Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

understanding the brain > Neurotransmission and Psychopharmacology > Flashcards

Neurotransmission and Psychopharmacology Flashcards

week 4

You may prefer our related Brainscape-certified flashcards:
The Brain flashcards
1
Q

what is the synapse?

A
  • Allows information to be passed (transmitted) from one neuron to the other
    • Information travels in one direction
    • Conduit of information from one neuron to another
    • Information travels in one direction
      ○ In deep sleep can be said to reset itself- go in both directions.
    • Junction between the terminal button of an axon and the membrane of another neuron
      ○ Occur on the terminal buttons
      No contact between the neurons (space between each neuron)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the significance of the presence of mitochondria within the synapse?

A
  • Presence of mitochondria within synapse suggests it needs energy.
    • Mitochondria= produced ATP (energy)
      ○ Allows for movement of the neurotransmitter.
      Neurotransmitter doesn’t go into the postsynaptic cell but binds with the receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the structure of the synapse?

A
  • In dendritic spines
  • Presynaptic axon
    ○ Terminal containing neurotransmitters , mitochondria and other organelles
    § Help shape the neurotransmitter
    • Postsynaptic ending
      ○ Receptor sites for neurotransmitters
    • Synaptic cleft
      Some neurotransmitters and made in the cell body/nucleus and others in the terminal buttons.
      vesicles are released into the synaptic cleft.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the first stage of synaptic transmission?

A
  1. Action potential arrives at axon terminal triggering Ca2+ ions to move into cell
    Leads to an influx of calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the second stage of synaptic transmission?

A
  1. Ca2+ ions cause the migration of vesicles (which contain NTs) to the pre-synaptic membrane
    • Causes the vesicles to move to the end of the terminal button- once stuck to the membrane they pop.
      Tension causes neurotransmitter to enter synaptic cleft.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the third stage of synaptic tansmission?

A
  1. The vesicles fuse to pre-synaptic membrane and break open emptying their neurotransmitters into the synaptic cleft
    • Lock and key= fit into specific receptors perfectly.
      Drugs can mimic effect by being similar in shape to neurotransmitter.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the fourth stage of synaptic transmission?

A
  1. Neurotransmitters diffuse across the synaptic cleft towards the post-synaptic membrane
    Fit into receptor sites in postsynaptic neuron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the fifth stage of synaptic transmission?

A
  1. Neurotransmitters bind to receptor sites on the post-synaptic membrane with ‘lock and key’ specificity – specific NT binds to specific receptors
    Neurotransmitters don’t then enter the postsynaptic neuron, once they are bound to the receptor, they open up channels that contain all the ions and diffuse/ electrostatic pressure either moves them in our out of the cell.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the sixth stage of synaptic transmission?

A

This binding opens NT-dependent ion channels which change the excitability of the post-synaptic cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is synaptic transmission?

A

the process by which one neuron communicates with another.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is direct postsynaptic receptors?

A

(ionotropic)
* Binding site for a NT
* Ion channel opens when NT molecule
binds
* Can act directly= inotropic response
Neurotransmitters bind to receptor channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are indirect postsynaptic recpetors?

A

(metabotropic)
* Only a binding site for a NT
* Activates enzyme
* Ion channel opens elsewhere
* Metabotropic=indirect effect of neurotransmitter
* Neurotransmitter send messages to G protein
Broken down metabolite opens the receptor leading to an influx of ions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the postsynaptic potential?

A
  • Graded potential- can help reach the threshold of the action potential.
    Postsynaptic potential = ions move across post synaptic membrane and alter the membrane potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is depolarisation of the postsynaptic potential?

A

(excitatory) = increased likelihood of AP
○ Start off the action potential if enough comes together
Influx of sodium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is hyperpolarisation of the posysynaptic potential?

A

(inhibitory) = decreased likelihood of AP
○ Outflux of potassium
* Depolarisation > threshold (-55mV) triggers AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does depolarisation/ hyperpolarisation epend on in the postsynaptic nueron?

A

Depolarisation/ hyperpolarisation depends on where neurotransmitter binds and what with (type of channel).
chemical to elctrical impulse
* Depends on which type of ion channel in the postsynaptic membrane is opened by the neurotransmitters
* Can open one of 3 channels:
○ Sodium - Na+
○ Potassium - K+
○ Chloride - Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are NA+ channels?

A
  • Produce excitatory postsynaptic potentials
    • Causes sodium to influx into the cell
    • Causes the resting potential to increase to -55mV
      ○ Increase in positive ions
      ○ Depolarisation of the cell
      ○ Increases the likelihood of action potential being released
      § Depends on depolarisation of other channels.
    • Binding cites is attached to by the neurotransmitter and opens the channel
18
Q

what are K+ channels?

