narrative
Chapter 1 – The Cellular Foundations of Behavior
1.1 The Biological Approach to Behavior
Imagine you’re watching someone cry, or a dog wag its tail, and you wonder:
“What are they thinking? What are they feeling?”
A biological psychologist answers that question in a very specific way.
Instead of saying, “He’s like this because his childhood was sad,” they look at four angles:
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Physiology: What is the body doing right now? Which brain areas are active, which
hormones and neurotransmitters are flowing?
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Ontogeny (Development): How did this behavior develop across this person’s life?
What changed from baby → child → adult?
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Evolution: How did this behavior appear across generations? Did our ancestors have
something similar?
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Function: Why did this behavior survive evolution? What advantage did it give?
Biological psychology (aka biopsychology, behavioral neuroscience, etc.) says:
You behave the way you do because of brain mechanisms that helped your
ancestors survive and reproduce.
Your brain is a giant city of neurons and glia.
Neurons are the ones sending messages to each other, to muscles, to glands.
Glia are like the support staff: cleaners, feeders, guides, insulators. They’re smaller, but without
them the city collapses.
Three things this field never shuts up about:
1. Perception happens in your brain, not in the world.
You don’t “see” light outside; you see what light makes your brain do.
Same with sound, touch, pain – it’s all patterns of brain activity.
2. Mind and brain are inseparable (monism).
Mental activity is brain activity, just described differently – like saying “temperature” vs
“molecule speed.”
Asking “does brain activity cause thoughts?” is like asking “does running cause moving
your legs?” They’re just two descriptions of the same process.
3. Differences in brains explain differences in people.
Why some people are super visual, some can’t recognize faces well, some are more
sensitive to pain → their brains are wired/organized slightly differently.
When biological psychologists explain behavior, they don’t say “he did it because he wanted to.”
They choose one (or combine) of these:
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Physiological:
“He’s aggressive because of increased testosterone affecting the amygdala and other
brain circuits.”
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Ontogenetic:
“Her language ability developed through genes + early environment + schooling.”
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Evolutionary:
“Goose bumps come from our ancestors who had thicker fur; raising hair made them
look bigger.”
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Functional:
“A camouflaged coat evolved because it made animals harder to see, so they were less
likely to be eaten.”
Then there are careers. Same science, different costumes:
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Researchers (usually PhD): neuroscientist, behavioral neuroscientist, cognitive
neuroscientist.
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Practitioners (PhD/PsyD/Master’s): clinical psychologist, neuropsychologist.
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Medical route (MD): neurologist, psychiatrist.
All of this leads to neuroethics: just because we can study brains, should we always?
Studying animals raises big questions. Why use them?
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Many mechanisms are similar to humans.
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Sometimes animals are just interesting in themselves.
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They teach us about human evolution.
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We can’t ethically slice open human brains or electrically stimulate people’s amygdala
just because we’re curious.
So we get conflict:
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Minimalists: “Some animal research is okay if suffering is low and benefit is high. Let’s
use the 3 Rs: Reduce, Replace, Refine.”
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Abolitionists: “Animals have the same rights as humans. No research, no exceptions.”
Even human research has ethical worries:
Is consent really voluntary? Is the sample diverse enough, especially for drug trials? Or is it
mostly one demographic?
The core idea of the chapter:
Your experiences, your personality, and even your moral questions about research
— all of it is being processed in the 1.3 kg of tissue sitting in your skull.
1.2 Neurons and Other Cells
Zoom in from “the brain” to the tiny citizens inside it: neurons and glia.
You have about 86 billion neurons.
Each one is like a tiny, living wire that can receive signals, process them, and pass them on.
Cajal, in the late 1800s, was the guy who proved the brain is made of separate cells instead of
one continuous blob. With a special stain on baby brains (smaller cells, easier to see), he saw:
Neurons aren’t fused—they’re close, but separated by tiny gaps (later called synapses).
Like all animal cells, neurons have:
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A membrane: the border control—protein gates decide who gets in and out.
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A nucleus: where the DNA (instruction manual) lives.
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Ribosomes: protein factories.
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Endoplasmic reticulum: the protein shipping network.
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Mitochondria: energy factories.
Brain work is energy-expensive; if mitochondria are struggling, mood and cognition
suffer.
