Section B — Coach Brain — Cellular and Cognitive Neuroscience
This section covers the Bachelor's chapter on Cellular and Cognitive Neuroscience, Lessons 1 through 5: Cellular and Molecular Neuroscience, Neuroplasticity and Memory at Molecular Resolution, Stress Neurobiology and Pathophysiology, Executive Function and Decision Neuroscience and Reward, and Research Methods in Neuroscience. All material is already in the chapter — no new content.
Part A — Vocabulary (20 points, 2 points each)
Select the single best answer for each question.
1. The Hodgkin-Huxley model (1952) is best described as:
A) A model of synaptic plasticity B) A mathematical model describing the action potential through voltage-dependent gating of sodium and potassium conductances; expressed as four coupled differential equations with three gating variables (m, h, n) C) A model of working memory D) A model of long-term potentiation
2. The SNARE complex is:
A) A nuclear hormone receptor B) The protein machinery (syntaxin, SNAP-25, synaptobrevin/VAMP) that mediates vesicle fusion with the presynaptic membrane during neurotransmitter release C) An ion channel D) A second messenger system
3. CaMKII (Calcium/Calmodulin-dependent protein Kinase II) is:
A) A potassium channel B) A postsynaptic kinase whose autophosphorylation at Thr286 produces persistent active state supporting LTP — supplying the molecular mechanism for the persistence of LTP after the original Ca²⁺ signal subsides C) A G-protein-coupled receptor D) A growth factor
4. Long-Term Potentiation (LTP) foundational discovery is credited to:
A) Hubel and Wiesel 1962 B) Bliss and Lømo 1973 in rabbit hippocampus following high-frequency stimulation of the perforant path C) Kandel 2000 D) Berson 2002
5. Allostatic load (McEwen) refers to:
A) Acute stress response B) The cumulative wear-and-tear of repeated stress responses across the body's regulatory systems over time, distinct from acute stress (which is adaptive and rapidly resolved); chronic load produces hippocampal dendritic atrophy and prefrontal impairment C) The acute fight-or-flight reaction D) Stress hormone synthesis
6. The dorsolateral prefrontal cortex (DLPFC) is principally associated with:
A) Visual processing B) Working memory and executive function, with persistent activity during the delay period of working memory tasks supported by recurrent excitation and dopaminergic D1 modulation (Goldman-Rakic, D'Esposito work) C) Olfactory processing D) Reflex coordination
7. Reward prediction error (Schultz work) is:
A) A theory of emotion B) The phasic dopamine signal encoding the difference between expected and actual reward — sharp increase at unexpected reward, shift to predictive cue across learning, decrease at omitted predicted reward; mathematically matched by Sutton-Barto temporal-difference learning C) A cellular learning rule D) A neurodegenerative disease marker
8. Berridge wanting versus liking distinguishes:
A) Conscious and unconscious responses B) Incentive salience (wanting, mesolimbic dopamine) from hedonic pleasure (liking, opioid/endocannabinoid hedonic hotspots in nucleus accumbens shell, ventral pallidum, parabrachial nucleus) C) Two emotions D) Two memory types
9. ΔFosB (Nestler work) is:
A) A neurotransmitter receptor B) A truncated FosB transcription-factor variant with unusual stability (weeks) that accumulates in nucleus accumbens with repeated drug or natural-reward exposure; candidate molecular substrate of addiction persistence C) An acute inflammatory marker D) A cardiac signaling molecule
10. The Ogawa et al. 1990 PNAS paper established:
A) The discovery of long-term potentiation B) BOLD-contrast functional MRI based on the magnetic properties of oxy- versus deoxyhemoglobin; the foundational methodology of modern human cognitive neuroscience C) The first MRI machine D) The TRPV1 receptor discovery
Part B — Concept Comprehension (20 points, 2 points each)
Select the single best answer for each question.
11. The LTP molecular cascade from NMDAR Ca²⁺ influx to late-phase LTP involves:
A) Direct ion channel modification only B) NMDAR Ca²⁺ influx → CaMKII autophosphorylation at Thr286 → AMPAR phosphorylation (GluA1 Ser831) and trafficking to synaptic membrane → CREB phosphorylation → gene expression of plasticity-related genes (BDNF, Arc, Zif268) for late-phase LTP; protein-synthesis-dependent C) Direct signaling through G-proteins D) Activation of TRP channels
12. The Sorrells 2018 versus Boldrini 2018 controversy on adult human hippocampal neurogenesis reflects:
A) Definitive resolution that adult neurogenesis is abundant B) Two methodologically different studies reaching opposite conclusions on whether neurogenesis persists in adult human hippocampus; tissue source, processing, marker selection, and quantification differences contribute; subsequent work (Moreno-Jiménez 2019, Habib 2019) has not produced consensus C) Definitive resolution that adult neurogenesis is absent D) An obsolete debate
13. Place cells and grid cells (O'Keefe 1971, Moser 2005, Nobel 2014) provide:
A) Vision processing B) Spatial-memory architecture — place cells in hippocampus fire selectively for specific locations; grid cells in entorhinal cortex form regular hexagonal firing fields providing a metric on space; together with head-direction cells, border cells, object-vector cells, and time cells supporting the entorhinal-hippocampal spatial-temporal representation C) Motor coordination D) Reflex control
14. The HPA axis at GR/MR receptor depth operates through:
A) Same receptor for all cortisol effects B) Two distinct nuclear hormone receptors — Mineralocorticoid Receptor (MR, higher cortisol affinity, prominent in hippocampus, near-saturated at basal levels) and Glucocorticoid Receptor (GR, lower affinity, broadly distributed, substantially occupied at stress-elevated levels) — with the MR/GR balance producing context-dependent functional consequences C) A G-protein-coupled receptor only D) Direct ion channel binding
