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Mans - Dr. Thompson exam 3 > Synapses - Action Potential and Drug Targets > Flashcards

Synapses - Action Potential and Drug Targets Flashcards

1
Q

What’s the resting membrane potential and what is it useful for?

A

– 70 mV ( is the charge difference across the membrane) one way the neurons communicate without using ATP

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2
Q

Resting state ion concentration (Na, K)

A

Na concentration high outside the membrane, K – high inside

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3
Q

Who sets the concentration?

A

Sodium potassium pump

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4
Q

What happens when a ligand/neurotransmitter binds to a receptor at the dendrite spine -

A

The membrane becomes depolarized or hyper polarized

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5
Q

How does excitatory action potential form?

A

Excitatory neurotransmitters open positively charged channels and depolarize the membrane

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6
Q

How does inhibitory action potential form?

A

Inhibitory neurotransmitters (Cl, K) are negative ions that hyper polarize the membrane

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7
Q

who makes the decision to propagate Action Potential or not?

A

the hillock by temporal or spatial summation

( The action potential is all or none)

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8
Q

What happens when threshold is reached?

A

Action potential

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9
Q

What happens at rising phase of Action Potential?

A

Na is rushing in

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10
Q

What happens when Na reaches its equilibrium?

A

Na channels become inactivated

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11
Q

What’s the difference between Inactive vs closed channels?

A

Inactive means can’t depolarize anymore, cannot respond to other/more stimulation =refractory phase = the flushing of toilet model

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12
Q

What’s the next step in the AP after depolarization?

A

the Na channels close

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13
Q

What’s next? After the Na channels close

A

Next the K channels open and remain open for a longer period causing the overshoot - the K leaves creating hyper-polarization,

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14
Q

What’s next? after hyperpolarization

A

At this point the Na K pumps use ATP to equalize the charge across the membrane

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15
Q

What needs to happen at the pre-synaptic membrane before releasing the neurotransmitters?

A

the voltage gated Ca channels need to open

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16
Q

What does increase in Ca concentration cause?

A

Readily releasable pool is emptied by the increase in Ca concentration- vesicles fuse with the membrane and empty

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17
Q

What are transporter proteins important for?

A

getting the neurotransmitter into vesicles = neurotransmitter storage

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18
Q

Types of Synapses (2)

A

Chemical and electrical

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19
Q

Characteristics of Chemical Synapses

A
  • Chemical synapses are unidirectional

- Rapid, prolonged stimulation /firing can activate the reserve pool

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20
Q

Electrical synapses characteristics (6)

A
  • Prevalent in hippocampus and other limbic structures
  • The speed is faster because the membranes are touching (the connexons form the tight junctions)
  • The origin or the type of the signal matches the response of the signal (either depolarization or hyperpolarization)
  • Bidirectional (if you have multiple neurons in a row = synchronous firing)
  • There is no signal renewal or salutatory conduction and over time and space the signal will weaken because of membrane resistance
  • Drugs that affect membrane dynamic will have a stronger effect because the membranes are close to each other
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21
Q

Places where synapses can be targeted by drugs (8)

A

NT release (Ca channels)

NT reuptake (clear a signal from the synapse)

NT degradation – (clear a signal from the synapse by enzymatic activity)

NT synthesis

NT storage – transporter proteins

Membranes

Postsynaptic receptors

Presynaptic auto-receptors (mobilize the reserve pool by prolonged stimulation)

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22
Q

How can we change the strength of the synapse?

A

Up-regulating the number of receptors by repeated stimulation
Strength of synapses can be increased with long term potentiation which is the foundation of learning and memory ( up-regulation of receptors) (neurons that fire together, wire together)

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23
Q

How else can we change the strength of synapse?

A

Down regulation of receptors = depression of activity/less activity or response to stimulation
Long term depression underlines addictions

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24
Q

What happens with neurons whose connections are not supported or stimulated?

A

die

25
Q

What is the role of microglia?

A

Glia have a supportive role (astrocytes that release a small amount of NT) are the ones that support new formed connection

26
Q

Can we grow new neurons?

