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BIO 203 > Lecture 19 > Flashcards

Lecture 19 Flashcards

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1
Q

What are the two ways messages are transmitted from one neuron to another? (2 types of synapses)

A

Electrical synapse
Chemical synapse

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2
Q

What happens in an electrical synapse?

A

Adjacent cells are joined by gap junctions and ions diffuse directly from 1 cell into the next

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3
Q

What are the advantages of electrical synapse?

A

Much faster
No delay for release, diffusion and binding of NT

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4
Q

What are the disadvantages of electrical synapse?

A

Cannot integrate information
Only quick propagation of the existing AP for a simultaneous response among multiple cells, similar to cardiomyocytes

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5
Q

What happens in a chemical synapse?

A

Gap between 2 neurons where information passes chemicals, in the form of neurotransmitter (NTs) molecules

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6
Q

What is the advantage of chemical synapse?

A

NTs released at the chemical synapse can be both excitation and inhibitory and their quantity can vary, allowing integration from multiple presynaptic neurons

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7
Q

What may a presynaptic neuron synapse with?

A

A dendrite, the soma, or the axon of a postsynaptic neuron

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8
Q

What size molecules are “classical” neurotransmitters?

A

Small

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9
Q

What are the 4 kinds of molecules that are the neurotransmitters?

A

Amino acids
Monoamines “biological amines”
Acetylcholine
ATP & it’s derivatives (adenosine)

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10
Q

What are the 3 types of amino acids and are they excitatory/inhibitory?

A

Glutamate - excitatory
Y-aminobutyric acid (GABA) - inhibitory
Glycine - inhibitory

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11
Q

Where are monoamines synthesized from?

A

Amino acids

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12
Q

What are the 5 monoamines?

A

Dopamine
Norepinephrine
Epinephrine
Serotonin
Histamine

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13
Q

What are the 3 catecholamines and where are they derived from?

A

Dopamine
Norepinephrine
Epinephrine

Derived from tryptophan

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14
Q

Where is serotonin (5-HT) derived from?

A

Tryptophan

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15
Q

Where is histamine derived from?

A

Histadine

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16
Q

Where are all of the 4 neurotransmitters derived from?

A

Carbohydrate substrates of intermediate metabolism

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17
Q

Where are peptides?

A

Short protein chains of 2-40 amino acids
(B endorphins, substance P)

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18
Q

What are modulators?

A

“Unconventional” neurotransmitters
(Gases like NO and CO)

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19
Q

What are the steps of the synthesis and release of the classical neurotransmitters?

A
  1. The enzymes are required for their synthesis are synthesized in the rough ER (neurosoma)
  2. They are transported to the Golgi apparatus
  3. In the Golgi apparatus, they are modified
  4. Soluble enzymes are transported along the axon to the nerve terminal by slow anterograde axonal transport via microtubules. The remaining enzymes are transported by fast anterograde axonal transport.
  5. The precursor needed for the synthesis of NTs is taken up via transporter proteins located in the plasma membrane of the nerve terminal. The NT is synthesized in the presynaptic nerve terminal from the precursor.
  6. The synthesized pool of the NT in the cytoplasm is take up into small vesicles by Vesicular MonoAmine Transported (VMAT)
  7. The appropriate stimulus results in the release of the NT by exocytosis
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20
Q

What are the two major enzymes responsible for catecholamine catabolism int he brain?

A

Cateschol-O-methylthransferase (COMT)

Monoamine oxidase A (MAOa)

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21
Q

What is epinephrine (adrenaline) synthesized from?

A

From norepinephrine within the adrenal medulla

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22
Q

What is the adrenal medulla?

A

Small glands associated with the kidneys

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23
Q

What are the 2 types of receptors that neurotransmitters bind to?

A

Ionotropic receptors

Metabotropic receptors

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24
Q

What are ionotropic receptors?

A

Ligand-gated ion channel receptors

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25
Q

What are metabotropic receptors?

A

G-protein coupled receptors

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26
Q

What are ionotropic receptors composed of?

A

3-5 protein subunits that form a pore

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27
Q

What do NTs binding to ionotropic receptors do?

A

They open the pore and directly induce ion fluxes

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28
Q

What do metabotropic receptors affect?

A

Affect channels by the activation of intermediate molecules called G-proteins

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29
Q

What can G-proteins activate?

A

The production of second messenger molecules

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30
Q

How does synaptic transmission finish? (3 ways)

A

Via NT transporters on the plasma membrane

Diffusion/Absorption
Degradation
Reuptake

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31
Q

What is diffusion/absorption?

