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BIOM 3400 > M2 Material > Flashcards

M2 Material Flashcards

1
Q

What cytoskeletal component makes up the space under the PSD

A

Actin

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2
Q

What is endocytic zone

A

Area neighboring PSD, hot spots for nt receptor endocytosis

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3
Q

Types of glutamate receptors? Subtypes of ionotropic?

A
  • Ionotropic (ligand-gated) (NMDA, AMPA, Kainate)
  • Metabotropic (G protein-coupled)
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4
Q

AMPA receptors:

A
  • they are responsible for bulk of fast excitatory synaptic transmission through CNS, their modulation is mechanism that underlies plasticity of excitatory neurotransmission in brain
  • can increase postsynaptic response to stimulus by: increasing amount of AMPA receptors, or increasing channel conductance (how long they’re open for)
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5
Q

NMDA receptors:

A
  • inactive at resting membrane potentials because pf voltage-dependent block of channel pore by Mg ions, preventing ions from flowing through
  • sustained activation of AMPA receptors , depolarizes postsynaptic cells, releasing channel inhibition and allowing NMDA activation
  • unlike AMPA receptors, NMDA receptors are permeable to calcium ions (and other ions). So NMDA receptor activation leads to a calcium influx into postsynaptic cell, a signal that is instrumental in the activation of a number of signaling cascades
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6
Q

Kainate receptors:

A
  • been implicated in epilepsy
  • important in synaptic plasticity, shown to be important in LTP.
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7
Q

G-protein coupled receptors:

A

INSERT IMAGE alpha subunit, depending on which G protein can activate 3 diff signaling pathways:
1. Alpha s activates adenyl cyclase, more cAMP, activate PKA, phosphorylates PKA targets

  1. Alpha I has opposite effect, inhibits adenyl cyclase, effects on ion channels and proteins
  2. Alpha q activate PLC (phospholipids C), breaks PIP2 down into 2 molecules, DAG and IP3. DAG activates PKC (phosphorylates targets), IP3 molecule binds to IP3 receptor on ER, leads to release on calcium from ER.
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8
Q

Types of GABA receptors:

A
  • GABAA: Ligand gated ion channels (ionotropic receptors)
  • GABAB: G protein-coupled (metabotropic) receptors
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9
Q

GABAa receptors:

A
  • 5 subunits, 2 alpha, 2 beta and 1 gamma
  • Allows chloride to flow through, cause hyperpolarization (inhibitory)
  • Synaptic: involved in fast inhibition. Extra synaptic (next to active zone): involved in tonic inhibition
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10
Q

How does activation of GABAa receptors produce a depolarization in immature but nor in adult neurons?

A

Normally when GABA activated, Cl enters and hyperpolarizes.
KCC2: allows Cl out. NKCC1 lets Cl in.
- In immature neurons, KCC2 expression is lower, and NKCC1 expression is higher therefore more chloride comes in (higher Cl conc inside). When GABA binds to receptors, Cl leaves. Results in depolarization. Excitatory.

  • In mature neurons, KCC2 expression is higher, maintains low Cl conc (transports Cl out), NKCC1 brings Cl in, but higher expression of KCC2 so low Cl concentration internally. When GABA Is activated, Cl enters, causes inhibitory/hyperpolarization.
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11
Q

GABAa receptor endocytosis

A
  • signal for receptor endocytosis is dephosphorylation of receptor
  • recycling of receptor involves similar proteins: clathrin, AP2, dynamin
  • involves endosomes, can be degraded or sent back to membrane
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12
Q

Mechanism for epilepsy (dysregulation of GABAa receptor trafficking)?

A

Repeated activation of pathways leads to dephosphorylation of receptors, now large numbers of GABAergic receptors being recycled or internalized. Fewer GABA receptors, less inhibition, more excitation.. mechanism for epilepsy

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13
Q

presynaptic GABAb receptors

A
  • can activate alpha i subunit, inhibits adenylyl cyclase (less cAMP)
  • beta gamma subunit can bind to voltage gated calcium channels (has inhibitory effect, less calcium coming in). or they can bind to snare proteins and have inhibitory effects. effects synaptic vesicle exocytosis
  • can have number of effects on presynaptic side that affects nt release.
  • on postsynaptic side, can have effects on signaling through adenylyl cyclase, and binds to ion channels.
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14
Q

Define long term potentiation and depression

A

Long-term potentiation: a long-lasting (hours or days) increase in the synaptic response of the neurons to stimulation of their affronts following a brief patterned stimulus (for example, 1s stimulation at 100 Hz).

