Lecture 2 Flashcards

Neuronal Synapses

1
Q

What is a synapse?

A

Where a neuron transfers
information to 1 or more
other neurons or a muscle

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2
Q

3 parts of a synpase

A
  1. presynaptic cleft
  2. synaptic cleft
  3. postsynaptic cleft
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3
Q

types of synapse

A

axodendritic, axosomatic, axoaxonic

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4
Q

Axodendritic synapse

A

axon to dendrites

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5
Q

Axosomatic syapse

A

axon to soma (body of the neuron)

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6
Q

Axoaxonic synapse

A

axon to axon

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7
Q

If synapse is neuromuscular, axosomatic, or axodendritic, the ions
flowing thru _____-_____ _____ cause local membrane
potentials.

A

ligand-gated channels

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8
Q

where does the presynaptic effect occur?

A

axoaxonic synapse

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9
Q

steps of synaptic transmission

A
  1. AP comes to the presynaptic terminal
  2. voltage-gated Ca2+ channels open
  3. Ca2+ ions directly trigger the movement of neurotransmitter vesicles.
  4. vesicles fuse with the presynaptic membrane –> release neurotransmitters to the synaptic cleft via exocytosis.
  5. neurotransmitters spreads across cleft
  6. neurotransmitter binds to appropriate postsynaptic receptors–>altering its shape AND:
    - opens associated ligand-gated ion channel OR
    - triggers associated intracellular messengers
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10
Q

Each neuron can have different numbers of inputs in each region. (T/F)

A

True

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11
Q

Strong excitatory stimuli in the presynaptic neuron lead to more action potentials (APs). (T/F)

A

True

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12
Q

The total number of APs that reach the presynaptic terminal directly relates to the amount of neurotransmitter released. (T/F)

A

True

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13
Q

Longer stimulation duration in the presynaptic cell results in a longer series of APs. (T/F)

A

True

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14
Q

EPSP

A

Excitatory postsynaptic potential
- Local depolarization occurs with flow of Na+ or Ca2+ into neuron
- Summation of EPSPs facilitates AP generation.
- Common throughout CNS and PNS

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15
Q

IPSP

A

Inhibitory postsynaptic potential
- Local hyperpolarization occurs with influx of Cl- into or K+ out of neuron.
- Summation with EPSPs determines if AP is generated or not

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16
Q

Synaptic integration occurs through

A

summation

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17
Q

Summation includes

A

of EPSPs and IPSPs

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18
Q

During presynaptic facilitation, 1st presynaptic neuron releases neurotransmitters that
causes slight local ________ of 2nd neuron’s
presynaptic terminal.

A

depolarization

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19
Q

During presynaptic facilitation, when APs arrive, AP duration increases allowing more
_____ influx and vesicles of neurotransmitter to move and
be released.

A

Ca2+

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20
Q

During presynaptic inhibition, 1st causes slight local _________.

A

hyperpolarization

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21
Q

During presynaptic inhibition, when APs arrive, AP duration decreases allowing less ______ influx and less neurotransmitter release.

A

Ca2+

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22
Q

Chemicals that transmit messages among neurons
- can be facilitative and inhibitory