A typical neuron has:
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Dendrites: tree-like branches receiving messages. They’re covered in receptors,
sometimes with tiny bumps (spines) to increase contact area.
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Soma / Cell body: contains nucleus, ribosomes, mitochondria. Also receives synapses.
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Axon: a long, thin cable that sends the message out. One axon per neuron, but it can
branch.
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Myelin sheath: fatty wrapping around many vertebrate axons → speeds up signal.
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Presynaptic terminals: little bulbs at the end where chemicals are released to the next
cell.
Information flow words:
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Afferent: brings info into a structure.
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Efferent: carries info away from a structure.
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Interneuron: stays inside one structure (local communicator).
Shape = destiny:
A Purkinje cell with huge branching dendrites can receive input from up to 200,000 other
neurons.
Then glia enter the chat:
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Astrocytes: star-shaped. They hug synapses, coordinate activity, and help bring more
nutrients to active brain areas.
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Microglia: the tiny clean-up crew and immune army. They eat dead cells, fight viruses,
and prune weak synapses.
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Oligodendrocytes / Schwann cells: build myelin (CNS vs PNS).
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Radial glia: developmental guides; they literally help neurons find their proper location
when the brain is forming.
Now, because neurons are fragile and irreplaceable, the brain builds a security fence: the
blood–brain barrier (BBB).
Capillary walls in the brain are tightly packed so almost nothing can slip through.
Only:
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Small, uncharged molecules (O₂, CO₂).
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Fat-soluble stuff (alcohol, some drugs).
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Things with active transport (glucose, amino acids, certain vitamins) can get in.
The brain runs almost entirely on glucose, and to use glucose well, it needs thiamine (vitamin
B₁).
Long-term thiamine deficiency can destroy neurons and cause severe memory problems (think
Korsakoff’s syndrome).
And surprisingly, your gut bacteria are part of this story too.
They make chemicals (vitamins, amino acids) that go into your blood and influence mood,
motivation, and inflammation. Stress can shift the microbiome toward more inflammation →
linked to depression.
So even “just your mood” might be: brain + mitochondria + BBB + gut bacteria all gossiping
together.
1.3 The Action Potential
Now we follow a message along the neuron.
At rest, a neuron is like a loaded bow: quiet, but ready.
The inside is about –70 mV, slightly negative compared to the outside. This is the resting
potential.
The membrane is selectively permeable and has a sodium–potassium pump constantly
working:
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Pumps 3 Na⁺ out
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Brings 2 K⁺ in
So you end up with:
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Lots of Na⁺ outside
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Lots of K⁺ inside
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Big, negative proteins trapped inside → inside stays negative
Forces on ions:
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Na⁺ wants to rush in (both electrical and concentration gradient).
●
K⁺ is pulled in electrically (inside is negative) but pushed out by concentration (there’s
more K⁺ inside).
The result: a small leak of K⁺ out, helping maintain the resting potential.
This resting state is not “doing nothing.”
It’s like a spring compressed and ready to explode when triggered.
When the neuron is stimulated enough and the membrane depolarizes to a certain point, it hits
threshold.
At threshold:
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Voltage-gated Na⁺ channels swing open.
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Na⁺ rushes in, pushed by both gradients.
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The inside flips from negative to positive.
This is the rising phase of the action potential.
Then:
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Na⁺ channels snap shut at the peak.
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Voltage-gated K⁺ channels are open, and now K⁺ is pushed out both electrically (inside
now positive) and by concentration gradient.
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K⁺ flows out → the membrane potential falls back down (and even overshoots:
hyperpolarization).
●
The Na⁺/K⁺ pump gradually returns the original ion distribution.
This big spike is the action potential: a sudden, brief reversal of membrane potential that
travels down the axon.
Key rule: All-or-none law.
If threshold is reached, the action potential goes full blast, same size, same speed.
Stronger stimulus doesn’t give bigger action potentials, it just makes them occur more often or
in different patterns.
After an action potential, we have:
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Absolute refractory period: no new AP possible (Na⁺ channels are inactivated).
●
Relative refractory period: possible, but only with a stronger stimulus (membrane is
more negative than rest).
