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Here is a structured summary of your study notes:

Summary of F1.pdf - Biochemistry & Neuroscience Study Notes

The document covers five interconnected themes:

1. Cell Signaling Pathways

Ca²⁺ / Calmodulin pathway: High intracellular Ca²⁺ activates calmodulin, which then activates protein kinases.
Gq pathway: Gαq activates PLC-β → generates IP3 and DAG. IP3 triggers Ca²⁺ release from the ER, and DAG (along with Ca²⁺) activates PKC.
cAMP pathway: cAMP activates PKA (protein kinase A).
β-arrestins: Mediate receptor desensitization and endocytosis after receptor activation.

2. Energy Sensing & Regulation (AMPK / mTOR)

AMPK is the master energy sensor - activated when energy (ATP) is low (high AMP:ATP ratio). It boosts catabolic pathways and is a major inhibitor of mTOR.
mTOR is activated when nutrients are abundant and drives anabolic/growth pathways.
Think of them as the "gas pedal" (mTOR) and "brake" (AMPK) for cell growth.

3. Glycolysis & Glycogen Metabolism

PFK-1 is inhibited by ATP (negative feedback when energy is high) to prevent excess glucose breakdown.
Glycogen synthase builds glycogen; AMP inhibits it as an energy-saving signal.
Pyruvate dehydrogenase (PDH) complex is activated by PDH phosphatase (PDP).
Citrate export from mitochondria to cytoplasm inhibits glycolysis - a brake when energy stores are full.
PFKFB3 in astrocytes drives glycolysis, producing lactate.

4. Ketone Body Metabolism

During starvation or a ketogenic diet, neurons switch from glucose to ketone bodies for fuel.
SCOT (Succinyl-CoA:3-oxoacid CoA-transferase) is the key enzyme linking ketone body utilization to the TCA cycle.
MCTs (Monocarboxylate Transporters) carry ketone bodies and lactate across the blood-brain barrier into neurons.

5. Astrocyte-Neuron Metabolic Coupling

Astrocyte-Neuron Lactate Shuttle: Astrocytes (via PFKFB3) are highly glycolytic and produce lactate, which is exported to neurons as their primary fuel.
Glutamate released by active neurons stimulates astrocyte glycolysis - a feedback loop matching neuronal activity to fuel supply.
If lactate import into neurons drops, the TCA cycle slows and neuronal function is impaired.
Lactate dehydrogenase A boosts astrocyte lactate production under hypoxia.
Pentose Phosphate Pathway (PPP): Produces NADPH and ribose-5-phosphate. NADPH is an antioxidant (regenerates active glutathione, eliminating ROS). G6PD is the key enzyme; its deficiency causes NADPH deficiency.
Astrocytes compensate for neurons' limited glucose-processing ability by supplying both lactate (fuel) and NADPH-derived antioxidants via the PPP.
Malate-aspartate shuttle: Transfers NADH from the cytosol into mitochondria for oxidative phosphorylation.
The stable expression of PFKFB3 and elevated fructose-2,6-bisphosphate (F2,6-BP) in astrocytes is what keeps them highly glycolytic, while neurons can focus on signaling tasks.

Key Enzyme/Molecule Quick Reference

Molecule/Enzyme	Role
AMPK	Energy sensor; activates catabolism, inhibits mTOR
SCOT	Ketone bodies → TCA cycle
PFKFB3	Drives glycolysis in astrocytes
G6PD	Entry into PPP; deficiency → NADPH deficiency
MCT	Transports lactate/ketones into neurons
PDH phosphatase	Activates PDH complex
β-arrestin	Receptor desensitization & endocytosis
Malate-aspartate shuttle	NADH transfer: cytosol → mitochondria

The overarching theme is brain energy metabolism - how neurons rely on astrocytes for fuel (lactate shuttle), how cells sense and respond to energy state (AMPK/mTOR, PFK-1, glycogen synthase), and how the brain protects itself from oxidative stress (PPP/NADPH/glutathione).

Quiz me on specific topics like AMPK/mTOR or the lactate shuttle

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Great - AMPK/mTOR, multiple choice. Here's your first question:

Question 1 of 5 - AMPK / mTOR

AMPK is activated under which condition?

A) High ATP and abundant nutrients
B) Low energy state with high AMP levels
C) High mTOR signaling
D) Excess glucose availability

Take your time - type the letter of your answer when ready!

✅ Correct!

AMPK is activated when energy is low - high AMP levels act as the cellular "alarm," triggering AMPK to enhance catabolic pathways and conserve energy.

Question 2 of 5 - AMPK / mTOR

What is the relationship between AMPK and mTOR?

A) AMPK activates mTOR to promote cell growth
B) They operate independently with no interaction
C) AMPK is a major inhibitor of mTOR
D) mTOR activates AMPK when nutrients are low

✅ Correct!

AMPK is a major inhibitor of mTOR. Think of it this way - when energy is scarce (AMPK on), the last thing the cell should do is grow and build things (mTOR off). The two pathways are functionally opposed.

Question 3 of 5 - AMPK / mTOR

Which of the following best describes mTOR's role?

A) It acts as the "brake" - slowing growth when nutrients are low
B) It acts as the "gas pedal" - driving growth and anabolism when nutrients are abundant
C) It inhibits protein synthesis under all conditions
D) It is activated by high AMP levels

✅ Correct!

mTOR is the "gas pedal" for growth and anabolic pathways - it fires up when nutrients are plentiful. AMPK is the "brake," shutting things down when energy is low. They work in opposing directions.

Question 4 of 5 - AMPK / mTOR

AMPK activation enhances which type of pathways?

A) Anabolic pathways (building molecules)
B) Catabolic pathways (breaking down molecules for energy)
C) DNA replication pathways
D) Receptor desensitization pathways

❌ Not quite - the answer is B.

When energy is low, AMPK enhances catabolic pathways - breaking down molecules (fats, glucose, etc.) to generate more ATP. Anabolic pathways (building things like proteins and glycogen) are energy-expensive, so AMPK suppresses those. That's exactly why AMPK inhibits mTOR, which drives anabolism.

Question 5 of 5 - AMPK / mTOR

AMP inhibits glycogen synthase. Which of the following best explains why this makes sense in the context of AMPK signaling?

A) Building glycogen requires energy; when AMP is high (low energy), the cell should stop storing glucose and instead use it for ATP production
B) AMP directly activates glycogen synthase to increase glucose storage
C) Glycogen synthase is only active when mTOR is inhibited
D) AMP inhibits glycogen synthase to prevent glucose from entering the PPP

❌ Not quite - the answer is A.

AMP inhibits glycogen synthase (it does not activate it). The logic: high AMP = low energy. Synthesizing glycogen costs energy and locks glucose away in storage - exactly the wrong move when the cell is already energy-starved. So AMP signals "stop storing, start burning."

AMPK / mTOR Quiz - Final Score

Q	Your Answer	Result
1	B	✅
2	C	✅
3	B	✅
4	A	❌ (correct: B - catabolic)
5	B	❌ (correct: A - AMP inhibits glycogen synthase)

Score: 3 / 5

Solid on the big-picture AMPK/mTOR concepts! The two misses were both about what AMPK does downstream - remember the core rule: low energy → AMPK on → break things down (catabolic), stop building things. Everything flows from that.

Want to move on to another topic? I can quiz you on the Astrocyte-Neuron Lactate Shuttle, Cell Signaling, Ketone Bodies, or PPP & NADPH.

I want question like seu exam

Got it - you want questions written in the style of your SEU (university) exam: clinical/applied scenarios, tricky distractors, and deeper reasoning rather than straightforward recall.

Let's go. Topic: AMPK / mTOR first, then I'll mix in the lactate shuttle.

Question 1

A researcher studies neurons under prolonged glucose deprivation. She finds that a key kinase becomes highly active, suppressing a growth-promoting pathway and redirecting metabolism toward fuel breakdown.

Which of the following best describes the molecular interaction she is observing?

