Neurobiology Study Guide Cards Flashcards

(48 cards)

1
Q

What are the three types of signaling in neurons?

A

Synaptic, paracrine, and endocrine signaling.

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2
Q

What are the main components of signaling cascades?

A

Signaling molecules, receptors, second messengers, protein kinases, phosphatases.

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3
Q

Name three types of signaling molecules.

A

Neurotransmitters, neuropeptides, hormones.

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4
Q

What are the two main types of receptors?

A

Ionotropic and metabotropic receptors.

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5
Q

What is the role of G proteins in signaling?

A

They can activate/inhibit enzymes and directly open/close ion channels

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6
Q

What regulates G protein activity?

A

GTP binding activates; GDP binding inactivates; regulated by GAPs (GTPase-activating proteins).

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7
Q

What is a kinase? What is a phosphatase?

A

A kinase adds phosphate groups; a phosphatase removes them.

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8
Q

Give an example of a metabotropic receptor and its neurotransmitter.

A

Dopamine receptors (metabotropic, dopamine).

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9
Q

What second messengers are derived from PIP2?

A

DAG and IP3.

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10
Q

What are the roles of cAMP and cGMP?

A

Activate PKA and PKG; can also open cyclic nucleotide-gated channels.

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11
Q

Which second messenger directly increases intracellular calcium?

A

IP3 (via IP3 receptors on ER).

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12
Q

What enzyme produces DAG and IP3?

A

Phospholipase C

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13
Q

What is CREB and why is it important?

A

A transcription factor activated during long-term plasticity and memory.

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14
Q

What distinguishes short-term plasticity from long-term plasticity?

A

Short-term: lasts seconds to minutes, involves post-translational modifications. (Rearrangement of furniture)

Long-term: lasts hours to years, involves gene transcription and protein synthesis. (Remodeled house)

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15
Q

What is synaptic facilitation?

A

A temporary increase in synaptic strength due to repeated stimulation.

due to accumulated presynaptic Ca²⁺, enhancing neurotransmitter release.

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16
Q

What is synaptic depression?

A

A temporary decrease in synaptic strength due to neurotransmitter depletion.

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17
Q

What type of plasticity occurs in Aplysia for habituation and sensitization?

A

Long-term plasticity involving serotonin and changes in transcription.

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18
Q

What is required for hippocampal long-term potentiation (LTP)?

A

High-frequency tetanic stimulation.

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19
Q

What are the properties of LTP?

A

Specificity and associativity.

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20
Q

Which receptors are critical for LTP initiation?

A

NMDA receptors (for Ca²⁺ influx) and AMPA receptors (for depolarization).

21
Q

How can LTP be blocked?

A

By blocking transcription factors like CREB or NMDA receptor activation.

22
Q

How is transcriptional regulation involved in long-term memory?

A

Via factors like CREB in both Aplysia and hippocampus during memory formation.

23
Q

Can a neurotransmitter be both excitatory and inhibitory?

A

Yes. For example, GABA is excitatory in early development due to chloride ion gradient and inhibitory in adults.

24
Q

What is a channelopathy involving inactivation?

A

Certain epilepsy forms caused by Na⁺ channel inactivation defects.

25
How can neurotransmitters modulate signal transduction?
Through G-protein coupled receptors that activate second messenger pathways.
26
What are the four important ions in neuronal communication and their roles?
Na⁺ (depolarization), K⁺ (repolarization), Ca²⁺ (neurotransmitter release), Cl⁻ (inhibitory responses).
27
What is HSAM?
Highly Superior Autobiographical Memory; ability to recall personal experiences in great detail.
28
What is memory reconsolidation?
The process where recalled memories become labile and can be altered before being stored again.
29
Synaptic signaling
- Local and fast, occurs at synapses between neurons.
30
Paracrine signaling
- Signals diffuse to nearby target cells without synaptic junctions.
31
Endocrine signaling
- Hormones released into the bloodstream act on distant cells.
32
Extracellular signaling molecule
- Neurotransmitter or Hormone
33
Receptor protein
- GPCR, ion channel
34
Intracellular second messengers
- cAMP, cGMP, Calcium, and IP3
35
Effector proteins
- kinases, phosphatases
36
Cellular response
- gene expression, ion channel modulation
37
Specificity
Only the actively stimulated synapse is strengthened during LTP, while inactive neighboring synapses remain unchanged. Example: If neuron A synapses onto neuron B at two different points (synapse 1 and synapse 2), and only synapse 1 receives strong stimulation, only synapse 1 will undergo LTP, not synapse 2.
38
Associativity
A weakly stimulated synapse can also undergo LTP if it is active at the same time as a strongly stimulated synapse on the same postsynaptic neuron. Example: If a weak input (e.g., bell ringing) and a strong input (e.g., food presentation) are activated together on the same postsynaptic neuron, the weak synapse can be potentiated too—"cells that fire together, wire together."
39
What kinases are classified as Ser/Thr kinases?
PKA (Protein Kinase A) PKC (Protein Kinase C) CaMKII (Calcium/calmodulin-dependent kinase II)
40
What are the targets of DAG and IP3, and where do they come from?
DAG and IP3 are generated from PIP2 cleavage by phospholipase C DAG activates PKC IP3 triggers Ca²⁺ release from the ER
41
How is calcium removed from the cell after signaling?
Pumped out via PMCA (plasma membrane Ca²⁺ ATPase) Sequestered into ER via SERCA pump Exchanged with Na⁺ via NCX (Na⁺/Ca²⁺ exchanger)
42
What are the two main types of acetylcholine (ACh) receptors and their functions?
Nicotinic (ionotropic): Cause EPSPs via Na⁺ influx Muscarinic (metabotropic): In the heart, open K⁺ channels to slow heart rate
43
Describe the difference between monomeric and trimeric G proteins.
Monomeric G proteins (e.g., Ras): Single subunit; important in growth pathways. Trimeric G proteins (α, β, γ): Activated by GPCRs; α binds GTP/GDP and regulates downstream effectors.
44
What are second messengers and what are some examples?
Small intracellular molecules that amplify and relay signals from receptors. Examples: Calcium (Ca²⁺): Released from intracellular stores, activates kinases like CaMKII cAMP/cGMP: Activate PKA/PKG and open cyclic nucleotide-gated ion channels DAG: Activates PKC IP3: Binds to IP3 receptors on the ER to release calcium
45
What are the structural differences between cAMP and cGMP, and how are they generated?
cAMP: made from ATP by adenylyl cyclase cGMP: made from GTP by guanylyl cyclase
46
What enzymes degrade cAMP and cGMP to terminate their signals?
Phosphodiesterases (PDEs) hydrolyze cAMP and cGMP into AMP and GMP, respectively.
47
What is the role of calcium-binding proteins like calmodulin?
Calmodulin binds Ca²⁺ and activates enzymes like CaMKII, which participate in memory and plasticity pathways.
48
What does CaMKII do in neuronal signaling?
CaMKII is a serine/threonine kinase activated by Ca²⁺/calmodulin. It phosphorylates ion channels and receptors, and is critical for LTP and memory formation.