Biopsychology Chpt 4 Flashcards

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1
Q

What is the membrane potential?

A

difference in electrical charge inside and outside of the cell

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2
Q

What causes the uneven distribution of ions?

A
  1. The membrane is selectively permeable to some ions (more permeable to K+)
  2. Sodium-Potasium pumps
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3
Q

What factors contribute to the even distribution of ions?

A
  1. Random motion > particles move down their concentration gradient
  2. electrostatic pressure > like repels like, opposites attract
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4
Q

What is equilibrium potential

A

the potential at which there is no movement of an ion> it will try to reach this point if allowed to move freely

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5
Q

What is the equilibrium potential of
Na+ (sodium)
K+ (potassium)

A
Na+ = 62 mV
K+ = -80mV
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6
Q

What is the resting membrane potential of the neurons we are studying?

A

-70mV

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7
Q

Is the sodium-potassium pump directly involved in the action potential?

A

no, but it helps to create the uneven distribution of ions that polarizes the cell and contributes to AP

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8
Q

What are factors acting on Sodium ions (NA+)

A
  1. Sodium in high concentration outside cell > wants to move down gradient to inside
  2. Sodium also attracted to -A protein inside cell
  3. Membrane is not very permeable to Sodium
  4. Sodium Potassium pump is sending Na+ out of cell
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9
Q

What are the factors acting on Potassum ions?

A
  1. Potassium in high concentration inside cell > wants to move out down the concentration gradient
  2. K+ is being brought in by the sodium-potassium pump
  3. K+ is attracted to A- protein
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10
Q

What are PSP’s

A

Post Synaptic Potentials > when neurotransmitters bind at postsynaptic receptors and cause electrical changes

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11
Q

How does an EPSP affect the electrical charge of the cell?

A

Excitatory PSP’s makes the membrane potential less negative (depolarization) and more likely that the neuron will fire

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12
Q

How does an IPSP affect the electrical charge of the cell?

A

Inhibitory PSP’s makes the membrane potential more negative (hyperpolarization) and less likely that the neuron will fire

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13
Q

What is the mechanism that causes IPSP’s to make the membrane potential more negative?

A

Protein channel opens to allow Cl- into the cell making it more polarized

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14
Q

What is the mechanism that causes EPSP’s to make the membrane potential more positive (depolarization)?

A

Protein channels open to allow Na+ in

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15
Q

What does it mean the PSPs are graded?

A

They vary in size

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16
Q

When will a neuron fire an action potential?

A

When the membrane potential reaches -65Mv at the AXON INITIAL SEGMENT

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17
Q

How do EPSPs and IPSPs travel?

A

Passively from their site of origin > get smaller as they travel

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18
Q

What is integration in regards to the action potential

A

integration of several post synaptic potentials is needed for a neuron to reach -65Mv and fire an action potential.

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19
Q

What are the two types of integration?

A

Spatial summation: integration of PSPs happening at different places
Temporal summation: integration of PSPs happening at different times

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20
Q

At what phase in the AP are sodium channels opened? When are they closed?

A

Opened: The rising phase
Closed: Peak of rising phase +50mV

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21
Q

When are the Potassium channels opened during the AP?

When are they closed?

A

Opened: delay open after Na+ channels
Closed: start to close at -70 mV, results in hyperpolarization and a potential of -80mV

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22
Q

Why does the neuron hyperpolarize to -80mV?

A

Because the potassium is being pushed quickly out by sodium ions and -80mV is it’s equilibrium potential (desired state)

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23
Q

What brings the neuron back to resting potential?

A

random motion (concentration gradient) and sodium-potassium pump

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24
Q

What is an absolute refractory period

A

> When it is impossible to initate another AP

>Sodium channels are inactivated/closed and need time until they will open again

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25
Q

What is the relative refractory period?

A

> period of time when the sodium channels are open but the cell is still depolarized below resting potential
harder for an AP to be fired

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26
Q

What does the refractory period do?

A

> Prevent the backwards movement of APs and limit the rate of firing

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27
Q

What are 3 features of Action Potentials

A

> Nondecremental
Conducted more slowly than PSPs
Passive and active

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28
Q

What is antidromic conduction?

Orthodromic conduction?

A

Antidromic: toward cell body
Orthodromic: down axon towards dendrites

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29
Q

What is Saltadory conduction?

A

> fast transmission of APs in myelinated axons

>because conduction jumps from node to node

30
Q

What are the nodes of ranvier?

A

spaces between myelin sheath

31
Q

What are the two most common synaptic transmissions?

A

axodendritic: axons on dendrites
axosomatic: axons on cell bodies

32
Q

What are two less common synaptic transmissions?

A

dendrodendritic: dendrite on dendrite
axoaxonic: axon on axon

33
Q

What is special about dendrodendritic transmissions?

A

can transmit in either direction

34
Q

what are axoaxonic transmissions potentially involved in?

A

presynaptic facilitation or inhibition

35
Q

How is an AP passive AND active?