A) mTOR activation leads to phosphorylation and inhibition of AMPK
B) AMPK activation leads to inhibition of mTOR, shifting the cell toward catabolic metabolism
C) PKA activation inhibits AMPK, causing mTOR to drive glycogen synthesis
D) AMPK inhibits PLC-β, reducing DAG-mediated activation of PKC

✅ Correct!

Glucose deprivation → high AMP → AMPK activates → mTOR inhibited → cell shifts to catabolism. Option D was a trap mixing in the Gq/PKC pathway - unrelated to AMPK.

Question 2

A patient with a genetic defect has astrocytes that cannot export lactate to neighboring neurons. Neuronal firing rates drop significantly despite normal blood glucose levels.

Which of the following best explains this finding?

A) Without lactate, neurons cannot synthesize glycogen, impairing long-term energy storage
B) Neurons rely on astrocyte-derived lactate as a primary fuel for their mitochondria; without it, the TCA cycle slows and ATP production falls
C) Lactate normally inhibits PFKFB3 in astrocytes; its absence causes uncontrolled glycolysis that depletes neuronal glucose
D) Without lactate import, neurons upregulate mTOR to compensate for the energy deficit

✅ Correct!

This is the core of the Astrocyte-Neuron Lactate Shuttle - neurons depend on astrocyte-derived lactate to feed their mitochondria. Normal blood glucose doesn't help if the shuttle is broken, because neurons have limited glycolytic capacity on their own. Option D was a trap - low energy suppresses mTOR, not the other way around.

Question 3

During a hypoxic episode in brain tissue, measurements show a sharp rise in astrocyte lactate output. A student proposes this is driven by increased activity of a specific enzyme.

Which enzyme is most directly responsible for this increased lactate production in hypoxia?

A) Pyruvate dehydrogenase phosphatase (PDP)
B) Succinyl-CoA:3-oxoacid CoA-transferase (SCOT)
C) Lactate dehydrogenase A (LDH-A)
D) Mitochondrial aconitase

✅ Correct!

LDH-A significantly increases astrocyte-derived lactate under hypoxia - it converts pyruvate to lactate, which is then exported to neurons. The other options were deliberate traps: PDP activates PDH (which actually pushes pyruvate away from lactate toward the TCA cycle), SCOT is for ketone body utilization, and aconitase works in the TCA cycle - none of these increase lactate output.

Question 4

A research group finds that neurons in a disease model have dysfunctional MCTs. Despite adequate astrocyte lactate production, neuronal ATP levels are critically low.

What is the most likely explanation?

A) Without functional MCTs, neurons cannot export excess glucose, causing toxic accumulation
B) MCTs are required to transport lactate and ketone bodies into neurons; their dysfunction prevents neurons from taking up these alternative fuels, even when available
C) Dysfunctional MCTs block the malate-aspartate shuttle, preventing NADH from entering mitochondria
D) Without MCTs, astrocytes cannot receive glutamate signals from neurons, so glycolysis in astrocytes shuts down

✅ Correct!

MCTs are the gateway for lactate and ketone bodies to enter neurons. If the shuttle produces fuel but neurons can't import it, ATP still crashes - the problem is at the transport step, not production. Option D was a clever trap that reversed the signaling direction - it's neurons releasing glutamate that stimulates astrocyte glycolysis, not the other way around via MCTs.

Question 5

A neuroscientist observes that in a brain region under oxidative stress, astrocytes dramatically increase flux through the Pentose Phosphate Pathway (PPP) while reducing glycolytic activity.

Which of the following best explains the functional significance of this shift?

A) The PPP produces ATP more efficiently than glycolysis, compensating for the energy deficit caused by oxidative stress
B) Increased PPP flux generates NADPH, which regenerates active glutathione to neutralize ROS, protecting both astrocytes and neighboring neurons from oxidative damage
C) The PPP produces pyruvate, which is converted to lactate and exported to neurons as an emergency fuel during oxidative stress
D) Shifting to PPP inhibits PFKFB3, preventing excess F2,6-BP accumulation and reducing glycolytic overload in neurons

✅ Correct!

The PPP's primary job under oxidative stress is antioxidant defense - it generates NADPH, which reduces oxidized glutathione back to its active form, neutralizing ROS. Option A was a trap: the PPP does NOT produce ATP efficiently - that's glycolysis and oxidative phosphorylation. Option C was also a trap - the PPP produces ribose-5-phosphate, not pyruvate.

SEU-Style Quiz - Final Score

Q	Topic	Your Answer	Result
1	AMPK/mTOR - scenario	B	✅
2	Lactate shuttle - genetic defect	B	✅
3	LDH-A in hypoxia	C	✅
4	MCT dysfunction	B	✅
5	PPP & NADPH under oxidative stress	B	✅

Score: 5 / 5 🎯

Excellent - perfect round on the scenario-based questions. You clearly understand the why behind the mechanisms, not just the facts. That's exactly what SEU-style exams test.

Want to keep going with harder questions, or switch to a new topic - Cell Signaling (Gq, cAMP, Ca²⁺) or Ketone Body Metabolism?

Explain for biochem seu exam

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This file covers Cell Signaling - GPCRs, G proteins, RAS/MAPK, and more. Here's a full SEU-exam-focused explanation of every concept:

F2 - Cell Signaling: SEU Exam Explanation

1. G Protein-Coupled Receptors (GPCRs) - The Basics

Inactive state: GPCR is unoccupied → the G protein inside the cell is bound to GDP (inactive).

Activation sequence:

Ligand binds GPCR
GPCR changes shape → acts as a GEF (Guanine nucleotide Exchange Factor) → kicks GDP off, GTP loads on
Gα-GTP separates from Gβγ dimer
Both Gα-GTP and free Gβγ can now activate downstream targets
Gα slowly hydrolyzes GTP → GDP → G protein reassembles → signaling OFF

Key anchor point: The γ-subunit (and α-subunit) have a membrane "tail" - the γ-subunit is attached by isoprenylation. This keeps the whole G protein complex docked at the membrane in the right position.

SEU tip: "Inactive GPCR = G protein bound to GDP" is a classic one-liner exam fact.

2. G Protein Subtypes & Their Downstream Effects

G Protein	Main Effect
Gαs	Activates adenylyl cyclase → ↑ cAMP → activates PKA
Gαi (e.g. M2 receptor)	Inhibits adenylyl cyclase → ↓ cAMP; Gβγ opens K⁺ channels
Gαq	Activates PLC-β → ↑ IP3, DAG, Ca²⁺, PKC
Gα12/13	Activates Rho-GEFs → Rho signaling (cytoskeleton)
Gαgust (gustducin)	Activates phosphodiesterases (taste signaling)

Gβγ dimer is not just a passive anchor - it has its own signaling:

Gates inward-rectifying K⁺ channels (important in cardiac muscle via M2/Gi)
The M2 receptor (via Gi) simultaneously affects adenylyl cyclase AND K⁺ channels - a classic exam example

Constitutively active Gαs - forces adenylyl cyclase to keep producing cAMP non-stop. This is the mechanism behind cholera toxin (Vibrio cholerae locks Gαs on).

3. Gq Pathway - Know This Cold

Gq → PLC-β → cleaves PIP2 into:

IP3 → goes to ER → releases Ca²⁺
DAG → stays in membrane → activates PKC (together with Ca²⁺)

"Revise action of DAG" from your notes = DAG directly activates PKC at the membrane. This is its primary role.

Ca²⁺ also activates calmodulin → calmodulin-dependent protein kinases (CaMK).

4. Termination of G Protein Signaling

Three key mechanisms to terminate the signal:

Mechanism	How it works
GRKs (G protein-coupled Receptor Kinases)	Phosphorylate the activated receptor → recruits β-arrestin
β-arrestin	Blocks further G protein coupling (desensitization) → triggers receptor endocytosis
RGS proteins	Bind Gα → accelerate GTP hydrolysis → shut off Gα faster
GAPs	Activate intrinsic GTPase of Ras/G proteins → converts GTP→GDP → signal OFF
PDEs (phosphodiesterases)	Degrade cAMP → terminating PKA signaling (activated alongside PKA)

Phosducin - sequesters Gβγ subunits, preventing them from reassociating with Gα or signaling on their own.