Long-term depression: a long-lasting decrease in the synaptic response of neurons to stimulation of their afferents following a long patterned stimulus (for example, 15 min stimulation at 15 Hz).

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15
Q

Molecular mechanisms of LTP:

A
  • glutamate binds to AMPA receptors.. depolarization.. removal of Mg block on NMDArs.
  • phosphorylation of AMPA leads to more expressed on plasma membrane, leads to increase in AMPA on membrane.
  • long lasting forms require new proteins, new gene transcription or local translation of existing transcripts.
  • BDNF also plays role in synaptic plasticity
  • structural change: bigger spine head and neck
  • functional change: more AMPA receptors
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16
Q

Molecular mechanisms of LTD:

A
  • induction of LTD triggered by activation of NMDAr
  • The Ca2+ transient determines the polarity of the induced plasticity, with low and prolonged Ca2+ transients inducing LTD and brief, steeper transients inducing LTP.
  • results partly from dephosphorylation of AMPA receptors
  • presynaptic mechanisms also contribute
17
Q

Glutamate excitotoxicity:

A
  • Too much stimulation
  • Leads to AMPA and NMDA being overactivated
  • Leads to calcium imbalance
  • Leads to increase in all those activities (ATPase, lipase, protease, DNAase), leads to neuronal cell death (PSD-95 and NOS might be mechanism)
18
Q

Short vs Long term memory

A

Short-term memory: protein synthesis independent, anesthesia sensitive

Long-term memory: protein synthesis dependent, anesthesia resistant

19
Q

What part of the brain does spatial learning and memory rely on

A

Hippocampus

20
Q

Mechanisms of short-term memory formation in Aplysia

A
  1. Presynaptic PKA activated
  2. Presynaptic Ca and CamKII
  3. Presynaptic PKC
  4. Postsynaptic Ca and CamKII
  5. Recruitment of pre and possibly postsynaptic molecules to new sites.
21
Q

Mechanisms of long-term memory formation:

A
  1. Nt release and short-term strengthening of synaptic connections
  2. Involvement of kinases and phosphatases
  3. Activation of nuclear transcription factors
  4. Activity-dependent induction of gene expression
  5. Chromatin alteration and epigenetic changes in gene expression
  6. Synaptic growth and the formation of new synapses
  7. Activation of pre-existing silent synapses
22
Q

Silent synapses definition?

A

structural specializations for neurotransmission that do not produce a physiological response in the receiving cell

23
Q

4 types of silent synapses:

A
  1. Presynaptically silent synapse (missing smthn on presynaptic side)
  2. Conditionally silent synapse (only have NMDA and not AMPA receptors, need AMPA to depolarize postsynaptic neuron to remove Mg block from NMDA)
  3. Postsynaptically silent synapse (no NMDA or AMPA receptors)
  4. Incompletely assembled synapse (can become active)
24
Q

Histone modification, heterochromatin vs euchromatin:

A

Heterochromatin: condensed chromatin and subsequent transcriptional repression. More methylation

Euchromatin: relaxed chromatin state that allows transcriptional machinery access to DNA for gene expression. Less methylation more acetylation and phosphorylation.

25
Q

5 neurological diseases:

A

Alzheimers, Fragile X, Huntingtons, Parkinsons, Amyotrophic later sclerosis

26
Q

What is Alzheimers characterized by:

A

Accumulation of plaques (amyloid beta peptides, cleaved from APP.. cleaved by complex family of enzymes.. gamma and beta secretases including presenilin) and tangles (insoluble filaments of tau protein)

27
Q

APP processing and formation of amyloid beta peptide

A

Has number of cleavage sites (beta, alpha and gamma sites)

Depending on what’s cleaved, can be pro (beta/gamma secretases) or anti amyloidogenic (alpha secretases) (anti=less plaques)

28
Q

Effects of presenilin:

A

Takeaway: presenilin is involved in a number of effects both presynaptically and postaynaptically. In some presynapse there was reduction in CICR, which leads to reduction in nt release, paired pulse facilitation, and facilitation. Postsynaptically, can effect amount of NMDAR and LTP (reduces).