A

neuromessengers

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23
Q

types of neuromessengers

A

neurotransmitters and neuromodulators

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24
Q

Neurotransmitters location of action

A

synapse

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25
Neurotransmitters method of action
EPSP or IPSP
26
Neurotransmitters time
ms to mins
27
neuromodulators location of action
extracellular space
28
neuromodulators method of action
alter gene expression open ion channels change metabolism affects many neurons
29
neuromodulators time
mins to days
30
same chemical can function as neurotransmitter or neuromodulator but depends on:
- if released at specific synapses or into extracellular space - what part of nervous system it is released in
31
Neurons can contain more than 1 neurotransmitter but can release only 1 type at a time. (T/F)
False - Neurons can contain more than 1 neurotransmitter and can release different types at a time
32
Receptors are name for what?
Neurotransmitters that bind to them
33
Most neurotransmitters can bind to different kinds of receptors. (T/F)
True
34
What is the effect of neurotransmitters related to?
Type of receptor Not the kind of chemical it is
35
Mechanisms receptors use to transducer signals
Ligand-gated ion channels (fast response) - also called ionotropic receptor G protein triggering of ion channels (slow) - also called metabotropic receptor
36
What is the lock and key analogy?
For the binding to occur, the neurotransmitters (key) must fit the receptor site (lock). One “key” might fit multiple “locks”
37
Ligand-gated ion channels
(fast response) - also called ionotropic receptor Made up of proteins that act as neurotransmitter receptors and as ion channels
38
At rest, Ligand-gated ion channels are _______ (open/close)
Closed
39
What happens when a specific neurotransmitter binds to postsynaptic receptors (ligand-gated)?
The gates open Specific ions flow in/out depending on their electrochemical gradient across neuron’s membrane
40
Ligand-gated ion channels are both excitatory and inhibitory. (T/F)
True
41
What are some other characteristics of Ligand-gated ion channels?
Most open/close rapidly when neurotransmitters are in the cleft Some have shut off mechanism Other become inactive when neurotransmitter is no longer in synaptic cleft due to binding at postsynapting receptors or resorption at presynaptic terminals
42
G protein (guanine nucleotide) activation of ion channels happens by
G proteins altering electrical excitability of neurons Subunits if G protein move between neurotransmitter receptors and specific ion channels
43
When neurotransmitter binds go G protein receptor:
1. Receptor protein alters its shape and internal G protein is triggered. 2. G protein subunit breaks away, moves, and binds to membrane ion channel. 3. Ion channel changes shape and opens
44
What is the G protein 2nd messenger system?
When neuromodulator binds at extracellular receptor, it initiates a sequence of intracellular events with G protein as 2nd messenger
45
Neuromodulator is the 1st messenger and chemical produced inside the neuron is the 2nd messenger. (T/F)
True
46
Cascade of events in the G protein 2nd messenger system
1. Cell produces neurotransmitters or other cellular products due to activation of genes. 2. Opens ion channels. 3. Releases Ca2+ to regulate metabolism and other processes.
47
Abnormalities in the G protein 2nd messenger system can lead to
Mental illness, mood disorders, Parkinson’s, Alzheimer’s, and others
48
Agonist
Drugs that bind to receptors and copy actions of neurotransmitters
49
Antagonist
Drugs that block the binding of neurotransmitters to receptors OR drugs that inhibit the release of neurotransmitters in presynaptic neurons Ex. Caffeine
50
Common neurotransmitters
Acetylcholine (Ach) Glutamate (amino acid) Y-aminobutyric acid (GABA) (amino acid) Dopamine (amines) Norepinephrine (amines) Serotonin (amines) Substance P (peptide)
51
Where is acetylcholine produced
Basal forebrain and midbrain
52
Functions related to Acetylcholine in regards to skeletal muscles
all neurons that synapse with skeletal muscles use Ach to elicit fast-acting effects on muscle membranes It is excitatory neurotransmitter found in neuromuscular junctions to promote muscle contractions
53
Blocking Ach receptors in skeletal muscles can cause
Weakness, fatigue or paralysis
54
What destroys Ach receptors
Myasthenia gravis
55
Ach in autonomic nervous system
Slows HR constricts pupils Increases smooth muscle contractions and digestive processes
56
Ach in brain
Arousal, pleasure, cognitive function Acts as slow neuromodulator in control of movement and attention Implicated in nicotine addictive and Alzheimer’s disease