GoLoco-containing RGS proteins - block Gβγ reassociation with Gα and keep free βγ available longer.

SEU tip: "GAPs and RGS proteins = termination of G protein signaling" - memorize this as a paired fact.

5. Receptor Tyrosine Kinases (RTKs) & RAS/MAPK

RTKs are different from GPCRs - they have intrinsic kinase activity.

RTK activation pathway:

Ligand binds → RTK dimerizes → autophosphorylation
Adaptor proteins dock → activate RAS (via GEF loading GTP onto RAS)
RAS-GTP activates Raf → MEK → ERK (the MAPK cascade)
ERK enters nucleus → gene expression → cell proliferation/differentiation

RTKs also activate PLC-γ (not PLC-β like Gq) → generates IP3 and DAG → PKC.

RAS regulation:

GAP turns RAS OFF by activating its GTPase (GTP → GDP)
No GAP activity (e.g. RAS mutation) → RAS stays GTP-bound → uncontrolled cell proliferation → cancer
GTP binding on RAS → activates MAPK pathway

SEU tip: Mutant RAS with no GTPase = constitutively active = oncogene. This is a very common exam scenario.

6. Metabolic Signaling (from F2 notes)

Citrate accumulation: Excessive neuronal citrate export from mitochondria into the cytoplasm blocks glycolytic flux (inhibits PFK-1). The cell is signaling "enough energy - slow down glucose breakdown."

F-2,6-BP (Fructose-2,6-bisphosphate): The most powerful activator of PFK-1 (the rate-limiting enzyme of glycolysis). Made by PFKFB3 in astrocytes.

PFKFB3 constitutive degradation: In neurons, PFKFB3 is constantly broken down → low F-2,6-BP → glycolysis is suppressed → glucose is redirected into the PPP for NADPH/antioxidant production. This is why neurons handle oxidative stress differently from astrocytes.

G6PD & NADPH:

G6PD = rate-limiting enzyme of PPP
Activated when NADP⁺ rises (low NADPH = oxidative stress → G6PD turns on to make more NADPH)
NADPH regenerates active glutathione → neutralizes ROS

Calcium & PDH:

Ca²⁺ in mitochondria → dephosphorylates/activates PDH complex (via PDH phosphatase)
This couples neuronal activity (Ca²⁺ influx during firing) directly to energy production

Glycogenolysis in astrocytes:

Astrocytes are the ONLY CNS cells that store glycogen
Glutamate signaling from active neurons → triggers astrocytic glycogenolysis
Glycogen → glucose → lactate → exported to neurons

7. Visual GPCR - Rhodopsin

Rhodopsin is activated by isomerization of 11-cis-retinal → all-trans-retinal (light does this)
Couples to transducin (Gt) → activates PDE → breaks down cGMP → closes Na⁺ channels → hyperpolarization → vision signal

Quick Memory Map for the Exam

Ligand → GPCR → GDP off / GTP on → Gα + Gβγ split

Gαs  → ↑cAMP → PKA
Gαi  → ↓cAMP + Gβγ → K⁺ channels open
Gαq  → PLC-β → IP3 (Ca²⁺) + DAG (PKC)
Gα12/13 → Rho

RTK → RAS-GTP → Raf-MEK-ERK → proliferation
No GAP → RAS stuck ON → cancer

OFF switches: GRKs + β-arrestin | RGS | GAP | PDE

Want me to now quiz you on F2 topics in SEU exam style, or combine both files for a mixed question set?

[11/07, 6:06 pm] Saurabh Wadile: If the membrane potential is 0 and the concentration of an ion is higher within the cell than outside the cell, the ions will (assume channels are open) 1. not move either in or out of the cell 2. move out of the cell. 3. move into the cell. How is this a? [11/07, 6:06 pm] Saurabh Wadile: Which of the following statements correctly describes action potentials? 1. Is only an excitatory event and has a threshold 2. . Has no refractory period 3. Amplitude varies with the size of the initiating event [11/07, 6:06 pm] Saurabh Wadile: Which structures take part in ammonia excretion from the brain? 1. Glutamate/Glutamine shuttle 2. Glucose-alanine shuttle 3. Lactate-alanine shuttle 4. Malate/Aspartate shuttle Help :") [11/07, 6:06 pm] Saurabh Wadile: Which subunit of Na/K-ATPase is responsible for regulation? 1. Gamma 2. Epsilon 3. Beta 4. Alpha :") isn't it a :") [11/07, 6:06 pm] Saurabh Wadile: Which of the following proteins is associated with dendritic cytoskeleton structures? 1. Tau 2. MAP2 3. Actinin 4. MAP1 :")

These are great neuroscience questions. Let me go through each one carefully.

Q1 - Membrane potential = 0, ion concentration higher INSIDE → answer is 2 (move OUT)

Here's why the answer is not A:

When membrane potential = 0, there is no electrical driving force - the electrical gradient is eliminated. But there is still a concentration gradient - the ion is more concentrated inside than outside.

Ions always follow their concentration gradient when there's no electrical force opposing it. Higher inside → ions flow out to equalize concentration.

Answer A ("not move") would only be correct if BOTH gradients cancel each other out - i.e., the electrical force pulling the ion in exactly equals the concentration force pushing it out. That equilibrium point is the Nernst potential for that ion. At membrane potential = 0, only the concentration gradient acts, so the ion moves out.

This is the electrochemical driving force concept:

Net driving force = membrane potential - equilibrium potential (Nernst potential)
If Vm = 0 and Nernst potential ≠ 0, net force exists → ions move

Q2 - Action potentials → answer is none of the listed options are fully correct, but closest exam answer is implied "has a threshold"

Let's break down each option:

Option	Verdict
1. Only excitatory + has a threshold	Partially correct - APs DO have a threshold, but they are NOT only excitatory (inhibitory neurons fire APs too). This is a trick.
2. Has no refractory period	Wrong - APs absolutely have a refractory period (absolute + relative)
3. Amplitude varies with initiating event size	Wrong - APs are all-or-nothing; amplitude does NOT vary with stimulus size

The key property being tested: APs are all-or-nothing and have a threshold. The "correct" answer the exam likely intends is 1, specifically for the threshold part - just ignore the "only excitatory" wording as an oversimplification. The other two are clearly wrong.

Remember: APs are all-or-nothing, have a threshold (~-55 mV), have both absolute and relative refractory periods, and propagate without decrement.

Q3 - Ammonia excretion from the brain → answer is 1 (Glutamate/Glutamine shuttle)

Here's the mechanism:

Neurons produce NH₃ as a toxic byproduct of amino acid metabolism. The brain handles this via:

Glutamate + NH₃ → Glutamine (catalyzed by glutamine synthetase, found in astrocytes)
Glutamine is exported from astrocytes → carried to the liver or kidney for detoxification
In neurons, glutaminase converts glutamine back to glutamate (for neurotransmission)

This cycle = the Glutamate/Glutamine shuttle - it serves dual purpose: recycles neurotransmitter glutamate AND detoxifies ammonia.

The other options:

Glucose-alanine shuttle = liver/muscle ammonia transport, not brain
Lactate-alanine shuttle = not a standard named shuttle
Malate-aspartate shuttle = transfers NADH into mitochondria, nothing to do with ammonia

Q4 - Na/K-ATPase regulatory subunit → answer is 1 (Gamma), NOT Alpha

You asked "isn't it Alpha?" - here's the breakdown:

Subunit	Role
α (Alpha)	Catalytic subunit - contains the ATP binding site, Na⁺/K⁺ binding sites, and does the actual pumping. It is the functional core.
β (Beta)	Structural/chaperone role - helps proper folding and membrane targeting of the α subunit
γ (Gamma)	Regulatory subunit - modulates pump activity, affects ion affinity

Alpha is the catalytic subunit, not the regulatory one. Gamma is the regulator. This is a common trap - alpha does the work, gamma controls it.

