L4 Flashcards
(111 cards)
1
Q
What determines the effect of a neurotransmitter on a post-synaptic neuron?
A
The receptor, not the neurotransmitter itself
2
Q
What are the two main types of post-synaptic receptors?
A
- Ionotropic receptors
- Metabotropic receptors
3
Q
What happens when a neurotransmitter binds to a receptor protein?
A
It causes a change in the shape of the receptor protein
4
Q
How do ionotropic receptors function?
A
They directly open ion channels when a ligand binds
5
Q
How do metabotropic receptors function?
A
They initiate a metabolistic cascade to activate enzymes
6
Q
What is a Post-Synaptic Potential (PSP)?
A
The change in post-synaptic membrane potential resulting from neurotransmitter binding
7
Q
How long does a typical PSP last?
A
About 20-40 ms (as long as transmitters are present)
8
Q
What causes an Excitatory Post-Synaptic Potential (EPSP)?
A
Ion channels specific for cations (Na+, K+) opening, causing depolarization
9
Q
What causes an Inhibitory Post-Synaptic Potential (IPSP)?
A
Ion channels specific for Cl- or K+ opening, causing hyperpolarization
10
Q
Why are nicotinic acetylcholine receptors considered “fast”?
A
Because binding and channel opening occur in the same protein complex
11
Q
What is the structure of nicotinic acetylcholine receptors?
A
They have a pore loop specific for cations and change from closed to open when acetylcholine binds
12
Q
What potential health benefit is associated with nicotinic receptors and smoking?
A
Smokers may be somewhat protected from Alzheimer’s disease
13
Q
What happens when acetylcholine binds to nicotinic receptors?
A
The channel changes from closed to open, allowing cations to pass through
14
Q
Why is the nicotinic receptor response considered “fast”?
A
Because binding and channel opening occur in the same protein complex
15
Q
What are the principal neurotransmitters that act on ionotropic receptors?
A
- Acetylcholine
- Glutamate
- GABA
- Glycine
16
Q
What determines the effect of a neurotransmitter in synaptic transmission?
A
The receptor, not the neurotransmitter itself
17
Q
What type of post-synaptic potential does GABA typically generate?
A
Inhibitory Post-Synaptic Potential (IPSP)
18
Q
What drug class enhances the effect of GABA?
A
Benzodiazepines
19
Q
What are the therapeutic effects of benzodiazepines?
A
Sedative, hypnotic, anti-anxiety, and muscle relaxant properties
20
Q
How do benzodiazepines work in the brain?
A
By increasing the efficiency of GABA to decrease neuronal excitability
21
Q
Can the same neurotransmitter act on both ionotropic and metabotropic receptors?
A
Yes, all the principal neurotransmitters can act on both receptor types
22
Q
What type of enzyme is typically activated by metabotropic receptors?
A
G-protein-coupled enzymes
23
Q
Name some common second messengers in metabotropic pathways
A
- cAMP
- cGMP
- InP3
24
Q
What do second messengers activate in metabotropic pathways?
A
Other enzymes like phosphokinases
25
How do phosphokinases affect ion channels?
They phosphorylate membrane proteins, modulating ion currents
26
Why are metabotropic effects slower than ionotropic effects?
They require time to go through enzymatic activity before influencing ion channels
27
What types of PSPs are associated with metabotropic receptors?
Slow EPSPs and slow IPSPs
28
Do metabotropic effects always change membrane potential?
No, they might only cause internal metabolic effects
29
What neurotransmitter activates β-adrenoreceptors?
Noradrenaline (NA)
30
What enzyme is activated when NA binds to β-receptors?
Adenylyl cyclase
31
What second messenger is produced in the β-adrenoreceptor pathway?
cAMP (cyclic AMP)
32
What do kinases phosphorylate in the β-adrenoreceptor pathway?
Membrane Ca++ channels
33
What is the effect of Ca++ channel phosphorylation in heart muscle?
Increased Ca++ influx, leading to increased contractility
34
How do beta-blockers work?