57
Glutamate is associated with
Principle fast excitatory neurotransmitter of CNS Virtually in every brain region Neural changes with learning and development
58
What if you have excessive glutamate?
Excitotoxicity and neuron death Epileptic seizure
59
Glutamate levels must be closely regulated because
Changes in transmission implicated in chronic pain, Parkinson’s, schizophrenia, and neuron death in acute stroke
60
Glycine
Inhibits post synaptic membranes mostly in brain stem and spinal cord
61
y-aminobutyric acid (GABA)
Primary inhibitory neurotransmitter in CNS, especially with interneurons in spinal cord
62
Functions of glycine and y-aminobutyric acid (GABA)
Low levels implicated in seizure, unwanted or involuntary muscle concentrations or anxiety Alcohol, barbiturates, benzodiazepines, anticonvulsant, and baclofen mimic GABA Huntington’s disease causes loss of neurons in striatum that use GABA with jerky involuntary movements and cognitive decline.
63
Where is dopamine produced?
Substantia migraine of brain
64
Dopamine affects
Motor function, cognition/attention, and behavior
65
Dopamine is associated with _______ _______ behaviors
reward seeking Can be good for eating, bad leading to addition
66
What are the receptors for dopamine
All are 2nd messenger system
67
Abnormalities in dopamine seen in
1. Parkinson’s (not enough produced with bradykinesia and other symptoms present - precursors to dopamine given medically) 2. Schizophrenia or psychoses - signaling pathways (drugs that prevent binding to receptors to alter thinking also impact motor function - tardive dyskinesia) 3. Excessive dopamine levels seen in cocaine or amphetamine abuse by preventing reuptake by presynaptic terminals 4. ADHD is associated with dysfunction and medications block re-uptake
68
Where is norepinephrine produced?
Brainstem, hypothalamus, and thalamus
69
What cells release norepinephrine?
Neurons of ANS and secreted by adrenal glands
70
What is norepinephrine responsible for?
Vigilance and “fight or flight”
71
Norepinephrine in excessive levels can cause
Over activity of system —> fear and panic Excessive NE found in people with PTSD Beta blockers reduce sympathetic nervous system activity seen when stressed
72
Low levels of norepinephrine:
sleeping and depression
73
Serotonin is involved in
mood, pain perception, arousal, motor activity
74
High levels of serotonin is seen when
alert
75
lowest serotonin level seen during
REM sleep and depression
76
Receptors for serotonin are some ______ & some ______ allowing different ways to respond to neuromodulator.
2nd messenger systems; ligand-gated
77
what do drugs for depression do?
selectively block receptors to keep more serotonin available
78
Endogenous opioid peptides include:
endorphins, enkephalins, and dynorphins
79
where are opioid peptides produced? what receptors do they bind?
within nervous system and bind same receptors as opium
80
where are the opioid peptide receptors mostly found? what do they do?
spinal cord, hypothalamus, and areas in brainstem; inhibit perception of pain
81
what does substance P do in the case of tissue injury?
stimulates nerve endings at injury site
82
what does substance P do as a neurotransmitter? where does it act as a neurotransmitter?
acts in CNS carrying information from spinal cord to brain
83
what does substance P do as a neuromodulator?
- pain syndromes - in hypothalamus & cerebral cortex - causing long duration excitation in postsynaptic neurons - modulates immune system and activity of neurons during times of high stress.
84
what are neuronal regulations of receptor activity?
Restriction # of receptors available increasing the # of receptors
85
how can we restrict the # of receptors available?
- internalize receptor into cell body: folds membrane and forms vesicle --> recycle or degraded and replaced - inactivate receptors: # of receptors unchanged - occurs with overstimulation of postsynaptic receptors
86
how can we increase # of receptors
- infrequent activation - low levels of neurotransmitter
87
In which synaptic function disorder do the antibodies inflict damage to voltage-gated Ca2+ channels in presynaptic terminal of neuromuscular junction?
Lambert-Eaton syndrome
88
In Lambert-Eaton syndrome, what happens?
- blockage of Ca2+ influx into terminal - decreased release of neurotransmitter - decreased muscle excitation - muscle weakness
89
In which disorder does the antibodies damage receptors on muscle cells?
Myasthenia Gravis
90
In Myasthenia Gravis, what happens?
- plenty of Ach is released but not enough places to bind. - repetitive muscle use causes muscle fatigue and weakness. - can be life threatening