Q5 - Dendritic cytoskeleton protein → answer is 2 (MAP2)

Protein	Location
MAP2	Specifically concentrated in dendrites - stabilizes microtubules in dendritic shafts
Tau	Found in axons - stabilizes axonal microtubules (Tau tangles = Alzheimer's)
MAP1	Found in both axons and dendrites, but not dendritic-specific
Actinin	Actin-binding protein, associated with actin filaments, not microtubule-based dendritic cytoskeleton

Memory trick: MAP2 = dendrites, Tau = axons. In Alzheimer's, Tau mislocalizes from axons into dendrites and aggregates - that's why this distinction matters clinically.

Summary Table

Question	Correct Answer	Key Concept
Ion movement at Vm=0, higher conc. inside	Move OUT	Concentration gradient drives movement when no electrical force
Action potential properties	Has a threshold (option 1, partial)	All-or-nothing, refractory period exists
Ammonia excretion from brain	Glutamate/Glutamine shuttle	Astrocytes fix NH₃ into glutamine via glutamine synthetase
Na/K-ATPase regulatory subunit	Gamma	Alpha = catalytic; Gamma = regulatory
Dendritic cytoskeleton protein	MAP2	MAP2 = dendrites; Tau = axons

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This is your actual SEU midterm with answer keys! I can see several answers that differ from what we discussed earlier - let me go through every question with a full explanation, flagging the ones that surprised you.

BIOCHEM & PHYSIO MIDTERM - Full Answer Explanations

Q1 - Membrane potential = 0, ion conc. higher inside → Answer: 1 (not move)

This contradicts what I explained earlier - here's why the exam says "not move":

The exam is implying this is the equilibrium (Nernst) condition. At Vm = 0, if the ion is a cation with higher concentration inside, the outward concentration force is exactly balanced by... wait - actually at Vm = 0, there IS no electrical force. So the ion SHOULD move out.

This answer (1) appears to be a questionable exam answer. The physiologically correct answer is that ions move OUT (option 2) when concentration is higher inside and there is no opposing electrical gradient. If your professor marks it as option 1, it may reflect the assumption that equilibrium is already established - but that reasoning is not standard. Be aware of this discrepancy and follow your professor's version for the exam.

Q2 - Role of Ca²⁺ at chemical synapse → Answer: 3 (facilitate transmitter release from pre-synaptic terminal)

Ca²⁺ enters via voltage-gated Ca²⁺ channels when the AP arrives → triggers vesicle fusion (via synaptotagmin sensing Ca²⁺) → neurotransmitter released into synaptic cleft. Classic.

Q3 - Action potential reaches presynaptic terminal → Answer: 1 (All answers correct)

All three happen sequentially:

Voltage-gated Ca²⁺ channels open
Vesicles fuse with the membrane
Fixed amount of neurotransmitter releases

Q4 - Cl⁻ channels open at resting potential of -55 mV → Answer: 1 (Cl⁻ enters, moves potential further from threshold)

Cl⁻ equilibrium potential is around -70 mV. At -55 mV, Cl⁻ is driven inward (toward its equilibrium). This makes the membrane more negative (hyperpolarizes it) → moves it further from threshold (~-55 mV) → inhibitory effect. This is how IPSPs work.

Q5 - Increase in magnitude of membrane potential → Answer: 2 (None of the listed responses is correct)

"Increase in magnitude" = membrane becomes more negative (e.g., -70 → -80 mV) = hyperpolarization. Option 1 says hyperpolarization, which is actually correct - but the exam says "none." This likely means the question is testing that "increase in magnitude" is specifically called hyperpolarization but the way option 1 is phrased may have been incomplete in the original. Follow your professor's answer key here.

Q6 - Neuron cell bodies inside CNS → Answer: 1 (a nucleus)

Nucleus = cluster of neuron cell bodies inside the CNS
Ganglion = cluster of neuron cell bodies outside the CNS (PNS)
Nerve = bundle of axons

Q7 - Saltatory conduction → Answer: 3 (only at nodes of Ranvier)

In myelinated axons, the AP "jumps" from node to node (saltatory = "to jump" in Latin). Myelin insulates between nodes, so ions only flow at the exposed nodes of Ranvier. This speeds up conduction dramatically.

Q8 & Q9 & Q12 - EPSP vs IPSP → Answer: 1 (EPSP is a depolarizing potential)

EPSP = depolarizing (moves toward threshold, e.g., -70 → -60 mV)
IPSP = hyperpolarizing (moves away from threshold, e.g., -70 → -80 mV)
Neither is all-or-nothing (that's the AP)
Both occur at postsynaptic membranes

Q10 - Neuroglial cells support → Answer: 3 (neurons)

Glia (astrocytes, oligodendrocytes, microglia, Schwann cells) provide structural support, nutrition, myelination, and immune defense - all for neurons.

Q11 - CNS function → Answer: 1 (Integration)

CNS = receives sensory input, integrates it, sends motor output. Integration (processing/decision-making) is the CNS's defining role.

Q13 - Hot stove reflex order → Answer: 3 (sensory input → integration → motor output)

The standard information flow in any nervous system response.

Q14 - Action potential properties → Answer: 3 (Amplitude varies with initiating event)

⚠️ This is the tricky one. This is marked correct in your exam key, but this is actually wrong physiologically - APs are all-or-nothing and amplitude does NOT vary. This may be a bad question or a misprint in the exam. In reality:

Option 1 is partially true (has a threshold)
Option 3 is physiologically incorrect

For your exam: write what the key says (option 3), but know the actual physiology is all-or-nothing.

Q15 - Repolarization of AP → Answer: 1 (efflux of K⁺ via voltage-gated K⁺ channels)

AP sequence:

Depolarization: Na⁺ rushes IN (voltage-gated Na⁺ channels open)
Repolarization: K⁺ rushes OUT (voltage-gated K⁺ channels open, Na⁺ channels inactivate)
Hyperpolarization (undershoot): K⁺ channels slow to close
Na⁺/K⁺-ATPase restores resting potential

Q17 - IPSP → Answer: 2 (membrane becomes more negative / negative deflection)

IPSP = inhibitory = hyperpolarizes the membrane = more negative inside = moves away from threshold.

Q18 - Oscilloscope pattern → Answer: 3 (polarity changes)

The rapid reversal of charge across the membrane (Na⁺ in → depolarization, K⁺ out → repolarization) creates the characteristic AP waveform on the oscilloscope.

Q19 - Refractory period → Answer: 1 (brief time when neuron cannot conduct an impulse)

Absolute refractory period: Na⁺ channels inactivated - no AP possible at any stimulus strength
Relative refractory period: requires stronger-than-normal stimulus

Q20 - Carries impulses AWAY from CNS → Answer: 2 (Motor)

Motor (efferent) = CNS → muscles/glands
Sensory (afferent) = receptors → CNS
Afferent = "arrive," Efferent = "exit"

Q21 - Information path in neuron → Answer: 2 (Dendrites → soma → axon)

Dendrites receive signals → soma integrates → axon transmits output.

Q22 - Cannot be controlled by conscious thought → Answer: 3 (autonomic nervous system)

ANS controls heart rate, digestion, glands - all involuntary. Somatic NS controls skeletal muscle (voluntary).

Q23 - Ammonia excretion from brain → Answer: 4 (Malate/Aspartate shuttle)

⚠️ Note: Your exam key says Malate/Aspartate shuttle. The standard teaching is Glutamate/Glutamine shuttle for ammonia detoxification. The malate-aspartate shuttle normally transfers NADH into mitochondria. This may reflect your professor's specific teaching - follow the key.

Q24 - Na/K-ATPase regulatory subunit → Answer: 3 (Beta)

⚠️ Another discrepancy from earlier. Your key says Beta. In most textbooks:

Alpha = catalytic
Beta = structural/membrane targeting + some regulatory modulation
Gamma = fine-tuning regulator

Your professor considers Beta the regulatory subunit. Follow the key.

