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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
What are metabotropic receptors?
G-protein coupled receptors
26
What are ionotropic receptors composed of?
3-5 protein subunits that form a pore
27
What do NTs binding to ionotropic receptors do?
They open the pore and directly induce ion fluxes
28
What do metabotropic receptors affect?
Affect channels by the activation of intermediate molecules called G-proteins
29
What can G-proteins activate?
The production of second messenger molecules
30
How does synaptic transmission finish? (3 ways)
Via NT transporters on the plasma membrane Diffusion/Absorption Degradation Reuptake
31
What is diffusion/absorption?
NT diffuse away from the synaptic cleft and are returned to presynaptic neuron
32
What is degradation?
NT are degraded by enzymatic reactions in the synaptic cleft
33
What is reuptake?
NTs are taken back into the presynaptic neuron
34
What does the monoamine hypothesis of depression suggest?
Suggests that depression was associated with a deficiency of monoamines such as serotonin and norepinephrine
35
How well are the causes of depression understood?
They are poorly understood
36
What are the steps in how serotonin works in the synapse?
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
37
Hero do neurons of the substantia nigra communicate with neurons of the basal ganglia?
By liberating the NT dopamine
38
What is this biochemical interaction responsible for?
Voluntary movement coordination of the body
39
Which NT is association with Parkinson’s disease and how?
Neurons of the substantia nigra degenerate
40
What happens with this degeneration?
Slowness or a sense of movement, rigidity and a resting tumor (especially in the hands and fingers)
41
What has been a central dogma for schizophrenia for decades?
The mesolimbic hypothesis
42
What does the mesolimbic hypothesis state?
Aberrant functioning of the midbrain dopamines projections to limbic regions causes psychotic symptoms
43
What are examples of positive symptoms in schizophrenia?
Hallucinations Delusions
44
What are negative/cognitive symptoms of schizophrenia?
Lack of motivation, cognitive impairment
45
What is the receptor in positive symptoms?
D2 (hyper-)
46
What is the receptor in negative/cognitive symptoms?
D1 (hypo-)
47
What is the brain region of positive symptoms?
Limbic system (nucleus accumbens)
48
What is the brain region of negative symptoms?
Prefrontal cortex
49
What are the 4 dopaminergic pathways in the brain?
Mesocortical Mesolimbic Tuberoinfundibular Nigrostriatal
50
What is the mesocortical pathway responsible for?
Cognition and executive function (planning) Emotions and affect
51
How does the mesocortical pathway relate to schizophrenia?
Decreases D1 - negative symptoms (apathy)
52
What is the function of the mesolimbic pathway?
Regulates limbic function or motivation, and reward
53
How does the mesolimbic pathway relate to schizophrenia?
Increases D2 - positive symptoms like hallucinations
54
What is the nigrostriatal pathway responsible for?
Motor movement
55
What will decreased or increased activity produce in the nigrostriatal pathway?
Produce movement abnormalities Hypokinetic: Parkinson’s symptoms Hyperkinetic: movement disorders
56
What is the function of the tuberoinfundibular pathway?
Inhibition of prolactin release
57
Where does the tuberoinfundibular project from?
From the hypothalamus to the anterior pituitary gland
58
What is the disorder of the tuberoinfundibular pathway?
Decreased DA: hyperprolactinemia
59
Which inhibitory NT is associated with epilepsy?
GABA
60
How does GABA external its inhibitory effects through the GABAa receptor?
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
What has AD progression been associated with?
Gradual damage in function and structure in the hippocampus and neocortex, the vulnerable brain areas used for memory and cognition
62
Acetylcholine acts on target neurons in the _____ and the ____
Hippocampus Neocortex
63
What does this do?
Strengthening the neural circuits that are involved in memory formation
64
What does the cholingeric hypothesis of Alzheimer’s postulate?
It centers on the progressive loss of limbic and neocortical cholingeric innervation
65
What is neuroplasticity?
The ability of the brain to change, or reward, throughout a person’s life
66
What is synaptic plasticity?
The process of neuroplasticity occurring at the single cell level (Individual synapse)
67
What is synaptic plasticity the basis of?
Basis of learning and brain repair after injuries
68
Changes in synaptic strength can be temporary or long lasting depending on what?
Depending on the intensity and reoccurrence of the signal the synapse receives
69
How long does temporary/short term memory last?
Seconds to hours
70
How long does long lasting/long term memory last?
Lifetime
71
What are the 2 types of neuroplastic changes?
Temporary Long-lasting
72
What happens in short term memory?
Neurons can temporarily enhance their connections by chemical/synaptic changes
73
What are the 3 chemical/synaptic changes in short term memory/
Releasing more neurotransmitter Activating a new receptor Modifying an existing receptor
74
What does long term memory require?
Strong or sustained activities that produce structural changes
75
How can neuroplastic changes be functional?
Neurons may adopt a new function when they are sufficiently stimulated
76
What is the new growth and changes in structural long term memory?
Growth of new dendritic spines and synaptic connections Changes in cortical area
77
What is associated with increased activity?
Enlargement (Shrinkage of areas that receive less or no activity
78
The hippocampus is an important memory forming center, but it doesn’t do what?
Doesn’t store memories
79
Where are long term memories consolidated and stored?
In various areas of the cerebral cortex
80
What are the 2 forms of long term memory?
Explicit (declarative) memory Implicit ( procedural or unconscious) memory
81
What does explicit memory refer to?
The conscious recollection of facts
82
What are the 2 types of explicit memory?
Semantic Episodic
83
What is semantic memory?
Facts and general knowledge
84
What is episodic memory?
Personally experienced events
85
What does implicit memory refer to?
The subconscious learning of skills, habits, or behaviors These actions develop with practice over time Your memory of how to do things
86
What is long term depression (LTD)?
Long term weakening of a synaptic connection
87
What is long-term potential (LTP)?
Is a persistent strengthening of a synaptic connection
88
What happens in long term memory if a memory is no longer needed?
Its corresponding synapses will slowly weaken and eventually disappear
89
What does long term depression allow for?
For unimportant connections to be lost and makes that synapses that have undergone LTP that much stronger by comparison
90
What is long term potentiation caused by?
High frequency signals (strong experience) Repeated stimulations (studying, stimulations)
91
How are new memories formed in LTP?
When neurons establish new connections or strengthen existing synapses
92
What rule does synaptic plasticity follow?
“Use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated
93
How is the strength of a synapse measured?
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
What is the main excitatory NT in the CNS?
The amino acid glutamate
95
What are the 2 main glutamate receptors that often coexist in a synapse?
AMPA and NMDA receptors (ligand gated ion channels)
96
What role do AMPA and NMDA play?
Major role in synaptic plasticity
97
What can calcium entry through polysynapttic NMDA receptors initiate?
Initiate 2 different forms of synaptic plasticity: LTP and LTD but also excitotoxicity (excessive Ca2+ influx)
98
What does excessive NMDAR activity cause?
Causes excitotoxicity and promote cell death
99
What is excessive NMDAR activity an underlying issue of?
Underlying a potential mechanisms of neurodegeneration occurred in Alzheimer’s disease
100
What does LTD induce?
Dendritic spine shrinkage and synaptic loss
101
What does the calcium that does not flow through NMDA receptors initiate?
Initiates a different cellular cascade (phosphates)
102
What type of firing rate does the presynaptic neuron have?
Low firing rate
103
Why is the postsynaptic neuron less responsive to glutamate?
Less receptor available

BIO 203 (6 decks)

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