They block the interaction of noradrenaline with β-receptors
35
What is a non-medical use of beta-blockers?
Used by performers to reduce nervousness
36
What is the main difference between ionotropic and metabotropic effects?
Ionotropic effects are immediate (direct channel opening), while metabotropic effects are slower (enzyme cascade)
37
What type of receptor is the muscarinic acetylcholine receptor?
Metabotropic receptor
38
Name three peptides that act as ligands for metabotropic receptors
Substance P, β-endorphin, and ADH
39
Which catecholamines serve as ligands for metabotropic receptors?
Noradrenaline and dopamine
40
What purines can act as ligands for metabotropic receptors?
Adenosine and ATP
41
Which gases function as ligands for metabotropic receptors?
NO (nitric oxide) and CO (carbon monoxide)
42
Why can't PSPs initiate an action potential directly?
They're generated in inexcitable membrane areas with low density of voltage-gated Na+ channels
43
Where are PSPs generated in neurons?
In neuronal dendrites and cell bodies
44
What type of potential is a PSP?
A graded potential (not an action potential)
45
What happens to PSP voltage as it moves away from the synapse?
It loses voltage/amplitude (degrades)
46
Where is the first location in a neuron that can generate an action potential?
The trigger zone
47
Why are dendrites and cell bodies considered "inexcitable" areas?
They lack sufficient voltage-gated sodium channels to fire an AP
48
Where is the nearest excitable membrane located in a neuron?
At the beginning of the axon (trigger zone)
49
What happens if the trigger zone is depolarized to threshold?
It will fire an action potential
50
What is the significance of the trigger zone in neuronal signaling?
It's the first location that can generate an action potential
51
How do PSPs spread to reach the trigger zone?
Through passive conduction across the membrane
52
What initiates a PSP in the postsynaptic membrane?
Binding of neurotransmitter to receptors
53
What must happen for a PSP to trigger an action potential?
It must reach the trigger zone with enough depolarization to reach threshold
54
What type of potential is generated when neurotransmitter binds to the postsynaptic membrane?
An EPSP (a graded potential)
55
Why do biological tissues have poor signal transmission compared to telephone cables?
They have poor cable properties
56
What happens to PSP current as it travels along the membrane?
Loss of current/potential (signal degradation)
57
Why is a single EPSP usually not enough to trigger an action potential?
It degrades too much before reaching the trigger zone
58
How do neurons overcome PSP signal degradation?
By adding EPSPs together via summation
59
How does signal degradation in PSPs differ from action potentials?
APs don't degrade; PSPs lose strength as they travel
60
What are the two types of PSP summation?
- Spatial summation
- Temporal summation
61
What is spatial summation?
Large number of EPSPs occurring simultaneously (in synchrony) on the dendritic tree
62
How many synchronous EPSPs are typically needed for spatial summation?
Minimum of 10-30 synchronous EPSPs
63
What happens when individual EPSPs are too small to reach threshold?
When combined through spatial summation, they can reach threshold and trigger an action potential
64
What is temporal summation?
Few active synapses generating EPSPs at high frequency, with summated potentials reaching threshold over time
65
What is required for EPSPs to effectively sum in spatial summation?
They must overlap in time and act in synchrony
66
How do the graded potentials interact at the trigger zone during spatial summation?
They arrive together and sum to create a suprathreshold signal
67
What is the key difference between spatial and temporal summation?
Spatial uses many synapses simultaneously; temporal uses few synapses at high frequency
68
What happens after graded potentials sum at the trigger zone?
An action potential is generated
69
Why might a single EPSP fail to trigger an action potential?
Individual EPSPs are often below threshold and require summation to reach firing threshold
70
How long do EPSPs typically last before dying out?
About 30-40 ms (or 40-50 ms according to professor's notes)
71
What is the typical time interval between successive inputs in temporal summation?
About 10 ms apart
72
What visual pattern do successive EPSPs create in temporal summation?
A staircase effect
73
How many synapses are needed for temporal summation compared to spatial summation?
Few synapses (don't need many)
74
What is required of synapses for effective temporal summation?