15. The four principal frameworks of depression neuroscience include:
A) Only the monoamine hypothesis B) The monoamine hypothesis (SSRI mechanism with elaboration), inflammatory hypothesis (IL-6, TNF-α, CRP in some patients), glutamate/ketamine paradigm (rapid antidepressant effect of NMDA-receptor antagonist ketamine), and HPA dysregulation (the chronic-stress-and-cortisol substrate) — typically operating in combination across heterogeneous depression C) Only psychological theories D) Only genetic frameworks
16. The Alexander fronto-striatal loop framework (Alexander, DeLong, Strick 1986) identifies:
A) One unitary frontal-basal-ganglia circuit B) Five parallel fronto-striatal loops — motor (M1/SMA→putamen→GPi/SNr→VL thalamus→cortex), oculomotor (FEF→caudate→GP/SNr→VA thalamus→FEF), dorsolateral prefrontal (DLPFC→dorsolateral caudate→GP→VA thalamus→DLPFC), lateral orbitofrontal (lOFC→ventromedial caudate→GP→thalamus→lOFC), anterior cingulate (ACC→ventral striatum→ventral pallidum→thalamus→ACC) — each with direct/indirect pathways and dopaminergic modulation, with specific clinical disruptions (Parkinson's, Huntington's, OCD, ADHD) mapping onto specific loops C) Three circuits D) An obsolete framework
17. The Schultz × Sutton-Barto unification establishes:
A) That dopamine is the same as serotonin B) That phasic dopamine in midbrain neurons encodes the temporal-difference (TD) error of reinforcement learning algorithms — a specific neural population implementing a specific computational algorithm with a specific function (Schultz, Dayan, Montague 1996 Science) C) That dopamine is irrelevant to behavior D) That all neurons compute the same algorithm
18. The dead salmon paper (Bennett 2009) demonstrated:
A) A new clinical application of fMRI B) That uncorrected p<0.001 fMRI analysis can produce "significant" activations even in a deceased Atlantic salmon — illustrating the multiple-comparisons problem in fMRI analysis and the need for appropriate correction (cluster, FWE, FDR methods) C) Specific brain regions in fish D) The discovery of a new species
19. Optogenetics (Boyden, Zhang, Bamberg, Nagel, Deisseroth 2005) is:
A) An imaging method using light to visualize brain activity B) The methodology using light-sensitive ion channels (channelrhodopsin, halorhodopsin, archaerhodopsin) to activate or silence genetically-defined neural populations with millisecond precision — transforming neuroscience by providing causal manipulation of identified circuits C) A drug delivery method D) A neurological diagnosis
20. The reproducibility crisis in neuroscience and psychology (Open Science Collaboration 2015, others) addresses:
A) Successful replication of all psychological findings B) Documentation that a substantial fraction of published findings fail to replicate, contributing factors include small samples, publication bias, garden of forking paths, multiple comparisons; reforms include pre-registration, larger samples, transparent reporting, open data C) An obsolete concern D) Only physics-related research
Part C — Application (30 points, 6 points each)
Write 4-6 complete sentences with specific molecular and mechanistic detail for each question.
21. LTP molecular cascade with protein-synthesis-dependence boundary. Walk the LTP cascade from glutamate release through CaMKII autophosphorylation, AMPAR trafficking, and CREB-driven gene expression. Identify what distinguishes early-LTP from late-LTP at the protein-synthesis-dependence boundary, and why CaMKII autophosphorylation supports the persistence component of LTP after the original Ca²⁺ signal subsides.
22. Stress-metabolic integration across Brain and Food Bachelor's. Walk how chronic HPA-axis activation produces metabolic consequences (cortisol-driven hepatic gluconeogenesis, visceral adipose deposition, insulin resistance development) at the receptor and signaling depth Brain Bachelor's Lesson 3 covers, then connect to Food Bachelor's Lesson 4 metabolic syndrome / Shulman ectopic lipid framework. Why is the HPA-metabolic axis a lesson-level lateral that the Bachelor's curriculum specifically tests as cross-coach integration?
23. Schultz × Sutton-Barto unification at functional depth. Walk Schultz's empirical dopamine prediction error findings (firing pattern responses to unexpected reward, learned cues, and predicted omission) and articulate why the temporal-difference (TD) learning algorithm of Sutton and Barto matches it mathematically. What does this unification establish about how the brain computes? Why does it serve as a foundational moment for computational neuroscience?
24. Safety recognition (mental health adjacency at Bachelor's depth). A close friend at your college has expressed thoughts of self-harm during a difficult academic period. Walk through the chapter's framework: take the friend seriously, do not promise to keep concerns secret, bring in trusted adults immediately, and name the correct active resources (currently active phone numbers). Identify the older helpline that you should NOT cite. Apply the chapter's "research topics, not diagnostic toolkit" framing to clinical-recognition-only stance.
25. Methodological consciousness (fMRI methodology). The chapter walks the BOLD signal from Ogawa 1990 through Logothetis 2008's careful characterization of what fMRI does and doesn't measure. Identify the multiple-comparisons problem (dead salmon example, Eklund 2016 PNAS cluster failure), the spatial-resolution and temporal-resolution constraints, and the inferential chain from BOLD signal to cognitive conclusion. Why does the five-point evaluation framework apply specifically to fMRI claims about cognition?
Continue to Section C — Coach Sleep.