A

NT diffuse away from the synaptic cleft and are returned to presynaptic neuron

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32
Q

What is degradation?

A

NT are degraded by enzymatic reactions in the synaptic cleft

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33
Q

What is reuptake?

A

NTs are taken back into the presynaptic neuron

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34
Q

What does the monoamine hypothesis of depression suggest?

A

Suggests that depression was associated with a deficiency of monoamines such as serotonin and norepinephrine

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35
Q

How well are the causes of depression understood?

A

They are poorly understood

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36
Q

What are the steps in how serotonin works in the synapse?

A
  1. Serotonin is produced directly in the neuron
  2. Vesicle membrane embedded transported protein transports serotonin into vesicles
  3. Vesicle releases serotonin into the synaptic cleft
  4. Serotonin binds to receptor and initiates a signal to the cell body of the post synaptic neuron
  5. Receptor clears. Serotonin is taken up by the presynaptic neuron, a glial cell of neuron leaves the cleft through diffusion.
  6. After reuptake, serotonin gets reloaded into vesicle or broken down
  7. MAO breaks down serotonin
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37
Q

Hero do neurons of the substantia nigra communicate with neurons of the basal ganglia?

A

By liberating the NT dopamine

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38
Q

What is this biochemical interaction responsible for?

A

Voluntary movement coordination of the body

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39
Q

Which NT is association with Parkinson’s disease and how?

A

Neurons of the substantia nigra degenerate

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40
Q

What happens with this degeneration?

A

Slowness or a sense of movement, rigidity and a resting tumor (especially in the hands and fingers)

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41
Q

What has been a central dogma for schizophrenia for decades?

A

The mesolimbic hypothesis

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42
Q

What does the mesolimbic hypothesis state?

A

Aberrant functioning of the midbrain dopamines projections to limbic regions causes psychotic symptoms

43
Q

What are examples of positive symptoms in schizophrenia?

A

Hallucinations
Delusions

44
Q

What are negative/cognitive symptoms of schizophrenia?

A

Lack of motivation, cognitive impairment

45
Q

What is the receptor in positive symptoms?

A

D2 (hyper-)

46
Q

What is the receptor in negative/cognitive symptoms?

A

D1 (hypo-)

47
Q

What is the brain region of positive symptoms?

A

Limbic system (nucleus accumbens)

48
Q

What is the brain region of negative symptoms?

A

Prefrontal cortex

49
Q

What are the 4 dopaminergic pathways in the brain?

A

Mesocortical
Mesolimbic
Tuberoinfundibular
Nigrostriatal

50
Q

What is the mesocortical pathway responsible for?

A

Cognition and executive function (planning)
Emotions and affect

51
Q

How does the mesocortical pathway relate to schizophrenia?

A

Decreases D1 - negative symptoms (apathy)

52
Q

What is the function of the mesolimbic pathway?

A

Regulates limbic function or motivation, and reward

53
Q

How does the mesolimbic pathway relate to schizophrenia?

A

Increases D2 - positive symptoms like hallucinations

54
Q

What is the nigrostriatal pathway responsible for?

A

Motor movement

55
Q

What will decreased or increased activity produce in the nigrostriatal pathway?

A

Produce movement abnormalities
Hypokinetic: Parkinson’s symptoms
Hyperkinetic: movement disorders

56
Q

What is the function of the tuberoinfundibular pathway?

A

Inhibition of prolactin release

57
Q

Where does the tuberoinfundibular project from?

A

From the hypothalamus to the anterior pituitary gland

58
Q

What is the disorder of the tuberoinfundibular pathway?

A

Decreased DA: hyperprolactinemia

59
Q

Which inhibitory NT is associated with epilepsy?

A

GABA

60
Q

How does GABA external its inhibitory effects through the GABAa receptor?

A

GABA binds to a sire near the junction of a and B subunits

This causes confrontation changes that open the chloride ion channel and lead to neuronal membrane hyperpolarization

61
Q

What has AD progression been associated with?

A

Gradual damage in function and structure in the hippocampus and neocortex, the vulnerable brain areas used for memory and cognition

62
Q

Acetylcholine acts on target neurons in the _____ and the ____

A

Hippocampus
Neocortex

63
Q

What does this do?

A

Strengthening the neural circuits that are involved in memory formation

64
Q

What does the cholingeric hypothesis of Alzheimer’s postulate?