As the action potential moves, Na⁺ entering at one point depolarizes the next bit of membrane,
causing that segment to fire. This is propagation. The impulse doesn’t get weaker because it’s
regenerated each step.
In myelinated axons, ions can only enter/exit at the nodes of Ranvier, so the AP appears to
“jump” from node to node. This is saltatory conduction: faster and energy-efficient.
Tiny local neurons without axons, however, don’t use full action potentials. They use graded
potentials (small changes that fade with distance).
Also: local anesthetics like Novocain block Na⁺ channels → no action potential → no pain
signal reaching the brain.
Chapter 2 – Synapses
2.1 The Concept of the Synapse
Cajal showed neurons are separate. Sherrington showed they communicate using tiny delays
→ the synapse.
He studied reflex arcs (sensory neuron → spinal cord → motor neuron → muscle).
He noticed:
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Reflexes are slower than a simple AP along one axon.
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Several weak stimuli can add up.
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When one muscle flexes, the opponent muscle relaxes.
From this, he inferred:
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There must be a gap (synapse) where transmission is slower.
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Synapses can sum inputs over time (temporal summation) and space (spatial
summation).
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Some synapses must be inhibitory to relax opposing muscles.
At excitatory synapses:
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The postsynaptic neuron gets a small depolarization (EPSP) because Na⁺ enters.
One EPSP may be too small, but multiple close together can add up and reach
threshold.
At inhibitory synapses:
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The postsynaptic neuron becomes more negative (IPSP), often via Cl⁻ entering.
This makes it harder to reach threshold.
Neurons are constantly receiving a mix of EPSPs and IPSPs, and the combined effect decides:
Fire an action potential or not?
That’s why we often say a neuron is like a decision maker.
2.2 Chemical Events at the Synapse
Sherrington thought it might be electrical, but Loewi proved it’s chemical (at most synapses).
His frog-heart experiment showed that stimulating a nerve released a substance into the fluid
that changed heart rate. That substance → neurotransmitter.
At a chemical synapse, the sequence is:
1. The presynaptic neuron makes neurotransmitters (from amino acids in food).
2. They’re stored in vesicles in the terminal.
3. An action potential arrives → opens Ca²⁺ channels.
4. Ca²⁺ enters → triggers exocytosis (vesicles fuse with membrane, releasing transmitter
into synaptic cleft).
5. Transmitter binds to receptors on the postsynaptic cell.
6. It detaches from the receptor.
7. It’s taken back up (reuptake) or broken down by enzymes.
8. There’s often negative feedback from postsynaptic cell or autoreceptors to control
future release.
Neurotransmitters include:
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Amino acids: glutamate, GABA, glycine.
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Modified amino acid: acetylcholine.
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Monoamines: dopamine, norepinephrine, epinephrine.
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Gases: nitric oxide (NO).
Diet → amino acids → neurotransmitters.
That’s why nutrition matters even on a molecular brain level.
Receptors can cause:
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Ionotropic effects: fast, brief, “on/off.”
Like a door that opens to Na⁺ (excitatory, often glutamate) or Cl⁻ (inhibitory, often
GABA).
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Metabotropic effects: slow, long-lasting.
The receptor activates a G protein → second messenger → affects channels,
metabolism, or gene expression.
Used by dopamine, serotonin, neuropeptides, etc., for things like mood, hunger,
attention.
Drugs can hijack this system:
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Hallucinogens mimic serotonin at certain receptors.
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Opiates (like morphine) bind to endorphin receptors.
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Stimulants like cocaine and amphetamine block reuptake of
dopamine/serotonin/norepinephrine → their effects last longer.
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Ritalin works similarly to cocaine but slower and more controlled.
The synapse also has feedback:
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Autoreceptors on the presynaptic terminal detect how much transmitter was released
and reduce future release when it’s too much.
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Postsynaptic cells can send reverse messengers (like anandamide) back to tell the
presynaptic cell to chill.
Cannabinoids (weed) mimic these reverse messengers.
Rarely, some synapses are electrical (gap junctions), where ions pass directly—used when
timing must be perfectly synchronized (like breathing rhythms).
Hormones are like “body-wide announcements” compared to neurotransmitters’ private
messages.
The pituitary attached to the hypothalamus releases hormones like oxytocin, vasopressin, and
others that regulate many systems.
