lecture 12 modulation Flashcards

(37 cards)

1
Q

things that can cause synaptic strength to change

A

diseases (myasthenia gravis, startle disease)
drugs (therapeutic, recreational)
prior or ongoing activity (experience changes thoughts and actions by altering synaptic function

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2
Q

what mechanisms lead to altered synaptic strength

A

addition or loss of synaptic connection
(can take hours to occur)

growth or shrinkage of synapse
(synaptic current directly proportional to number of open receptors)

rapid change in synaptic efficacy with no structural change
(no new proteins)

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3
Q

how to measure synaptic strength between 2 neurons

A

1) stimulate axon with electricity
2) fires action potential
3) releases neurotransmitters
4) epsp detected by recording electrode in post synaptic cell

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4
Q

how is facilitation different from temporal summation

A

facilitation piggybacks but the amplitude gets bigger every time and the second one starts after the first has gone back to rest (presynaptic because it relies on residual calcium)
vs
temporal summation where the epsps piggyback on top of each other and the next one starts before the first one has ended (postsynaptic because it relies on open lgic)

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5
Q

spatial summation

A

several weaker signals from different locations vs temporal several weak signals from one source that add up

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6
Q

facilitation increases quantal content why

A

the residual calcium hypothesis- ca enters to trigger neurotransmitter release then is removed
when second stimulus arrives soon after the first, new ca enters before the initial pulse is fully removed

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7
Q

this causes smaller synaptic potentials with repetitive stimulation

A

short term depression

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8
Q

ionotropic receptors

A

fast, ion channels

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9
Q

metabotropic receptors

A

slower, ligand gated, can activate a g proteins

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10
Q

g protein coupled receptors steps

A

1) binding of neurotransmitter to the extracellular receptor protein
2) activation of g proteins
3) activation of effector systems

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11
Q

secondary messengers

A

the activated proteins are enzymes that generate small molecules (second messengers like cyclic amp)
camp activates protein kinase a (pka) which phosphorylates proteins by adding phosphate groups and changes the properties of the proteins so it can activate other proteins

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12
Q

the 3 general second messenger systems that interact with specific g proteins

A

increases camp (gs)
decreases camp (gi/go)
stimulates phospholipase c, dag, ip3, pkc

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13
Q

opiate receptors are…

A

GPCRs and the ligands are small peptides called enkephalins and endorphins

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14
Q

pain modulation by opiate receptors

A

drg cells sense pain
spinal interneuron releases enkephalin
enkephalin binds GPCR
g protein (go) inhibits VGca channel
less neurotransmitter release when activated (weaker pain signals w opioid receptor activation)

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15
Q

aplysia

A

giant sea slug that has simple nervous system and large neurons, stereotyped behaviors

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16
Q

habituation

A

repetitive stimulation leads to decreased response

17
Q

what does habituation lead to

A

smaller epsps, decreased quantal content due to short term depression

18
Q

sensitization

A

intensified response after harmful stimulus

19
Q

Synaptic Strength

A

the average change in membrane potential of a postsynaptic neuron
elicited by a presynaptic action potential

20
Q

changes in strength or efficacy of neuronal connections. Can be
caused by a variety of physiologic and signaling mechanisms at time scales that vary from ms
to days or longer

A

Synaptic modulation

21
Q

Short-term plasticity

A

a change in synaptic
strength (time scale of milliseconds to
seconds) caused by presynaptic mechanisms
which alter the quantal content (average # of
vesicles released by one presynaptic action
potential

22
Q

Facilitation

A

increased synaptic strength
(EPSP amplitude) apparent after two or more
presynaptic action potentials. Caused by
elevation of residual Ca2+ in the presynaptic
termina

23
Q

Short-term depression

A

decreased synaptic
strength (EPSP amplitude) apparent after two
or more pre-synaptic action potentials.
Caused by depletion of vesicles from the
presynaptic terminal

24
Q

Ionotropic receptor

A

a neurotransmitter-gated ion channel which directly leads to changes in
membrane potential

25
Metabotropic receptor
a neurotransmitter receptor that effects neuron excitability or membrane potential indirectly through intracellular signaling cascades
26
Neuropeptides
large classification of neurotransmitter molecules that are made up of a short polypeptide chain. Neuropeptides active GPCRs (see below) for diverse effects on varying timescales.
27
G-protein coupled receptor (GPCR)
Type of metabotropic receptor with 7 transmembrane domains that interacts with G proteins. GPCRs are a diverse group with each subtype activated by one of a variety of ligands (light, specific neuropeptides, sugars, or lipids)
28
Second messenger
one of the intracellular signaling molecules that is activated by an extracellular signal (i.e. activation of GPCR) and triggers a signaling cascade to alter a neuron’s excitability or physiology
29
Aplysia
a type of sea slug used as an experimental animal to study the molecular underpinnings of behavioral learning or plasticity. A relatively simple circuit causes a reflexive retraction of the gills when the animal’s siphon is touched. This response and the underlying synaptic strengths can be modulated
30
Habituation
a decrease in the magnitude of behavioral responses to repeated stimuli. In Aplysia, repeated stimulation of the siphon causes a reduced gill retraction after multiple stimulations. This is due in part to a decrease in the synaptic strength between the sensory and motor neurons
31
Habituation
a decrease in the magnitude of behavioral responses to repeated stimuli. In Aplysia, repeated stimulation of the siphon causes a reduced gill retraction after multiple stimulations. This is due in part to a decrease in the synaptic strength between the sensory and motor neurons
32
Sensitization
an increase in the magnitude of a behavioral response to a stimulus after a separate, often noxious stimulus has been applied. In Aplysia, pairing a shock to the tail with stimulation of the siphon, causes a increase in gill retraction when then stimulating the siphon alone
33
Heterosynaptic plasticity
when synaptic strength between two neurons maybe be regulated by a third neuron/synapse. (e.g. sensitization in Aplysia)
34
Know the mechanisms underlying synaptic facilitation and short-term depression and be able to graph the effects of each on EPSPs
35
Predict how changes in the presynaptic terminal and [Ca2+] affect the magnitude of the EPSP
36
Explain the differences between slow and fast synaptic responses, including any advantages of slow, metabotropic signaling
37
Diagram how a synapse can be purely modulatory including mechanisms that would either increase (potentiate) or decrease (depress) a post synaptic response