A

It centers on the progressive loss of limbic and neocortical cholingeric innervation

65
Q

What is neuroplasticity?

A

The ability of the brain to change, or reward, throughout a person’s life

66
Q

What is synaptic plasticity?

A

The process of neuroplasticity occurring at the single cell level
(Individual synapse)

67
Q

What is synaptic plasticity the basis of?

A

Basis of learning and brain repair after injuries

68
Q

Changes in synaptic strength can be temporary or long lasting depending on what?

A

Depending on the intensity and reoccurrence of the signal the synapse receives

69
Q

How long does temporary/short term memory last?

A

Seconds to hours

70
Q

How long does long lasting/long term memory last?

A

Lifetime

71
Q

What are the 2 types of neuroplastic changes?

A

Temporary
Long-lasting

72
Q

What happens in short term memory?

A

Neurons can temporarily enhance their connections by chemical/synaptic changes

73
Q

What are the 3 chemical/synaptic changes in short term memory/

A

Releasing more neurotransmitter
Activating a new receptor
Modifying an existing receptor

74
Q

What does long term memory require?

A

Strong or sustained activities that produce structural changes

75
Q

How can neuroplastic changes be functional?

A

Neurons may adopt a new function when they are sufficiently stimulated

76
Q

What is the new growth and changes in structural long term memory?

A

Growth of new dendritic spines and synaptic connections
Changes in cortical area

77
Q

What is associated with increased activity?

A

Enlargement
(Shrinkage of areas that receive less or no activity

78
Q

The hippocampus is an important memory forming center, but it doesn’t do what?

A

Doesn’t store memories

79
Q

Where are long term memories consolidated and stored?

A

In various areas of the cerebral cortex

80
Q

What are the 2 forms of long term memory?

A

Explicit (declarative) memory

Implicit ( procedural or unconscious) memory

81
Q

What does explicit memory refer to?

A

The conscious recollection of facts

82
Q

What are the 2 types of explicit memory?

A

Semantic

Episodic

83
Q

What is semantic memory?

A

Facts and general knowledge

84
Q

What is episodic memory?

A

Personally experienced events

85
Q

What does implicit memory refer to?

A

The subconscious learning of skills, habits, or behaviors

These actions develop with practice over time
Your memory of how to do things

86
Q

What is long term depression (LTD)?

A

Long term weakening of a synaptic connection

87
Q

What is long-term potential (LTP)?

A

Is a persistent strengthening of a synaptic connection

88
Q

What happens in long term memory if a memory is no longer needed?

A

Its corresponding synapses will slowly weaken and eventually disappear

89
Q

What does long term depression allow for?

A

For unimportant connections to be lost and makes that synapses that have undergone LTP that much stronger by comparison

90
Q

What is long term potentiation caused by?

A

High frequency signals (strong experience)
Repeated stimulations (studying, stimulations)

91
Q

How are new memories formed in LTP?

A

When neurons establish new connections or strengthen existing synapses

92
Q

What rule does synaptic plasticity follow?

A

“Use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated

93
Q

How is the strength of a synapse measured?

A

By the level of excitability or responsiveness of the post-synaptic neuron in response to a give stimulus (NT) from the pre-synaptic neuron

94
Q

What is the main excitatory NT in the CNS?

A

The amino acid glutamate

95
Q

What are the 2 main glutamate receptors that often coexist in a synapse?

A

AMPA and NMDA receptors (ligand gated ion channels)

96
Q

What role do AMPA and NMDA play?

A

Major role in synaptic plasticity

97
Q

What can calcium entry through polysynapttic NMDA receptors initiate?

A

Initiate 2 different forms of synaptic plasticity: LTP and LTD but also excitotoxicity (excessive Ca2+ influx)

98
Q

What does excessive NMDAR activity cause?

A

Causes excitotoxicity and promote cell death

99
Q

What is excessive NMDAR activity an underlying issue of?

A

Underlying a potential mechanisms of neurodegeneration occurred in Alzheimer’s disease

100
Q

What does LTD induce?

A

Dendritic spine shrinkage and synaptic loss

101
Q

What does the calcium that does not flow through NMDA receptors initiate?

A

Initiates a different cellular cascade (phosphates)

102
Q

What type of firing rate does the presynaptic neuron have?

A

Low firing rate

103
Q

Why is the postsynaptic neuron less responsive to glutamate?

A

Less receptor available

BIO 203 (6 decks)

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