Q25 - Cerebroside in myelin → Answer: 4 (3'-sulfatide)

Cerebrosides are glycosphingolipids in myelin. Sulfatide (3'-sulfated galactocerebroside) is the predominant form in mature CNS myelin. Sulfatide loss is seen in metachromatic leukodystrophy.

Q26 - Why beta-hydroxybutyrate can't be standalone brain fuel → Answer: 3

Ketone bodies (including beta-hydroxybutyrate) enter the TCA cycle via SCOT → succinyl-CoA. But succinyl-CoA must come from the TCA cycle itself, which requires at least some glucose-derived oxaloacetate to keep the cycle running. Without any glucose, the TCA cycle can't sustain itself to accept ketone bodies. A small amount of glucose is always needed to "prime" the cycle.

Q27 - Calcium storage in neuronal intracellular stores → Answer: 1 (SERCA type 2b)

SERCA = Smooth Endoplasmic Reticulum Ca²⁺ ATPase - pumps Ca²⁺ from cytosol INTO the ER lumen. The type 2b isoform is the predominant neuronal form, responsible for maintaining ER Ca²⁺ stores used for IP3-triggered release.

Q28 - Myelin protein in neuron-oligodendrocyte crosstalk → Answer: 1 (MAG)

MAG (Myelin-Associated Glycoprotein) is located at the innermost myelin layer (closest to the axon) and mediates direct contact/signaling between the oligodendrocyte and the neuron during myelination. It's essential for the crosstalk that maintains axonal integrity.

Q29 - Dendritic cytoskeleton protein → Answer: 1 (Tau)

⚠️ Opposite of what I told you earlier! Your exam key says Tau for dendrites. Standard neuroscience teaches MAP2 for dendrites and Tau for axons - but your professor's key assigns Tau to dendrites. Follow the key for this exam.

Q30 - GFAP accumulation disorder → Answer: 2 (Alexander's disease)

Alexander's disease is caused by mutations in the GFAP gene → abnormal GFAP accumulates → forms Rosenthal fibers in astrocytes → white matter destruction. It is a rare leukodystrophy.

Q31 - PMCA sensitivity to small Ca²⁺ elevations → Answer: 3 (Ca²⁺ binding to calcium-sensitive site on PMCA)

PMCA (Plasma Membrane Ca²⁺ ATPase) has a built-in calmodulin-binding domain. At low Ca²⁺, calmodulin binds → conformational change → increases PMCA affinity (decreases Km) for Ca²⁺. This allows detection of even tiny Ca²⁺ rises.

Q32 - Astrocytes overcome glutamate excitotoxicity → Answer: 2 (Absorb glutamate → convert to glutamine)

Astrocytes express glutamate transporters (EAATs) that rapidly clear excess synaptic glutamate → inside astrocyte, glutamine synthetase converts glutamate + NH₃ → glutamine (non-toxic) → returned to neurons. This is the glutamate-glutamine cycle and prevents excitotoxic neuronal death.

Q33 - Neural plasma membrane proteins activating FGF receptors → Answer: 3 (Neural cell adhesion molecules / NCAMs)

NCAMs (N-CAM) can act as co-receptors or activators of FGF receptors, triggering downstream signaling for neurite outgrowth, synaptogenesis, and plasticity.

Q34 - Na/K-ATPase mutations in parkinsonism → Answer: 1 (alpha-3 subunit)

Mutations in the ATP1A3 gene (α3 subunit) cause Rapid-onset Dystonia-Parkinsonism (RDP) and CAPOS syndrome. The α3 isoform is enriched in neurons, explaining why its mutation causes neurological disease.

Q35 - Astrocyte pyruvate carboxylase → Answer: 4 (provides metabolites for neuronal TCA cycle and neurotransmitter synthesis)

Astrocytes use pyruvate carboxylase to convert pyruvate → oxaloacetate (CO₂ fixation). This replenishes TCA cycle intermediates (anaplerosis). Neurons lack pyruvate carboxylase, so they depend on astrocytes to supply these intermediates (e.g., alpha-ketoglutarate for glutamate synthesis).

Q36 - ApoE function in ABC transporters → Answer: 3 (enables ABC transporters to bind ligands and transport them)

ApoE acts as a ligand/chaperone that helps ABC transporters (like ABCA1) recognize and shuttle cholesterol and phospholipids across the plasma membrane.

Q37 - Glucose supply under hypoglycemia → Answer: 3 (Astrocytic glycogenolysis)

Astrocytes are the ONLY CNS cells that store glycogen. Under hypoglycemia, astrocytes break down glycogen → glucose → lactate → neurons. Liver glycogenolysis helps systemically but astrocytes are the local brain source.

Q38 - GABA shunt enzymes → Answer: 1 (GABA transaminase + succinate semialdehyde dehydrogenase + glutamate decarboxylase)

GABA shunt: Glutamate → glutamate decarboxylase → GABA → GABA transaminase → succinic semialdehyde → succinate semialdehyde dehydrogenase → succinate (enters TCA). This bypasses the alpha-ketoglutarate → succinate step of the TCA cycle.

Q39 - Primary energy supply to brain → Answer: 1 (Aerobic glycolysis)

The brain predominantly uses aerobic glycolysis (glucose + O₂ → CO₂ + H₂O + ATP). It cannot use fatty acid beta-oxidation (no significant uptake) and uses anaerobic only briefly.

Q40 - Tryptophan uptake during protein-rich diet → Answer: 1

Tryptophan crosses the BBB via the large neutral amino acid (LNAA) transporter. During a protein-rich diet, other large neutral amino acids (leucine, valine, isoleucine, etc.) flood the blood and compete with tryptophan for the same transporter. Since most dietary proteins are relatively low in tryptophan but high in other LNAAs, tryptophan uptake drops.

Glioma chemotherapy resistance → Answer: 3 (Overexpression of MDR3 transporter)

MDR (Multi-Drug Resistance) transporters are ABC transporters that pump chemotherapy drugs OUT of cancer cells. Glioma cells overexpressing MDR3 actively expel chemo agents before they can act. This is a major mechanism of treatment resistance in brain tumors.

Myelin proteolipid protein (PLP) function → Answer: 1 (Strengthen myelin sheath and define intraperiod lines)

PLP is the most abundant CNS myelin protein. It sits in the extracellular face of the myelin membrane and holds the intraperiod lines (where outer leaflets of adjacent myelin wraps appose each other) together, giving myelin its compact, stable structure.

Astrocytes balance extracellular K⁺ → Answer: 4 (Large negative membrane potential)

Astrocytes have a very negative resting membrane potential (~-85 mV) primarily set by K⁺ conductance. This large driving force allows them to rapidly take up excess K⁺ released during neuronal firing via spatial buffering (K⁺ enters where [K⁺] is high, exits where it's low through the astrocytic syncytium).

Ca²⁺ waves in astroglia → Answer: 3 (Gap junctions)

Astrocytes are connected by gap junctions (mainly connexin 43). Ca²⁺ waves propagate through the astrocytic network via these direct cytoplasmic connections, allowing coordinated responses across large brain regions.

Key Discrepancies to Remember for Your Exam

Q	Standard teaching	Your exam key
Q23	Glutamate/Glutamine shuttle = ammonia	Malate/Aspartate shuttle
Q24	Gamma = regulatory subunit	Beta = regulatory
Q29	MAP2 = dendrites, Tau = axons	Tau = dendrites
Q14	APs are all-or-nothing	Key says amplitude varies (likely misprint)

For your SEU exam, follow your professor's answer key on these - but know the standard physiology too in case essay questions come up.

1-Ampk related - MTOR inhibition 2.Phospholipase C beta related - Gq 1. Some qs with mitochondria in option( but that’s not the option) 2. ⁠lactate dehydrogenase A- hypoxia 3. GAP turns off ?? ( RAS is ans) 6.Beta gama dimer of Gi/o - K+ is the ans 7.Goloco- Ans is Maintains free Beta gama 8.depolarization- ans is cation 9.SOCS protein - inhibits JAK activity 10.NO TGF- beta receptor type 1 phosphorylation- ans is no SMAD2/3 activation 11.RTK related - multiple sclerosis 12.Schwann - PNS 13.oligo- CNS 14.Some qs related to Serca 15.PGP - used for drugs

These look like topics/answers from your upcoming exam. Let me explain every single one clearly for SEU exam level.

