midterm 2 Flashcards

1
Q

forms of short term synaptic plasticity resulting from repeated neuron stimulation

A

synaptic facilitation- residual calcium causes extra NT release.
synaptic depression- depletion of NT vesicles so they cant be used as fast
post tetanic potentiation- increase in efficacy due to repeated synaptic activity
augmentation- like potentiation, but much shorter and faster.

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2
Q

habituation

A

decreased response with repeated or prolonged exposure to the same stimulus.

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3
Q

sensitization

A

increased response to noxious stimulus

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4
Q

How does pairing siphon touch with tail shock modify the presynaptic neuron?

A

A facilitator neuron releases serotonin, which activates a G-protein-coupled receptor (GPCR) in the presynaptic neuron.

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5
Q

What is the role of serotonin in sensitization?

A

Serotonin activates GPCR, which stimulates adenylyl cyclase to produce cAMP, leading to activation of PKA. PKA phosphorylates a K⁺ channel, reducing its probability of opening, which prolongs depolarization in the presynaptic neuron.

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6
Q

Why does prolonged depolarization lead to increased neurotransmitter release?

A

More Ca²⁺ influx occurs due to the extended depolarization, increasing neurotransmitter release.

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7
Q

Why is short-term sensitization temporary?

A

The potassium channels eventually become dephosphorylated, and the increased neurotransmitter release returns to normal.

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8
Q

What molecular change converts short-term sensitization into long-term sensitization?

A

Persistent PKA phosphorylates CREB, a transcription factor that promotes gene expression.

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9
Q

What role does ubiquitin hydrolase play in long-term sensitization?

A

It degrades regulatory subunits of PKA, keeping PKA persistently active and sustaining phosphorylation effects.

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10
Q

REVIEW NMDA receptor

A
  • Permeable to Na+, K+ and Ca2+
  • Mg2+ block at resting membrane potential
  • postsynaptic depolarization relieves Mg2+ block
  • Requires a co-agonist glycine
  • Requirement of glutamate plus depolarization
  • Some Glutamatergic synapses have only AMPA/Kainate or NMDA receptors
  • Most have both AMPA and NMDA
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11
Q

what is a silent synapse

A

In utero there are synapses in the brain that have only NMDA receptors and no AMPA receptors. This means the synapse could not be activated as there would be no depolarization from the AMPA receptor. The silent synapses are turned on by the addition of AMPA receptors.

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12
Q

What is Long-Term Potentiation (LTP)?

A

LTP is a long-lasting increase in synaptic strength following high-frequency stimulation of synapses.

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13
Q

What hippocampal pathway is involved in LTP?

A

The trisynaptic circuit, including CA1 pyramidal neurons and Schaffer collaterals.

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14
Q

How is LTP induced experimentally

A

A brief high-frequency train of stimuli (tetanus) results in increased EPSP amplitude.

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15
Q

What happens when a tetanic stimulus is applied to one pathway?

A

Only that pathway shows increased synaptic response; unstimulated pathways remain unchanged.

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16
Q

schaffer collateral and presynaptic and postsynaptic dependency

A

Presynaptic stimulation alone is insufficient—LTP occurs when postsynaptic depolarization coincides with presynaptic activity.

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17
Q

What does it mean that LTP is synapse/input specific

A

When LTP is induced by activating one synapse, it does not occur in another. Therefore, each of the thousands of synapses of a neuron can store information

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18
Q

What is Associativity in LTP?

A

A weak stimulus alone does not induce LTP, but if a nearby synapse is strongly stimulated simultaneously, the weakly stimulated synapse is strengthened (slug)

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19
Q

What receptor is required for LTP induction?

A

NMDA receptors for Ca influx

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20
Q

How does AMPA receptor trafficking contribute to LTP

A

1.AMPA receptors are stored in recycling endosomes.
2.Synaptotagmin, activated by Ca²⁺, inserts AMPA receptors into the synapse.
3.More AMPA receptors = Stronger postsynaptic response to glutamate.

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21
Q

How do kinases contribute to LTP

A

calcium activates CaMKII and PKC phosphorylate AMPA receptors, increasing their conductance and insertion into the synapse.

22
Q

What retrograde signal strengthens the presynaptic response in LTP?

A

NO enhances presynaptic glutamate release

23
Q

How does LTP lead to long-term structural changes?

A

Persistent PKA activation leads to CREB-mediated gene expression, forming new synapses.

24
Q

What is the key difference between LTP and LTD regarding Ca²⁺ signaling?

A

LTP: Large, fast Ca²⁺ influx activates kinases.
LTD: Small, slow Ca²⁺ increase activates phosphatases, leading to AMPA receptor internalization.