The big idea of this chapter:
Behavior is shaped not just by action potentials, but by which chemicals are
released, where, how fast, and how long they act.
Chapter 3 – Anatomy and Research Methods
3.1 Structure of the Vertebrate Nervous System
First, a simple split:
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CNS = brain + spinal cord.
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PNS = everything else (nerves connecting CNS to body).
PNS splits into:
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Somatic nervous system: controls muscles + carries sensory info.
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Autonomic nervous system: controls organs (heart, intestines, etc.).
Autonomic has:
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Sympathetic (“fight or flight”): increases heart rate, decreases digestion, mainly uses
norepinephrine.
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Parasympathetic (“rest and digest”): slows heart, increases digestion, uses
acetylcholine.
The spinal cord is like a highway:
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Dorsal roots: sensory info into spinal cord.
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Ventral roots: motor commands out to muscles.
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Center = gray matter (cell bodies, dendrites).
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Surrounding = white matter (myelinated axons) sending info up/down.
Then the brain itself is divided into:
●
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Hindbrain (medulla, pons, cerebellum)
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Medulla: vital reflexes (breathing, heart rate, vomiting).
○
Pons: “bridge” where many axons cross sides.
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Cerebellum: movement, balance, coordination, but also timing and attention.
Midbrain
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Tectum: superior colliculus (vision), inferior colliculus (hearing).
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Tegmentum.
○
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Substantia nigra: dopamine path for movement (degeneration here →
Parkinson’s).
Forebrain
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Thalamus: relay station for most sensory info.
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Hypothalamus: motivated behavior (eating, drinking, sex, temperature) and
hormone control via pituitary.
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Amygdala: emotional evaluation, especially fear.
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Basal ganglia: habits, learning, vigor of movement.
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Hippocampus: memory for events and spatial navigation.
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Basal forebrain (nucleus basalis): arousal and attention.
The brain also has ventricles and a central canal filled with cerebrospinal fluid (CSF).
CSF cushions the brain, supports its weight, and carries nutrients.
3.2 The Cerebral Cortex
The cerebral cortex is the wrinkly outer layer that makes humans extra dramatic and
complicated.
Two hemispheres are connected by:
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Corpus callosum
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Anterior commissure
The cortex is layered and columned:
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Certain layers are thicker in sensory areas (like layer IV).
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Some are thicker in motor areas (like layer V).
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Cells in a vertical column often respond to the same type of input (like the same patch
of skin).
Main lobes:
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Occipital lobe: vision. Damage → cortical blindness.
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Parietal lobe: body senses & spatial processing. The postcentral gyrus receives touch &
body-position info.
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Temporal lobe: hearing, language (left side mostly), complex vision (faces, movement),
emotional/motivational behavior. Damage can cause strange emotional changes
(Klüver–Bucy).
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Frontal lobe: movement (primary motor cortex) + planning, decision-making, working
memory, emotion regulation (prefrontal cortex).
The prefrontal cortex has subregions for:
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Movement planning,
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Using memory to guide behavior,
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Evaluating future consequences and making decisions.
History detour: prefrontal lobotomies damaged connections here to “treat” severe mental
illness → patients became apathetic, impulsive, emotionally flat. This practice stopped once the
side effects were obvious and drugs became available.
The binding problem:
How does the brain combine color, shape, location, and sound into one unified object?
Answer: it tends to bind sensations that occur at the same time and same place.
3.3 Research Methods
How do we actually know which brain areas do what?
1. Study the effects of damage
○
Natural (stroke, trauma) or intentional (lesions in animals, TMS in humans).
○
See which functions are lost or changed.
2. Stimulate the brain
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Weak electrical or magnetic stimulation, or optogenetics (light-controlled
neurons) in animals.
3. Record brain activity
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EEG: scalp electrodes; great timing, poor spatial detail.
○
MEG: detects magnetic fields; also great timing.
○
PET: radioactive tracer; shows where glucose use (activity) is high.
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fMRI: detects blood-oxygen changes; good spatial detail and widely used.
4. Often, researchers compare brain activity in task vs control condition and subtract to
see what's specifically related to that task.
5. Look at brain anatomy
○
CT scans: X-ray images for tumors/structural damage.
○
MRI: high-resolution structural images.