Presenilin can have number of effects presynaptically and postsynaptically.

29
Q

mGluR theory for Fragile X syndrome:

A
  • mGluR receptor on postsynaptic stimulated by glutamate, induces local mRNA translation
  • protein synthesis stimulates internalization of AMPA receptors
  • FMRP negatively regulates that translation and reduces the internalization of AMPA receptors
  • So in fmr1 KO mice, neurons from patients with FXS have increased internalization of AMPA receptors in the absence of FMRP. This therefore weakens the synapse.
30
Q

Characterization of FXS

A

FXS usually caused by a 50 untranslated region (UTR) trinucleotide repeat expansion in the FMR1 gene, resulting in loss of FMRP

31
Q

Cellular mechanisms of huntingtons

A

huntington fragments forming due to CAG repeats, important effect they have: mitochondrial toxicity/energy imbalance effects, axonal transport impairment, synaptic dysfunction

32
Q

6 hypotheses for AD:

A

AB-amyloid hypothesis, AB-oligomer hypothesis, presenilin hypothesis, calcium dysregulation hypothesis, lysosome hypothesis, Tau hypothesis.

33
Q

Parkinson Disease- inherited mutations

A
  • alpha-synuclein
  • Leucin-rich repeat kinase 2 (LRRK2)
  • Parkin
  • DJ1
  • PREN-induced kinase 1 (PINK1)

5 proteins linked to PD, mutations in genes can have effects at synapses/effect synaptic function, can lead to tangles and aggregation, effects on ubiquitin and proteasome, effect on mitochondria, all effects collectively can lead to neuronal death.

34
Q

Take away for ALS

A

ALS is disease of motor neurons, characterized by degeneration of motor neurons, which leads to muscle weakness and paralysis, can affect number of things, can be involved in oxidative stress, mitochondrial dysfunction, affects on DNA, RNA.

35
Q

Short term plasticity in pain (facilitation and depression)

A

Short term facilitation> Paired Pulse Facilitation: two stimuli occur in short interval, second stimulus induces larger response

Stf>Wind up: repeated low freq stimulation, you get larger response.

Short term depression>Paired Pulse Depression: two stimuli occurring in short interval, second stimuli results in smaller response.

Std>Steady state depression: repeated stimulation results in smaller response

36
Q

Presynaptic mechanisms of synaptic plasticity

A

Nt release, binds to AMPA and NMDAR, leads to pathways on postsynaptic cell. Ca entering activates NO synthase, NO diffuses through membrane, goes into presynaptic terminal, activates Guanyl cyclase enzyme, makes cGMP, activates PKG, lead to phosphorylation of various targets, leads to increase in NT release.

Glia can contribute by releasing NO

37
Q

Microglia-neuron interactions crucial for pain hypersensitivity induced by peripheral nerve injury

A

EXP: in mice how injury induces increase in pain sensitivity.

There’s nociceptor innervating neurons. You have nerve injury

During nerve injury, you get increased expression of p2X4 receptor on microglia

They are purinergic receptors, can bind ATP.

Following nerve injury, increase in p2X4 receptor expressed on microglia, leads to more of their activation, leads to more calcium entering microglia

Leads to increase in neurotrophic factor release (BDNF)

BDNF can bind to TrkB receptors on postsynaptic neuron.

TrkB receptors are tyrosine kinase receptors, can phosphorylate other targets

TrkB has few effects: activates another kinase known as Fin

Fin phosphorylates NMDA receptors, increase in their activity

TrkB can have inhibitory effect on KCC2 (pumps Cl and K out of neurons, keep Cl concentration low) when GABA neurons enter neuron, hyperpolarizes

But since KCC2 is inhibited, there will be increase in Cl conc in neuron

More excitation bc activating NMDA receptors, and less inhibition bc inhibiting KCC2

Essentially, u have mechanism of pain hypersensitivity induced by nerve injury.

BIOM 3400 (2 decks)

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