A

Yes
- In the dentate gyrus of the hippocampus and,
- The olfactory bulb
There are stem cells that when stimulated could form new neurons here

27
Q

What can adults do to stimulate neuro-genesis?

A 
Read 
Use non dominant hand 
Exercise 
Solve puzzles 
Use your brain
28
Q

What is important when designing a Drug for the neurologic system?

A

Getting it to the target tissue / organ; Need to pass the BBB

29
Q

What is the BBB?

A

A highly selective permeability barrier that separates the brain from the circulatory system and protects the central nervous system (CNS) from potentially harmful chemicals while regulating transport of essential molecules and maintaining a stable environment. - BBB is formed by highly specialized endothelial cells that line brain capillaries and transduce signals from the vascular system and from the brain

30
Q

What are tight junctions?

A

Tight junctions = series of cross linked proteins that hold things close together, hold peripheral membrane proteins (found at the surface of the membrane) together with the actin cytoskeleton to form the ocludent family of proteins

31
Q

4 Ways of trespassing the BBB

A

Hyperosmotic solution
Microcatheterization
Micro Bubbles
Trojan Horse

32
Q

which substance easily get through the BBB?

A

Non-polar (lipids) through simple diffusion

33
Q

How do glucose and amino acids get through BBB?

A

Through facilitated diffusion –active transport

34
Q

Other pharmacological consideration when designing a drug

A

The risk of getting cleaned out once in the brain is also important

35
Q

Name the cells of the nervous system and their functions

A

Neurons (transmission cells)
NeuroGlia (support cells)
~Astrocytes: in CNS; provides structure and support. Have “feet” that make contact with the blood vessels
~Microglia: small, mobile, Like phagocytes (engulf and consume foreign microorganisms and damaged or dead neurons)
~Oligodendrocytes: in CSN; forms myelin in CNS, like CNS version of schawnn cells
~Ependymal cells: in CNS: These cells are involved in the creation and secretion of cerebrospinal fluid (CSF) and beat their cilia to help circulate the CSF and make up the blood-CSF barrier.
~Satellite cells: in PNF; small cells that surround neurons in sensory, sympathetic, and parasympathetic ganglia.[22] These cells help regulate the external chemical environment. kind of like astrocytes but in PNF
~Schwann Cells: in PNF; forms myelin in PNS, like PNF version of Oligodendrocytes

(sorry, didn’t realize these were covered in next deck)

36
Q

Where are ligand-gated channels commonly found and some examples of which ions pass through them.

A

We mostly talked about them on post-synaptic neuron.

Ligand-gated ion channels (LGICs) are a group of transmembrane ion channel proteins which open to allow ions such as Na+, K+, Ca2+, or Cl− to pass through the membrane in response to the binding of a chemical messenger (i.e. a ligand), such as a neurotransmitter

37
Q

Where are voltage gated channels usually found?

A

Often found in neurons, especially in the axon (I think).

Examples include:
~the sodium and potassium voltage-gated channels of nerve and muscle.
~the voltage-gated calcium channels that play a role in neurotransmitter release in pre-synaptic nerve endings.

38
Q

G and F Table 28-3
Anatomic site of damage: Frontal Lobe

How does damage affect Memory Finding? (4)

A

Lateralized deficit in working memory
~Right spatial defects
~left verbal defects
~impaired recall with spared recognition

39
Q

G and F Table 28-3
Anatomic site of damage: Frontal Lobe

How does damage affect Other Neurological and Medical Findings? (4 - 7)

A

~Personality change
~Perservation
~Chorea, dystonia
~Bradykinesia, tremor, rigidity

40
Q

G and F Table 28-3
Anatomic site of damage: Basal Forebrain

How does damage affect Memory Finding?

A

Declarative memory defiict

41
Q

G and F Table 28-3
Anatomic site of damage: Basal Forebrain

How does damage affect Other Neurological and Medical Findings?