A

Passive when it moves along myelin sheath, active when it moves between nodes of ranvier

36
Q

What is it called when the site of neurotransmitter release and reception are close?

A

directed synapse

37
Q

What is it called when the site of neurotransmitter release and reception are far away?

A

nondirected synapse

38
Q

Where are small neurotransmitter molecules synthesized and packaged?

A

small: synthesized in terminal button, packaged in vesicles

39
Q

Where are large neurotransmitter molecules synthesized and packaged?

A

Large: synthesized in the cell body and packaged in vesicles to be transported to the axon terminal

40
Q

How does exocytosis occur?

A

AP causes voltage-activated CA2+ channels to open which causes vesicles to fuse with the terminal membrane and release contents

41
Q

What is a ligand?

A

A molecule that binds to a receptor (neurotransmitters)

42
Q

What are ionotropic receptors?

A

associated with ligand-activated ion channels (ligand triggers channel to open to allow ion to pass)

43
Q

What are metabotropic receptors?

A

> They do NOT have a channel that opens
By binding with receptor they activiate G-protein which then
G protein activates secondary messenger
may or may not open an ion channel somewhere else on the membrane

44
Q

What is a signalling cascade

A

When a metabotropic receptor causes a g-protein to activate a chain of messenger molecules (not a direct opening of an ion channel by G-protein)

45
Q

What is the function of autoreceptors?

A

> regulate concentration of NT in the synapse
bind to neuron’s own NT
on presynaptic membrane

46
Q

What are two mechanisms for terminating NT action in the synapse?

A
  1. Reuptake by autoreceptors

2. Enzymatic degradation

47
Q

What are gap junctions?

A

Electrical synapses that allow electrical signals and small molecules to pass directly between cells

48
Q

Why are gap junctions necessary?

A

When simultaneous firing of neurons is necessary

ex. embryonic development, heart muscle

49
Q

What two types of neurons often use gap junctions?

A
  1. astrocytes > star-like glial cells of CNS

2. Oligodendrocytes > myelin sheath creating CNS glial cells

50
Q

Where can gap junctions occur?

A

Between neurons, glia, and neurons and glia

51
Q

What is a tripartite synapse?

A

a synapse that includes a presynaptic terminal + post synaptic terminal + astrocyte

52
Q

What does the astrocyte do in a tripartite synapse?

A

releases NT glutamate and ATP to modulate activity of pre and post synaptic terminal

53
Q

What are three characteristics of small molecule NT?

A
  1. directed synapses
  2. ionotropic and metabotropic receptors
  3. fast and brief signals
54
Q

What are three characteristics of large molecule NT?

A
  1. non-directed synapse
  2. metabotropic receptors
  3. slow and lasting signals
55
Q

What are three classes of small molecule NT?

A
  1. Amino Acids
  2. Monamines (dopamine, seratonin)
  3. Acetylcholine
56
Q

What is the one large molecule NT class?

A

Neuropeptides

57
Q

What is a prevalent excitatory amino acid NT and where is it found?

A

Glutamate > fast acting directed synapses in the CNS

58
Q

What is a prevalent inhibitory amino acid NT and where is it found?

A

GABA > synthesized from glutamate in the CNS

59
Q

What are two more common amino acid NT?

A

Aspartate and glycine

60
Q

What are two classes of Monoamines?

A
Catecholamines > synthesized from Tyrosine
1. dopamine
2. norepinephrine
3. epinephrine
Indolmines > synthesized from tryptophan
1. seratonin
61
Q

Where is acetylcholine important?

A

at neuromuscular junctions

62
Q

What are two types of unconventional NT?

A
  1. Endocannabinoids

2. soluble gases (Nitric Oxide, Carbon Monoxide)

63
Q

What do endocannabinoids and soluble gases do?

A

They inhibit synaptic transmission through backwards messaging

64
Q

What are 5 categories of neuropeptides?

A
Pituitary peptides
hypothalamic peptides
Brain-gut peptides
Opioid peptides
Misc. Peptides
65
Q

What are two examples of agonist drugs?

A
  1. Cocaine > catecholamine agonist > blocks reuptake preventing NT from being turned off
  2. Benzodiazepines > GABA agonists > increases frequency of GABA channel openings
66
Q

What are two examples of antagonist drugs?

A
  1. Atropine > Ach antagonist > women used to put in eyes to make the pupils larger > disrupts memory
  2. Curare > Ach antagonist > causes paralysis
67
Q

What are two families of endogenous Opioids and what do they do

A
  1. enkephalins
  2. endorphins
    produce anelgesia
68
Q

What kind of molecules are enodogenous opioids and what kinn of receptors do they bind to?

A

large molecules > neuropeptides > bind to metabotropic receptors

69
Q

What kind of symptoms do antischizophrenic drugs produce?

A

parkinsonian > because drugs disrupts the dopaminergic pathway from substantia nigra to the hypothalamus

70
Q

What kind of agonists produce schizophrenic sympotms?

A

dopamine agonists