High enough frequencies so new EPSPs can add on top of existing ones before they die out
75
What happens when subthreshold potentials arrive at the trigger zone within a short period?
They may sum and initiate an action potential
76
What is the end result of successful temporal summation?
A larger EPSP that can bring the trigger zone to threshold
77
What is the key timing requirement for temporal summation?
New inputs must arrive before previous EPSPs have time to die out
78
How does temporal summation help overcome the problem of signal degradation?
By building successive small EPSPs on top of each other to reach threshold
79
Where are IPSPs preferentially located?
On the cell soma, halfway between where EPSPs are generated and the trigger zone
80
What strategic advantage do IPSPs have due to their location?
They can shunt depolarizing EPSP currents out of the cell
81
What is the main function of IPSPs in relation to EPSPs?
They stop EPSPs from reaching the trigger zone
82
What ion channel is primarily involved in IPSPs?
Chloride (Cl-) channels
83
What is the equilibrium potential for Cl-?
Very close to the resting membrane potential (-70 mV)
84
What happens when Cl- channels open at resting membrane potential?
Little change occurs in the membrane potential
85
What happens when Cl- channels open during membrane depolarization?
They bring the membrane potential back down to -70 mV
86
Why are chloride ions more concentrated outside the cell?
They are repelled by negatively charged proteins inside the cell
87
What is the net effect of Cl- channel activation?
To "clamp" the membrane potential, preventing excitation and depolarization
88
How do strategically located IPSPs block signals from EPSPs?
By positioning directly on the soma between EPSPs and the trigger zone
89
What must happen to the membrane for IPSPs to be effective?
The membrane must become more negative
90
How do IPSPs contribute to information processing in neurons?
They provide precise control by blocking specific excitatory signals
91
Why are IPSPs considered more important than EPSPs in the nervous system?
They control and shape information processing with greater precision
92
How do IPSPs differ from EPSPs in terms of precision?
IPSPs tend to be very precise and accurate, while EPSPs are more general
93
What happens to neural inhibition when alcohol is consumed?
We lose our inhibition (neural control decreases)
94
What role do IPSPs play in information processing?
They provide control and shaping of information
95
What is a spike train?
A continuous stream of action potentials in response to a powerful, sustained input
96
How long can a powerful synaptic input last to generate a spike train?
Up to 500 ms
97
What happens to voltage-gated Na+ channels after an action potential fires?
They inactivate (enter refractory period)
98
What must happen to the membrane to generate multiple action potentials in a spike train?
It must be hyperpolarized between spikes
99
Why is hyperpolarization necessary for generating a spike train?
To restore/reactivate Na+ channels for the next action potential
100
What does a spike train signal to the brain?
That the stimulus is very powerful and long-lasting
101
What prevents continuous firing when the membrane is held above threshold?
Na+ channel inactivation during the refractory period
102
What must happen to the membrane potential before another action potential can fire?
It must repolarize below threshold
103
What problem must be overcome to generate a spike train?
The depolarization block, where voltage-gated Na+ channels become inactivated after the first action potential
104
What happens if you keep the trigger zone depolarized without a mechanism to overcome the block?
Only one action potential fires, then Na+ channels remain inactivated until the 500 ms depolarization ends
105
How do potassium channels help generate a spike train?
They open during depolarization, quickly repolarizing the membrane below threshold to reconfigure Na+ channels
106
What causes after-hyperpolarization in neurons?
Voltage-gated K+ channels at the trigger zone
107
What is the function of after-hyperpolarization following an action potential?
It ensures Na+ channels reconfigure and membrane excitability is restored
108
What happens after the hyperpolarization fades away?
The membrane potential can quickly return to threshold, allowing another spike to fire
109
Why is after-hyperpolarization necessary for generating a spike train?
Without it, Na+ channels would remain inactivated during sustained depolarization
110
What type of stimulus results in a spike train?
A very strong and long-lasting stimulus (approximately 500 ms).
111
What closes the voltage-gated K+ channels after hyperpolarization?
They close when the membrane is repolarized