SEU Exam - Topic-by-Topic Explanations

1. AMPK → mTOR Inhibition

The logic chain:

Low energy → AMP rises → AMPK activates
AMPK phosphorylates and inhibits mTORC1 (via TSC1/2 complex activation and direct Raptor phosphorylation)
mTOR suppressed → no protein synthesis, no cell growth
Cell shifts to catabolism (break things down for ATP)

SEU exam phrasing: "AMPK acts as a major inhibitor of mTOR" - if mTOR is in an option but the question asks what AMPK does to energy balance → answer involves mTOR inhibition.

Remember: AMPK on = energy crisis mode = mTOR off = no growth.

2. Phospholipase C-β → Gq Pathway

Full Gq cascade:

Gαq → activates PLC-β → cleaves PIP2 into:
        ├── IP3 → ER → Ca²⁺ release → CaMK activation
        └── DAG → stays in membrane → activates PKC

PLC-β is specifically activated by Gαq (not RTKs - those use PLC-γ)
If a question mentions PLC-β → answer is Gq
If a question mentions PLC-γ → answer is RTK

Key distinction: β = GPCR (Gq), γ = RTK

3. Mitochondria in Options (but NOT the answer)

This is a classic distractor. Common examples:

Question about	Mitochondria trap	Actual answer
Where does glycolysis occur?	Mitochondria (wrong)	Cytoplasm
Where does beta-oxidation occur?	Cytoplasm (wrong)	Mitochondrial matrix
Lactate production site	Mitochondria (wrong)	Cytoplasm (LDH converts pyruvate→lactate in cytoplasm)
Ketone body USE (SCOT)	Cytoplasm (wrong)	Mitochondria

When you see mitochondria as an option, ask: "Is this a cytoplasmic process?" Glycolysis, PPP, lactate production = cytoplasm. TCA, oxidative phosphorylation, beta-oxidation = mitochondria.

4. Lactate Dehydrogenase A (LDH-A) → Hypoxia

The mechanism:

In hypoxia, O₂ is low → mitochondria can't run oxidative phosphorylation
Pyruvate can't enter TCA cycle efficiently
LDH-A converts pyruvate → lactate + regenerates NAD⁺ (so glycolysis can keep going)
In astrocytes: LDH-A activity surges → massively increased lactate production → exported to neurons via MCTs

Why LDH-A specifically?

LDH-A (also called LDH-5) has high affinity for pyruvate → optimized for pyruvate-to-lactate direction
LDH-B (LDH-1) prefers lactate-to-pyruvate (heart muscle, neurons)

Exam answer: hypoxia → LDH-A → ↑ lactate production in astrocytes

5. GAP turns off → RAS

GAP = GTPase-Activating Protein

RAS is active when bound to GTP
RAS has weak intrinsic GTPase activity (slow self-inactivation)
GAP accelerates GTP hydrolysis on RAS → GTP → GDP → RAS turns OFF
No GAP (e.g. RAS mutation) → RAS stays GTP-bound → constitutively active → uncontrolled MAPK signaling → cancer

RAS-GTP (active) --[GAP]--> RAS-GDP (inactive)

If a question asks "what does GAP turn off?" → RAS If it asks "what happens when GAP is absent?" → excessive RAS-GTP signaling → cell proliferation

6. Gβγ dimer of Gi/o → K⁺ channels

When Gi/o is activated (e.g. by M2 muscarinic receptor in heart):

Gαi → inhibits adenylyl cyclase → ↓ cAMP
Gβγ → directly opens inward-rectifying K⁺ channels (IKACh)

Opening K⁺ channels → K⁺ exits → hyperpolarization → slows heart rate (this is how vagus nerve slows the heart).

Exam answer: Gβγ of Gi/o → K⁺ channels (not Ca²⁺, not Na⁺)

7. GoLoco → Maintains free Gβγ

GoLoco motif (found in some RGS proteins):

Binds to Gα-GDP (the inactive form)
Prevents Gα-GDP from reassociating with Gβγ
Result: free Gβγ remains available to keep signaling independently

Normal: Gα-GDP + Gβγ → reassemble → inactive complex
GoLoco: Gα-GDP is sequestered → Gβγ stays FREE → continues signaling

Exam answer: GoLoco-containing RGS proteins → maintain free Gβγ (by blocking Gβγ reassociation with Gα)

8. Depolarization → Cation (influx)

Depolarization = membrane becomes less negative (e.g. -70 → -55 mV → 0 → +30 mV)

This is caused by cation influx - specifically:

Na⁺ rushes IN during AP upstroke (positive charge entering = less negative inside)
Ca²⁺ can also cause depolarization

Depolarization = cation (Na⁺ or Ca²⁺) entering the cell Hyperpolarization = cation leaving OR anion (Cl⁻) entering

9. SOCS protein → Inhibits JAK activity

JAK-STAT pathway:

Cytokine → receptor → JAK kinases activate → phosphorylate STAT → STAT enters nucleus → gene expression

SOCS (Suppressor of Cytokine Signaling) proteins are the negative feedback:

Induced by STAT activation (feedback loop)
Bind directly to JAK kinases → inhibit their kinase activity
Also target the receptor complex for degradation

Exam answer: SOCS → inhibits JAK (not STAT directly, not the receptor itself - JAK is the target)

10. No TGF-β receptor type 1 phosphorylation → No SMAD2/3 activation

TGF-β signaling:

TGF-β → binds Type II receptor → recruits & phosphorylates Type I receptor (ALK5)
→ Type I receptor phosphorylates SMAD2/3
→ SMAD2/3 + SMAD4 → nucleus → gene expression (growth arrest, fibrosis, etc.)

If Type I receptor is NOT phosphorylated:

The entire downstream cascade fails
SMAD2/3 cannot be phosphorylated → not activated
No SMAD2/3-SMAD4 complex → no transcriptional response

Exam answer: No TGF-β R1 phosphorylation → no SMAD2/3 activation

11. RTK → Multiple Sclerosis connection

RTKs (especially ErbB/PDGFR family) are involved in:

Oligodendrocyte survival and myelination (PDGF-R signaling promotes oligodendrocyte progenitor proliferation)
In MS, oligodendrocytes are destroyed → demyelination
RTK signaling (especially ErbB2/ErbB3 via Neuregulin-1) is essential for Schwann cell myelination in PNS and oligodendrocyte function in CNS

The likely exam question: RTK signaling related to myelination → failure → MS (demyelinating disease)

12. Schwann Cells → PNS

Cell	Location	Function
Schwann cells	PNS	Myelinate peripheral axons (1 Schwann cell per 1 axon segment)
Oligodendrocytes	CNS	Myelinate central axons (1 oligodendrocyte wraps multiple axons)

If a question mentions Schwann cells → answer is PNS

13. Oligodendrocytes → CNS

Key differences to remember:

Feature	Schwann (PNS)	Oligodendrocyte (CNS)
Location	PNS	CNS
Axons per cell	1	Up to 50
Regeneration	Good (Schwann cells guide regrowth)	Poor
Myelin protein	P0, PMP22	MBP, PLP, MAG
MS damage	Not affected	Primary target

14. SERCA - Key Facts

SERCA = Smooth Endoplasmic Reticulum Ca²⁺ ATPase

Pumps Ca²⁺ from cytosol INTO the ER lumen (against concentration gradient, uses ATP)
Maintains low cytosolic Ca²⁺ at rest
SERCA2b = neuronal isoform (predominant in neurons)
Regulated by phospholamban (in cardiac muscle) - when phospholamban is phosphorylated by PKA, it releases SERCA → SERCA works faster → faster Ca²⁺ reuptake
Thapsigargin = SERCA inhibitor (causes ER Ca²⁺ store depletion - experimental tool)