A
  • K+ rushes out- leads to hyperpolarisation
    ○ Decreases likelihood of action potential being released.
    Produced inhibitory postsynaptic potentials
    1. k+ channels open
    2. k+ leaves neuron
    3. hyperpolarisation reduces AP liklihood
19
Q

what are Cl- channels?

A
  • At rest balance of Cl- in intra and extracellular fluid
    Leads to an influx within the postsynaptic cell
    at rest:
    1. cl- channel opens -> nothing happens as the forces are balaned

depolarisation
cl- channel opens -> cl- enters neuron -> stabilisation reduces the liklihood of AP

20
Q

what are the who ways in which neurotransmitters act?

A
  1. excitatory: help propagate AP
    e.g.: glutamate
  2. inhibitory: reduced AP liklihood
    e.g.: GABA
21
Q

what are the main neurotransmitters?

A
  1. acetlycholine (ACh)
  2. dopamine (monoamine)
  3. seretonine (monomanie)
  4. norepinephrine (noradrenaline) (monomaine)
  5. glutamate
  6. GABA (gamma-aminobutryic acid)
  7. endorphins (mood enhancers)
22
Q

what is acetylcholine (ACh)?

A
  • Mostly excitatory
    ○ Regulates heart rate and digestion
    • Found in peripheral & central NS
    • PNS: neurons controlling muscle contraction, excretion of certain hormones
    • CNS: widespread - role in REM sleep, sexual desire, activating cerebral cortex, learning, memory
    • Alzheimer’s disease is associated with a lack of ACh in certain brain regions
      ○ Due to imbalances within acetylcholine.
    • Centre of motivation
      Can inhibit the inhibitory part of the frontal cortex.
23
Q

what is the monoamine seretonin?

A
  • Excitatory or Inhibitory
    ○ Can be both
    • Cell bodies of neurons in midbrain, pons, medulla
      ○ Below the forebrain- joining it with the hindbrain
      ○ Regulatory purpose
    • regulates mood, sleep patterns, libido, anxiety, appetite and pain.
    • 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).
      ○ Used to regulate it
      ○ Reuptake of serotonin in the synaptic cleft- more lasting effect.
24
Q

what is the monoamine dopamine?

A
  • Excitatory or Inhibitory
    ○ Dual processes
    • Neuron cell bodies in mid brain
    • 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).
25
Q

what is the monoamine epinephrine?

A

(aka adrenaline) and Norepinephrine
○ Adrenaline/ noradrenaline
* Epinephrine= only when sympathetic system is activated (flight or fight)
* Found in peripheral NS (autonomic NS) & CNS (pons & medulla)
* Also released into blood (as a hormone), causing blood vessel contraction & increased heart rate
○ Is also a hormone.
○ Particularly in extreme situations
* Responsible for “fight-or-flight response” to fear and stress.
* Found in peripheral NS (autonomic NS) & CNS (pons & medulla)
* Important for attentiveness, emotions, sleeping, dreaming & learning
* Also released into blood (as a hormone), causing blood vessel contraction & increased heart rate
* Stimulates body’s response by increasing heart rate, breathing, blood pressure, blood sugar, blood flow to muscles, heightened attention and focus.
○ Sympathetic nervous system processes.
* Excess epinephrine can lead to high blood pressure, diabetes, heart disease and other health problems.
○ Reciprocal effects of the above conditions.
* As a drug, epinephrine is used to treat anaphylaxis, asthma attacks, cardiac arrest and severe infections
* Role in mood disorders
○ e.g., bipolar disorder

26
Q

what is the peptide endorphins?

A

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.

27
Q

what is the amino acid glutamate?

A
  • Most common excitatory neurotransmitter
    • Indirectly has excitatory and inhibitory regulations
    • 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 (epilepsy)
28
Q

what is the amino acid GABA?

A
  • Simple in structure
    • Gamma-aminobutyric acid (GABA).
      ○ From glutamate
      ○ Synthesised from glutamate and vitamin B6
    • The most common inhibitory neurotransmitter of the nervous system, particularly in the brain.
      ○ Similar regions as glutamate
    • Regulates brain activity to prevent problems in the areas of anxiety, irritability, concentration, sleep, seizures and depression.
    • Most important neurotransmitter in brain
    • Widely distributed in neurons of cortex
    • 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
29
Q

what is regulating postsynaptic potentials?

A
  • How might neurotransmitters be removed from a synapse?
    3 processes in which they are taken away from the synaptic cleft- cant constantly be there as it needs clearing out.
30
Q

what are the processes in which neurotransmitters are removed from the synapse?