A

none listed

42
Q

G and F Table 28-3
Anatomic site of damage: Ventromedial Cortex

How does damage affect Memory Finding? (1)

A

Frontal lobe-type declarative memory deficit

43
Q

G and F Table 28-3
Anatomic site of damage: Ventromedial Cortex

How does damage affect Other Neurological and Medical Findings? (1)

A

Upper visual field defects

44
Q

G and F Table 28-3
Anatomic site of damage: Hippocampus and parahippocampal cortex

How does damage affect Memory Findings? (4)

A

~Bilateral lesions yield global amnesia
~Unilateral lesions show lateralizations of deficit
~Left: verbal deficit
~Right: spacial deficit

45
Q

G and F Table 28-3
Anatomic site of damage: Hippocampus and parahippocampal cortex

How does damage affect Other Neurological and Medical Findings? (4)

A

~myoclonus
~depressed level of consciousness
~cortical blindness
~automations

46
Q

G and F Table 28-3
Anatomic site of damage: Fornix

How does damage affect Memory Findings? (1)

A

~Global Amnesia

47
Q

G and F Table 28-3
Anatomic site of damage: Fornix

How does damage affect Other Neurological and Medical Findings?

A

none listed

48
Q

G and F Table 28-3
Anatomic site of damage: Mammillary Bodies

How does damage affect Memory Findings? (1)

A

~Declarative memory deficit

49
Q

G and F Table 28-3
Anatomic site of damage: Mammillary Bodies

How does damage affect Other Neurological and Medical Findings? (4)

A

~Confabulation,
~Ataxia
~nystagmus
~signs of alcohol withdrawal

50
Q

G and F Table 28-3
Anatomic site of damage: Dorsal and medial dorsal nucleus (of thalamus)

How does damage affect Memory Findings? (1)

A

~Declarative memory deficit

51
Q

G and F Table 28-3
Anatomic site of damage: Dorsal and medial dorsal nucleus (of thalamus)

How does damage affect Other Neurological and Medical Findings? (1)

A

~Confabulation

52
Q

G and F Table 28-3
Anatomic site of damage: Anterior Thalamus

How does damage affect Memory Findings? (1)

A

Declarative memory deficit

53
Q

G and F Table 28-3
Anatomic site of damage: Anterior Thalamus

How does damage affect Other Neurological and Medical Findings?

A

none listed

54
Q

G and F Table 28-3
Anatomic site of damage: Lateral temporal cortex

How does damage affect Memory Findings? (1)

A

Deficit in autobiographical memory

55
Q

G and F Table 28-3
Anatomic site of damage: Lateral temporal cortex

How does damage affect Other Neurological and Medical Findings?

A

none listed

56
Q

G and F Table 28-3

What are the 9 Anatomic Sites of Damage?

A
  1. Frontal Lobe
  2. Basal Forebrain
  3. Ventromedial Cortex
  4. Hippocampus and parahippocampal cortex
  5. Fornix
  6. Mammillary Bodies
  7. Dorsal and Medial dorsal nucleus (of thalamus)
  8. Anterior thalamus
  9. Lateral temporal cortex
57
Q

G and F Table 28-3

What five Anatomic Sites of Damage have declarative memory deficit as a Memory Finding?

A
  1. Basal forebrain
  2. Vntromedial cortex (frontal lobe-type declarative memory deficit)
  3. Mammillary Bodies
  4. Dorsal and medial dorsal nucleus (of thalamus)
  5. Anterior Thalamus
58
Q

G and F Table 28-3

What two Anatomic Sites of Damage had Confabulation as an Other Neurological and Medical Finding?

A
  1. Mammillary Bodies (also included atxia, nystagmus, signs of alcohol withdrawal)
  2. Dorsal and medial dorsal nucleus (of thalamus)
59
Q

G and F Table 28-3

What Four Anatomic Sites of Damage had nothing listed under Other Neurological and Medical Finding?

A
  1. Basal Forebrain
  2. Fornix
  3. Anterior Thalamus
  4. Lateral Temporal cortex

Mans - Dr. Thompson exam 3 (8 decks)

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