Common exam scenario: SERCA blocked → Ca²⁺ can't return to ER → prolonged cytosolic Ca²⁺ elevation → overactivation of Ca²⁺-dependent enzymes

15. PGP (P-glycoprotein) → Used for drug transport

PGP = P-glycoprotein = MDR1 = ABCB1

ABC transporter on the plasma membrane
Acts as an efflux pump - actively pumps drugs/toxins OUT of cells
Found at the blood-brain barrier (BBB) → limits drug entry into the brain
Glioma cells overexpress PGP → chemotherapy resistance (drugs pumped out before they can work)
Clinically relevant: PGP inhibitors are being studied to improve CNS drug delivery

Exam answer: PGP → efflux pump → pumps drugs out → used/relevant in drug resistance and BBB permeability

One-Line Memory Summary

Topic	Key answer
AMPK	Inhibits mTOR → catabolism
PLC-β	Gq pathway (not RTK)
Mitochondria trap	Glycolysis/lactate = cytoplasm
LDH-A	Hypoxia → ↑ lactate in astrocytes
GAP turns off	RAS
Gβγ of Gi/o	Opens K⁺ channels
GoLoco	Keeps Gβγ free
Depolarization	Cation influx (Na⁺)
SOCS	Inhibits JAK
No TGF-β R1 phospho	No SMAD2/3 activation
RTK + demyelination	MS / oligodendrocyte link
Schwann cells	PNS
Oligodendrocytes	CNS
SERCA	Pumps Ca²⁺ into ER
PGP	Drug efflux pump at BBB

Good luck on your midterm! Let me know if you want me to quiz you on any of these. 🎯

Running Command

python3 -c " import pdfplumber with pdfplumber.open('/home/daytona/workspace/att…

Running Command

cd /home/daytona/workspace && mkdir -p notes_scan && python3 /home/daytona/skill…

Running Command

pdftoppm -jpeg -r 150 '/home/daytona/workspace/attachments/0ea230d3-1b1a-4cd8-96…

analyse_media

Running Command

which tesseract && tesseract --version 2>&1 | head -3

Running Command

for i in $(seq -w 1 16); do echo "=== PAGE $i ===" tesseract /home/daytona/w…

This is a full question bank - 16 pages of MCQs covering neurophysiology and neurobiochemistry. These are clearly from your actual SEU exam pool. Here is a complete answer key with explanations for every question:

Complete Answer Key - Notes_241218 (SEU Question Bank)

PAGES 1-2 (Set 1)

Q	Question	Answer
1	Increase in magnitude of membrane potential	d) None - it's called hyperpolarization, but that option isn't listed correctly here
2	Neuron cell bodies inside CNS	a) Nucleus
3	Saltatory conduction	b) Only at nodes of Ranvier
4	Neuroglial cells support	c) Neurons
5	CNS function	a) Integration
6	Hot stove reflex order	c) Sensory input → integration → motor output
7	Action potential properties	d) None - all listed options are wrong (APs are all-or-nothing with threshold and refractory period)
8-9	Oscilloscope pattern	c) Polarity changes
9	Refractory period	a) Brief time neuron cannot conduct impulse
10	Carries impulses away from CNS	b) Motor
11	Path of information in neuron	b) Dendrites → soma → axon
12	Cannot be controlled consciously	c) Autonomic nervous system

PAGES 2-4 (Biochemistry Set 1)

Q	Question	Answer	Key explanation
13	Cerebroside in myelin	d) 3-Sulfatide	Sulfatide = 3'-sulfated galactocerebroside, dominant in CNS myelin
14	Beta-hydroxybutyrate not standalone	c) Needs glucose for succinyl-CoA via TCA	SCOT needs succinyl-CoA pool; glucose keeps TCA primed
15	Ca²⁺ storage in neurons	a) SERCA type 2b	Neuronal isoform of SERCA pumps Ca²⁺ into ER
16	Neuron-oligodendrocyte crosstalk	a) MAG	MAG at innermost myelin contacts axon directly
17	Dendritic cytoskeleton protein	c) Tau (your exam key)	MAP2 is standard teaching, but follow your key
18	GFAP accumulation disorder	b) Alexander's disease	GFAP mutations → Rosenthal fibers in astrocytes
19	PMCA sensitivity to low Ca²⁺	c) Ca²⁺ binding to calcium-sensitive site on PMCA	Calmodulin binding lowers Km - but this option describes direct Ca²⁺ sensing
20	Astrocytes overcome glutamate excitotoxicity	b) Absorb glutamate → convert to glutamine	Via EAATs + glutamine synthetase
21	Proteins activating FGF receptors	c) NCAMs	Neural cell adhesion molecules act as FGF co-receptors
22	Na/K-ATPase mutation in parkinsonism	a) Alpha-3 subunit	ATP1A3 mutations → Rapid-onset Dystonia-Parkinsonism
23	Pyruvate carboxylase in astrocytes	d) Provides metabolites for neuronal TCA + neurotransmitter synthesis	Anaplerosis - replenishes oxaloacetate; neurons lack pyruvate carboxylase
24	ApoE in ABC transporter maintenance	c) Enables ABC transporters to bind ligands and transport them	ApoE is a lipid-binding chaperone for ABCA1
25	Glucose under hypoglycemia	c) Astrocytic glycogenolysis	Astrocytes = only CNS glycogen store
26	GABA shunt enzymes	a) GABA transaminase + succinate semialdehyde dehydrogenase + glutamate decarboxylase	Full GABA shunt pathway
27	Brain energy supply	a) Aerobic glycolysis	Brain = obligate glucose user (aerobic)
28	Tryptophan downregulation in protein-rich diet	a) Other LNAAs compete for same transporter	Large neutral amino acid transporter (LAT1) has shared substrates

PAGE 5-7 (Set 2 - Neurophysiology)

Q	Question	Answer	Key explanation
1	Axons inside CNS	a) Tracts	Tracks/Tracts = axon bundles inside CNS; nerves = PNS
2	AP reaches presynaptic terminal	d) All answers correct	Ca²⁺ channels open → vesicles fuse → NT released
3	During IPSP	a) Membrane becomes more negative	Hyperpolarization = inhibitory
4	Role of Ca²⁺ at synapse	a) Facilitate transmitter release	Ca²⁺ triggers vesicle fusion (synaptotagmin)
5	Cl⁻ channels open at -55 mV	c) Cl⁻ enters, moves potential further from threshold	Cl⁻ equilibrium ~-70 mV; at -55 mV, Cl⁻ flows in → hyperpolarizes
6	What becomes insulation in myelination	d) The myelin sheath	Schwann cell membrane wraps axon → myelin
7	Neuron transmitting from environment to CNS	c) Sensory neuron	Afferent/sensory neurons carry signals TO CNS
8	Increase in magnitude of membrane potential	a) Hyperpolarization	More negative = larger magnitude
9	Refractory period	b) Brief time neuron cannot conduct impulse
10	Immediately after NT binds receptor	c) Chemically gated ion channels open	NT binding → conformational change → ion channel opens
11	Neuroglia forming myelin in CNS	b) Oligodendrocytes	Schwann cells = PNS; Oligodendrocytes = CNS
12	Vm=0, ion higher inside	c) Move out of cell	Concentration gradient drives outward flow when no electrical force
13	Where AP is generated on axon	b) Axon hillock	Highest density of voltage-gated Na⁺ channels
14	EPSP vs IPSP	b) Is a depolarizing potential	EPSP = depolarizing; IPSP = hyperpolarizing
15	Autonomic nervous system	a) Cannot be controlled by conscious thought
16	Ca²⁺ role at synapse	b) Facilitate transmitter release
17	Repolarization of AP	c) Efflux of K⁺ via voltage-gated K⁺ channels	K⁺ rushes out → membrane repolarizes
18	Divisions of ANS	b) Sympathetic and parasympathetic
19	Cell bodies inside CNS	c) Nucleus
20	Carry impulses away from CNS	b) Motor
21	When axon terminal depolarizes	b) Ca²⁺ enters → NT secreted	Voltage-gated Ca²⁺ channels open at terminal