25
How does LTD occur in the cerebellum
When climbing and parallel fibers are stimulated together, LTD occurs at the parallel fiber-Purkinje cell synapse.
26
What is the signaling pathway for cerebellar LTD
-Glutamate released from Climbing and Parallel fibers -Activates AMPA and mGlu receptors on postsynaptic Purkinje neuron dendrites. -mGlu receptors activate PLC. IP3 and DAG generated -Spreading depolarization from Climbing fiber opens voltage-gated Ca2+ channels leads to Ca2+ influx -Voltage-gated calcium channel together with IP3 activate IP3 receptors on ER – Ca2+ potentiates IP3 mediated Ca2+ release from the endoplasmic reticulum -PKC activated by Ca2+ from 2 sources and DAG -PKC phosphorylates protein targets, triggering internalization of AMPA receptors -Fewer AMPA receptors at synapse - Parallel fiber synapse weakened: LTD
27
What is Spike Timing-Dependent Plasticity (STDP)?
STDP is a form of synaptic plasticity where the timing of presynaptic and postsynaptic spikes determines whether a synapse is strengthened (LTP) or weakened (LTD).
28
How does the timing of spikes determine whether LTP or LTD occurs?
Presynaptic spike → Postsynaptic spike (within ~20 ms): LTP occurs (synaptic strengthening). Postsynaptic spike → Presynaptic spike: LTD occurs (synaptic weakening). follows the rules: If the presynaptic neuron fires first, it likely contributed to the postsynaptic firing → Strengthen the synapse (LTP). If the postsynaptic neuron fires first, it suggests the presynaptic neuron was less important → Weaken the synapse (LTD).
29
5 classes of cells in the retina
photoreceptors bipolar cells ganglion cells horizontal cells amacrine cells
30
What happens to rods and cones when they are activated by light?
Light hyperpolarizes rods and cones, reducing neurotransmitter release. In darkness, they remain depolarized due to open cGMP-gated channels, which close upon light activation.
31
What is the first molecular event that occurs when light hits the photoreceptor
Retinal (inside opsin) undergoes photoisomerization, changing from cis to trans, activating rhodopsin.
32
What is the phototransduction cascade
Photon absorption → cis-retinal → trans-retinal Activates rhodopsin Rhodopsin activates transducin Transducin activates phosphodiesterase (PDE) PDE breaks down cGMP Less cGMP = cGMP-gated channels close Hyperpolarization = Less NT release
33
How is the phototransduction signal turned off?
Rhodopsin kinase phosphorylates rhodopsin which allows arrestin binding Arrestin binds to rhodopsin, preventing further activation of transducin Trans-retinal is converted back to cis-retinal in the epithelial cells for reuse
34
How does the retina adapt to excessive light? (Photoadaptation)
Increased guanylate cyclase activity → More cGMP produced Increased rhodopsin kinase activity → More arrestin binding Increased cGMP-gated channel affinity for cGMP Reduced intracellular Ca²⁺, reducing sensitivity
35
How does phototransduction differ in invertebrates?
Unlike vertebrates, invertebrate photoreceptors depolarize in response to light. Some invertebrates, like octopi, have photoreceptors on their arms.
36
how does trans retinal get transformed back to cis retinal
Trans retinal gets turned back to cis retinal by a chaperone protein that moves it into the epithelial cell to get turned back.
37
on center ganglion cell
increases firing of action potentials as light is increased in the receptive field
38
off center ganglion cell
decreases firing of action potentials as light is decreased
39
on vs off bipolar cells
on bipolar cell has mglu receptors, off has ampa kainate receptors.
40
why is glutamate received differently in on and off bipolar cells
on bipolar cells have mglu receptors which give an inhibitory response in the bipolar cell whereas off bipolar cells have AMPA receptors which give an excitatory response in the bipolar cell.
41
neurons visual receptive field
For a photoreceptor, the receptive field is a point of light in the visual field that falls on the outer segment on the photoreceptors
42
foveation
shifting your gaze so that any new object of interest in the visual field is on the fovea.
43
saccades
quick ballistic eye movements used to align the fovea with a particular part of a scene
44
otolith organs: utricle and saccule
detect translational accelerations of the head and head position related to gravity. utricle is horizontal saccule is vertical
45
semicircular canals
detect rotational accelerations of the head
46
otolith organs structure
sensory epithelium (macula) consisting of hair cells and supporting cells, gel layer over hair cells, calcium carbonate crystals (otoconia) for weight.
47
what happens in the semicircular canal when you tilt your head
there is a viscous liquid that lags behind as you bend your head which causes hair cells to bend and cause changes in polarization.
48
3 major classes of reflexes vestibular system participates in
1. maintain gaze during movement 2. maintain/adjust body posture 3. maintain muscle tone
49
vestibulor-ocular reflex (VOR)
helps maintain steady image on retina during body movements. driven by vestibular input. for example, right rotation of the head causes compensatory eye movements to the left.
50
optokinetic reflex
holds image stable on retina during sustained head movements/rotations, is driven by visual stimuli “retinal slip”, and results in eye stabalization on the visual scene.
51