A
  1. Reuptake: NT quickly pumped back into nearby glia or the axon terminal that released it
    ○ Through process of transporter proteins is taken to terminal buttons in presynaptic cell.
    ○ Glial cells and vesicles (synaptic vesicles)
  2. Deactivation: NT destroyed (inactivated) by enzymes near receptors so its not recognized by receptor
    * (Acetylcholine A breaks down acetylcholine)
  3. Removal: diffuses into surrounding area (e.g., blood)
  • Capillaries diffuse neurotransmitters into the bloodstream.
    So it can return back to its resting level
31
Q

what is psychopharmacology?

A
  • Study of the effects of drugs on the nervous system and behaviour
    ○ Neurosciences overlap with rugs (psychopharmacology)
    • Primarily focusing on behaviours
    • Important field in neuroscience
      ○ Responsible for development of psychotherapeutic drugs to treat psychological & behavioural disorders
      Address imbalances to alleviate symptoms.
32
Q

what are drugs?

A
  • Drugs are exogenous chemicals (definition)
    ○ Means they aren’t manufactured within the body.
    • Unnecessary for normal functioning
      ○ Need them for medical conditions?
      ○ Readdress imbalance to make function work normally
    • Alter molecular functions of the synapse
    • Effects are physiological (biomolecular level- synapse takes place) or behavioural (excites or inhibits certain behaviours of the brain)
    • Natural vs artificial
      ○ Natural: opium, cannabis, heroine, ginger, cloves, turmeric
      Artificial: morpheme, aspirin, ibuprofen
33
Q

whata re the sites fo drug action?

A
  • Site of action
    ○ Where drug interacts with molecules
    ○ Synaptic cleft/ postsynaptic or presynaptic vesicles
    • Drugs affecting behaviour normally affect synaptic transmission
      Excitatory and inhibitory.
34
Q

what is the agonist in drug and synaptic transmission?

A
  • Facilitate of mimic action of a nuerotransmitter
  • facilitate postsynaptic effects
35
Q

what are antagonsist of drugs and synaptic trasmission?

A
  • inhibit action of a neurotransmitter
  • block postsynaptic effect
36
Q

what are the 6 stages of the mechanisms of drug actions?

A
  1. synthesis
  2. storage
  3. release
  4. receptors
  5. reuptake
  6. destruction
37
Q

what is the synthesis of drug actions?

A
  • Alter neurotransmitter synthesis in presynaptic neuron
    ○ So it cant effectively make the neurotransmitter in the first place
    ○ Less neurotransmitter being made in the cell organelles and vesicles.
    Modifies concentration in synaptic cleft
    • NT produced from specific precursor molecules
      ○ Changes through enzymatic reactions
      ○ Inactivate enzyme to get more in system
    • Enzymes required for change from precursor to neurotransmitters.
      Modes of alteration
      1. Inactivate the enzymes (antagonist)
      2. Introduce precursor molecules (agonist)
38
Q

what is the storage of drug actions?

A
  • Alter neurotransmitter storage in presynaptic neuron
    ○ In presynaptic terminal
    • Modifies concentration in synaptic cleft
    • Transporter proteins in vesicle membranes move NT from cytoplasm into vesicles
    • Antagonist inactivate transporters- still neurotransmitter in the extracellular fluid.
      ○ Vesicles remain empty
      Cant release as the vesicles aren’t stored with the neurotransmitter.
39
Q

what is the release of drug actions?

A
  • Changes neurotransmitter release from presynaptic cell
    ○ Inhibit or increase the release
    • Modifies concentration in synaptic cleft
      Modes of alteration
      1. Prevent release of NT (antagonist)
      2. Trigger NT release (agonist)
      Very toxic chemical that triggers release- can be used as a medicine despite it toxicity level.
40
Q

what are the receptors of drug actions?

A
  • Act on neurotransmitter receptors
  • Modify postsynaptic potentials
  • Direct agonist= influx of Na or K+
  • Direct antagonist= closes receptor cites
  • Indirect= needs neurotransmitter and drug to open channels.
41
Q

what is the reuptake fo drug actions?

A
  • Modify removal of neurotransmitters from synaptic cleft
  • Prevent serotonin from being reuptake into postsynaptic neuron
  • Work on transporter neurons.
  • Change neurotransmitter concentrations in the cleft
  • Agonists reduce or block reuptake
42
Q

what is the destruction of drug actions?

A
  • Modify neurotransmitter destruction in synaptic cleft
    • Prevent destruction of the neurotransmitter.- inhibit the breakdown
    • Enzymes typically inactivate neurotransmitters (agonist)
    • Enzyme Acetylcholinesterase (AChE) in postsynaptic membrane deactivates Ach
      ○ Neostigmine: inactivates AChE - deactivates the enzymes that break it down.
      § Remains in synaptic cleft longer
      ○ ACh remains in synaptic cleft longer
    • Myasthenia Gravis
      Muscle tremors.

understanding the brain (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions