neurontransmission and psychopharmacology Flashcards

lecture 4

1
Q

synapse

A
  • junction between the terminal button of a neuron and the membrane of another neuron
  • conduit of info from one neuron to another
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2
Q

structure of synapses

A

-presynaptic axon: contains neurotransmitters, mitochondira and other organelles
- postsynaptic ending: receives neurotransmitters
- synaptic cleft: the tiny gap where neurotransmitters diffuse across

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3
Q

synaptic transmission 1.

A

action potential arrives at axon terminal, triggering Ca+ ions to move into cell

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4
Q

synaptic transmission 2.

A

Ca+ ions cause the migration of vesicles to the pre-synaptic membrane

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5
Q

synaptic transmission 3.

A

neurotransmitters diffuse across the synaptic cleft towards the post-synaptic membrane

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6
Q

synaptic transmission

A

neurotransmitters bind to receptor sites on the post-synaptic membrane with ‘lock and key’ specificity

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7
Q

synaptic transmission 5.

A

this binding opens NT dependent ion channels which change the excitability of the post-synaptic cleft

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8
Q

postsynaptic receptors

direct receptor (ionotropic)

A
  • binding site for a neutrotransmitter
  • ion channel opens when neutotransmitter molecule binds
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9
Q

postsynaptic receptors

indirect receptor (metabotropic)

A
  • only a binding site for a NT
  • activates enzyme
  • ion channel opens elsewhere
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10
Q

postsynaptic potential

A
  • this refers to ions moving acorss post synaptic membrane and after the membrane potential
  • depolarising (excitatory) = increased likelihood of AP
  • hyperpolarising (inhibitory = decreases likelihood of AP
  • depolarisation > threshold (-55mV triggers AP
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11
Q

depolarisation vs hyperpolarisation

A
  • depends on which type of ion channel is opened by the neurotransmitter
  • Na+, K+, Cl-
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12
Q

Na+ channels

A
  • produces excitatory postsynaptic potentials
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13
Q

K+ channels

A
  • produces inhibotry postsynaptic potentials
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14
Q

Cl- channels

A
  • either stabilisation or rest
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15
Q

neurotransmitters

A
  • acetylcholine
  • serotonin
  • dopamine
  • nor/epinephrine
  • GABA
  • glutmate
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16
Q

acetylcholine

A
  • excitatory
  • released in ANS, regulating heart rate, blood pressure, and gut mobility
  • imbalances linked with Alzheimer’s disease, seizures and muscle spasms
17
Q

serotonin

monoamines

A
  • excitatory or inhibitory
  • produced in neurons in midbrain, pons, medulla
  • regulates mood, sleep patterns, anxiety, pain
  • imbalance include SAD, anxiety, depression
18
Q

dopamine

monoamines

A
  • excitatory or inhibitory
  • produced in neurons in mid brain
  • faciliates focus, concentration, memory, sleep
  • reward system
  • imbalance include parkinson’s disease, schizophreina, bipolar disorder, ADHD
19
Q

epinephrine and norepinephrine

monoamines

A
  • realsed into blood stream
  • responsible for “fight or flight response”
  • stimulates body’s response
  • excess epinephrine can lead to high blood pressure, diabetes, heart disease
20
Q

endorphins

peptides

A
  • pain relievers
  • released by hypothalamus and pituitary gland
  • inhibitors
21
Q

glutamine

amino acids

A
  • excitatory
  • most common
  • key role in cognitive functions like thinking, learning and memory
  • imbalances associates with alzheimer’s disease, dementia, parkinson’s
22
Q

GABA (gamma-aminobutyric acid)

amino acids

A
  • most common inhibitory NT
  • regulates brain acitivity to prevent anxiety, irritability, concentration, sleep, depression
  • contributes to motor control, vision
23
Q

NT removal from synapse

A
  1. reuptake: NT pumped back into glia or the axon terminal that released it
  2. deactivation: NT destroyed by enzymes near receptors
  3. removal: diffuses into surrounding area
24
Q

psychopharmacology

A
  • study of the effects of drugs on the nervous system and behaviour
25
drugs
- exogenous chemicals - alter molecular functions - effects are physicological or behavioural - natural vs artifical
26
sites of drug action
- where drug intreacts with molecules - drugs affecting behaviour normally affect synaptic transmission '
27
drugs and synaptic transmission | agonists
- facilitate or mimics action of a neurotransmitter - facilitates postsynaptic effects
28
drugs and synaptic transmission | antagonists
- inhibits action of a neruotransmitter - block postsynaotic effects
29
mechanisms of drug action: 1. synthesis
- alter NT synthesis in presynaptic neuron - modifies concentration in synaptic cleft - NT produced from specific precursor molecules - enzymes required for change from precursor to NT - modes of alteration: 1. inactivate the enzymes 2. introduce precursor molecules
30
mechanisms of drug action: 2. storage
- alter neurotransmitter storage in presynaptic terminal - modifies cocnentration in synaptic cleft - transporter proteins in vesicle move NT from cytoplasm into vesicles - antagonsit inactivate transporters - vesicles remain empty
31
mechanisms of drug action: 3. release
- changes NT release from presynaptic cell - modifies concentration un synaptic cleft - modes of alteration: 1. prevent release of NT 2. trigger NT release
32
mechanism of drug action: 4. receptors
- act on neurotransmitter receptors - modify postsynaptic potentials
33
mechanism of drug action: 5. reuptake
- modify removal of neurotransmitters from synaptic cleft - changes NT concentrations in the cleft - agonists reduce or block reuptake
34
mechanism of drug action: 6. destruction
- modify NT destruction in synaptic cleft - enzyme typically inactivate neurotransmitters - enzyme acetylcholinesterase in postsynaptic membrane deactivates Ach - neostigmine: deactivates AchE - ACh remains in synaptic cleft longer - myasthenia gravis