PAGES 8-9 (Set 3 - Mixed)

Q	Question	Answer	Key explanation
22	Dendritic cytoskeleton protein	c) Tau (exam key)
23	Glucose under hypoglycemia	d) Astrocytic glycogenolysis
24	Low rate of small neutral AA transport through BBB	c) To prevent changes in neurotransmitter content	Glycine, GABA are neurotransmitters - keeping them out of BBB prevents disruption
25	Beta-hydroxybutyrate not standalone	d) Needs glucose for succinyl-CoA
26	Astrocytes balance K⁺	a) Large negative membrane potential	K⁺ spatial buffering driven by high K⁺ conductance and very negative Vm
27	Astrocytes overcome glutamate excitotoxicity	a) Absorb glutamate → convert to glutamine
28	Glucose transporter to neurons	b) GLUT3	GLUT3 = high-affinity, neuron-specific; GLUT1 = astrocytes/BBB
29	ABC transporter upregulated during myelination	a) ABCA2	ABCA2 transports sphingomyelin/lipids needed for myelin assembly in oligodendrocytes
30	Na/K-ATPase mutations in parkinsonism	c) Alpha-3 subunit
31	Phospholipid in inner leaflet of myelin	a) Ethanolamine-containing plasmalogen	Plasmalogens (vinyl-ether phospholipids) are enriched in CNS inner membrane leaflet, protect against ROS
32	Neuronal H⁺-ATPase function	c) Maintains high H⁺ for pumping NTs into storage vesicles	V-type H⁺-ATPase acidifies vesicle lumen → H⁺ gradient drives NT uptake via antiport
33	Rapidly decreasing cytoplasmic Ca²⁺	d) Na/Ca exchanger (fast) + c) PMCA	NCX = fast/high capacity; PMCA = high affinity/slow. NCX is the primary RAPID system
34	Lipids NOT synthesized by neural cells	b) Linoleic and linolenic acid	These are essential fatty acids (omega-6, omega-3) - must come from diet

PAGE 9-10 (Set 4)

Q	Question	Answer	Key explanation
1	PMCA sensitivity	d) Ca²⁺ binding to calcium-sensitive site
2	Pyruvate carboxylase	b) Provides metabolites for TCA + neurotransmitter synthesis
3	Microglia protect neurons	a) Cytokines, neurotrophins, phagocytosis of damaged cells	Microglia = brain's immune cells; phagocytose debris, provide trophic support
4	Thiamine deficiency downregulates	d) Succinate dehydrogenase and alpha-ketoglutarate dehydrogenase	Thiamine (B1) = cofactor for PDH, alpha-KG dehydrogenase, transketolase - TCA enzymes affected
5	Phenylketonuria → less NT production	a) Downregulation of essential AA transport via L-amino acid transporters	High phenylalanine competes with Tyr, Trp (precursors of dopamine, serotonin) at LAT1

PAGES 10-11 (Set 5)

Q	Question	Answer	Key explanation
1	NOT in knee-jerk reflex	c) Interneuron (and d) Brain)	Knee-jerk is a monosynaptic reflex - only sensory + motor neuron; no interneuron, no brain
2	Axons outside CNS	b) Nerves	Nerves = axon bundles in PNS
3	EPSP vs IPSP	c) Depolarizing potential
4	Myelin-forming in CNS	c) Oligodendrocytes
5	AP at presynaptic terminal	d) All answers correct
6	ANS divisions	a) Sympathetic and parasympathetic
7	Refractory period	a) Brief time cannot conduct
8	CNS function	c) Integration
9	Away from CNS	a) Motor
10	AP generated at	b) Axon hillock
11	Depolarization: gates open for	c) Sodium ions	Na⁺ rushes IN → depolarization
12	Schwann cells are	b) Neuroglial	Schwann cells = PNS neuroglia
13	IPSP membrane potential	a) More negative
14	Ca²⁺ at synapse	b) Facilitate transmitter release
15	Cl⁻ channels at -55 mV	b) Enter, move potential further from threshold
16	Repolarization	b) Efflux of K⁺
17	After NT binds receptor	b) Chemically gated channels open

PAGES 13-16 (Advanced Biochemistry)

Q	Question	Answer	Key explanation
18	Path of info in neuron	c) Dendrites → soma → axon
19	Increase in magnitude	a) Hyperpolarization
20	Beta-hydroxybutyrate	a) Needs glucose for succinyl-CoA
1	NT reuptake mechanism	b) Na-dependent symport	Na⁺ gradient drives NT co-transport back into presynaptic terminal (e.g., serotonin, dopamine transporters = Na⁺ symporters)
2	Myelin proteolipid protein function	c) Strengthen myelin + define intraperiod lines	PLP holds extracellular leaflets together
3	Prevents ADP accumulation	d) Adenylyl kinase (adenylate kinase)	2ADP → ATP + AMP; keeps ADP from accumulating; also creatine kinase is important but adenylyl/adenylate kinase is the specific answer here
4	Myelin protein in MS	c) Myelin-oligodendrocyte glycoprotein (MOG)	MOG is a major target of autoantibodies in MS and MOG-antibody disease
1	Glutamate compartmentalization	c) Distribution of glutamate-metabolizing enzymes in different brain regions and cells	Glutamine synthetase in astrocytes; glutaminase in neurons - anatomically separated
2	PMCA sensitivity	d) Ca²⁺ binding to calcium-sensitive site
3	Pyruvate carboxylase	c) Provides metabolites for TCA + NT synthesis
4	Ketone bodies - reason + form	b) High liver FA catabolism + hypoglycemia → converted to acetyl-CoA	Starvation/hypoglycemia → liver makes ketones → brain uses them → enter TCA as acetyl-CoA via SCOT
5	Higher glutamine synthetase	d) Astrocytes	Glutamine synthetase is astrocyte-specific in brain
6	Neurons provide acetyl group to myelin cells	a) N-acetyl aspartate (NAA)	NAA made in neurons, exported to oligodendrocytes → cleaved by aspartoacylase → acetyl-CoA for myelin lipid synthesis
7	Neuronal H⁺-ATPase function	d) Maintains H⁺ for pumping NTs into vesicles
8	Acetyl-CoA carbon skeleton transporter	b) Citrate	Citrate = main acetyl-CoA carrier out of mitochondria to cytoplasm (for fatty acid synthesis)
9	Cerebroside in myelin	a) 3-sulfatide
10	Flippases in neurons	d) ABCA1 transporter	ABCA1 translocates phosphatidylserine from outer to inner leaflet (flippase activity)
11	Myelin protein in MS	b) MOG
12	ABC transporter in oligodendrocyte myelination	b) ABCA2
13	Tryptophan downregulation	d) Competing LNAAs
14	Glial cells prevent K⁺ excitotoxicity	b) Influx of K⁺ and water → efflux to distal regions	Spatial buffering: K⁺ + water enter astrocytes at active site, flow through gap junctions, exit distally
15	Neuron-oligodendrocyte crosstalk	c) MAG

Top Concepts to Nail for the Exam

High-frequency topics across all pages:

EPSP = depolarizing; IPSP = hyperpolarizing (more negative)
Repolarization = K⁺ efflux (not Na⁺ exit)
AP site = axon hillock
CNS bodies = nucleus; PNS bodies = ganglion; CNS axons = tracts; PNS axons = nerves
Ca²⁺ at synapse = triggers NT release (not a NT itself)
Oligodendrocytes = CNS myelin; Schwann cells = PNS myelin
Astrocytic glycogenolysis = brain glucose under hypoglycemia
GLUT3 = neurons; GLUT1 = BBB/astrocytes
Knee-jerk = monosynaptic = NO interneuron, NO brain
MOG = MS target; MAG = neuron-oligodendrocyte crosstalk
ABCA2 upregulated in oligodendrocytes during myelination
NAA = acetyl group carrier from neurons to oligodendrocytes
Adenylate kinase = prevents ADP accumulation
Na-dependent symport = NT reuptake mechanism

Good luck on your midterm - you've got a strong grasp of this material! 🎯

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