the post-synaptic excitatory or inhibitory

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6
Q

Postsynaptic receptors

A

-Direct receptors (ionotropic)
-Binding site for a NT
-Ion channels open when NT molecule binds, ionotropic receptor

Indirect Receptor (metabotropic)
-Only a binding site for NT
-Activates enzyme
-Called this because it involves steps that require the cell to expend metabolic energy

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7
Q

Problems that could occur:

A

-Too much or not enough of one or more neurotransmitters
-The receptor on the receiver cell isn’t working properly
-The cell receptors aren’t taking up enough neurotransmitter due to inflammation and damage of the synaptic cleft
-NT’S are reabsorbed too quickly
-Enzymes limit the number of neurotransmitters from reaching their target cell
-Problems with other part of nerves

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8
Q

Diseases that can occur

A

-Not enough acetylcholine can lead to the loss of memory that’s seen in Alzheimer’s disease
-Too much serotonin is possibly associated with autism
-An increase in glutamate can cause seizures
-Too much dopamine and abnormal glutamate transmission contributes to mania

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9
Q

Endorphins/ Peptides

A
  • Pain relievers and 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
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10
Q

Amino acids/ glutamate / GABA

A

-most common excitatory neurotransmitter
-used by brain to synthesise GABA
-most abundant NT in the 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, seizures

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11
Q

Gamma-aminobutryic acid (GABA)

A

-Synthesised from glutamate and vitamin B6
-The most common inhibitory neurotransmitter of the nervous system, particularly the brain
-Regulates brain activity to prevent problems in the areas of anxiety, irritability, concentration, sleep and depression
-Contributes to motor control, vision, regulation of anxiety, and many other cortical functions
-Drugs that increase GABA in the brain are used to treat epilepsy and calm trembling in Huntington’s disease

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12
Q

NT removal from synapse

A
  1. Reuptake: NT is quickly pumped back into nearby glia or the axon terminal that released it
  2. Deactivation: NT destroyed by enzymes near receptors, so its not recognised by receptor
  3. Removal: diffuses into surrounding area, blood
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13
Q

Enzymatic deactivation

A

-Enzymatic deactivation is accomplished by an enzyme that destroys molecules of the neurotransmitter
-E.g. Acetylcholinesterase (AChE) deactivates the neurotransmitter acetycholine (ACh) by breaking it into choline and acetate

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14
Q

Psychopharmacology definition

A

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

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15
Q

What are drugs

A

-Exogenous chemicals
-Unnecessary for normal functioning
-Alter molecular functions
-Effects are physiological or behavioural
-Natural VS Artificial

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16
Q
  1. Agonists VS 2. Antagonists
A
  1. Facilitate or mimics action of NT and facilitates postsynaptic effects
  2. Inhibit action of a NT and block postsynaptic effects
17
Q

Mechanisms of drug actions

A
  1. Synthesis
  2. Storage
  3. Release
  4. Receptors
  5. Reuptake
  6. Destruction
18
Q
  1. Synthesis
A
  • Alter neurotransmitter synthesis in presynaptic neuron
    -Modifies concentration in synaptic cleft
    -NT produced from specific precursor molecules
    -Enzymes required for change from precursor to NT
19
Q
  1. Storage
A
  • Alter neurotransmitter storage in presynaptic terminal
    -Modifies concentration in synaptic cleft
    -Transporter proteins in vesicle membranes move NT from cytoplasm into vesicles
    -Antagonist inactive transporters
    -Vesicles remain empty
20
Q

Release

A
  • Changes NT release from presynaptic cell
    -Modifies concentration in synaptic cleft
21
Q
  1. Receptors
A

-Act on neurotransmitter receptors
-Modify postsynaptic potentials

22
Q
  1. Reuptake
A

-Modify removal of NT from synaptic cleft
-Changes NT concentrations in the cleft
-Agonists reduce or block reuptake

23
Q
  1. Destruction
A
  • Modify NT destruction in synaptic cleft
    -Enzymes typically inactivates nt
    -Acetylcholinesterase in post synaptic membrane deactivates ACH
24
Q

Myasthenia Gravis

A
  • A rare autoimmune neuromuscular junction disorder
25
Drugs of abuse
- Central Nervous System depressants -Central Nervous System stimulants -Opiates and Opioids (Narcotics) -Hallucinogens -Marijuana
26
Categories of Psychotherapeutic Drugs:
-The anatomical therapeutic chemical (ACT) Classification system - International Pharmacopeia (WHO) -European Pharmacopeia -United states Pharmacopeia (USP)
27
4 Key Concepts of Pharmacology
-Dose -Tolerance -Sensitivity -Withdrawal
28
Tolerance
-the diminished response to drugs over the course of repeated or prolonged exposure -accounted for by adapting physiological process that achieves stability in a constantly changing environment
29
Types
-Acute/ Tachyphylaxis: Instant short term effect of drug on NT and synaptic junction -Pharmacodynamic (dispositional): Reduction in cellular response to drug -Pharmacokinetic (metabolic): absorption, distribution, metabolism and excretion of drugs - Behavioural (conditioned): Tolerance to a behavioural effect of a drug, occurs through drug-independent learning or as a form of pharmacodynamic tolerance in the brain
30
Sensitivity
-An increased response to a drug with repeated administration. -Amplified effects, including therapeutic benefits and side effects. -Mechanisms behind sensitization are not fully understood but thought to involve neuroadaptive changes. -Understanding tolerance and sensitization is crucial for optimizing drug therapy as they impact dosing, effectiveness, and potential side effects
31
Withdrawal
-With increased tolerance and dependence on a drug the reduction of that drug typically causes an opposite effect to the drug itself. - Internal systems perpetuate homeostasis by using counter regulatory methods to create a new state of balance based on the presence of the drug in the system. - Adaptions include levels of neurotransmitters, hormones, and other substances to adjust for the addition of the drug to the body
32
FACTS
-Fentanyl is 50x stronger than heroin -Caffeine = Antagonist -SSRI = Agonist -Morphine = Agonist - Benzodiazepine = Agonist