Phrenology (reading bumps on the skull) was a failed early attempt, but it had the right intuition:
that different brain areas might be linked to different mental functions. Modern methods are just
much more accurate.
The chapter’s main message:
Our understanding of the brain grows as our tools for measuring it get better.
If you want, next step we can:
●
Turn this into Q&A-style prompts so you can test yourself.
●
Or do super short “exam-cram” versions of each chapter with just “If exam asks X,
answer Y.”
CHAPTER 4 — NARRATIVE STORY
VERSION
“How a brain becomes a brain — and why you are who you are.”
1. Genes & Evolution: Why You Act the Way You Do
Everything you do — your quirks, habits, fears, and talents — comes from two parents:
your genes and your environment.
Before Mendel, people thought traits blended like strawberry + milk → smoothie.
WRONG.
Mendel showed traits come in packaged units called genes, sitting on chromosomes like
beads on a string.
Inside the chromosome sits DNA → makes RNA → makes proteins (the real bosses that run
everything in your body).
You can have:
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Homozygous: same gene twice
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Heterozygous: two different versions
Some genes are dominant (they show up even if you have only one copy),
others are recessive (they appear only when you have two copies).
But there is basically no such thing as “a gene for intelligence” or “a gene for anxiety.”
Everything is teamwork — many genes + life experiences.
2. Sex-Linked & Sex-Limited — the drama genes
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Sex-linked genes live on the X or Y chromosome.
→ Why red-green color deficiency is more common in males: they only have one X, so
no backup copy.
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Sex-limited genes exist in both sexes but show up only when the hormones activate
them.
→ e.g., chest hair in men, lactation in women.
They’re like actors waiting backstage for the right lighting.
3. When Genes Change: Mutation, Duplication,
Deletion
Genes can change through:
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Mutation (typo in DNA) — usually BAD
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Microduplication (extra copy)
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Microdeletion (missing copy)
These little mistakes can completely change development.
4. Epigenetics — the “gene on/off switch”
Your DNA doesn’t change, but its activity does.
DNA wraps around histones like a spool:
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Add acetyl group → loosen DNA → gene turns ON
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Add methyl group → tighten DNA → gene turns OFF
Life experiences (stress, diet, nurturing) can change these tags.
Meaning: experience literally changes your gene expression.
5. Heritability — what % of differences are genetic?
Heritability measures variation, not destiny.
Twin studies and adoption studies help estimate it.
High heritability = differences in the population mostly due to genes
BUT environment can still change the trait.
Perfect example:
PKU — genetically can’t break down phenylalanine → cognitive impairment
BUT if you avoid the amino acid → totally normal.
So genetic does NOT mean fixed.
6. Evolution — your ancestors whispering in your DNA
Evolution = genes becoming more or less common over generations.
Darwin called it "descent with modification."
Natural selection keeps traits that help survival/reproduction.
Doesn’t mean “better” — only “better for reproduction at that time.”
Misconceptions:
●
Using a trait doesn’t make it bigger in your kids (Lamarck was wrong)
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Evolution cares about genes, not individuals
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Goosebumps and infant grasp reflex = leftovers from ancestors
Altruism (helping others) is explained by:
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Kin selection (protect your genes through family)
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Reciprocal altruism (I help you now → you help me later)
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Group selection
Module 4.2 — How Your Brain Is Born
1. The baby brain starts early
At 2 weeks, a little tube forms → becomes spinal cord + brain ventricles.
By 7.5 weeks, babies already move because of spinal cord activity (not because of senses).
2. Birth of Neurons — the Five Steps
1. Proliferation – making tons of new cells
2. Migration – traveling to their assigned brain region
3. Differentiation – growing axons, dendrites
4. Synaptogenesis – forming connections
5. Myelination – glia add myelin for faster communication
This continues for decades.
3. Do adults grow new neurons?
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Yes in the nose (olfactory receptors).
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NO in the adult cortex (proved by radioactive carbon levels).
●
Maybe in human hippocampus, but after age 7 → super unsure.
4. How Axons Find Their Target — the legendary
experiment
Roger Sperry rotated a newt’s eye 180°
→ its vision was upside down forever
→ because axons regrew to their original targets, not new ones.
Moral: axons follow chemical trails, not logic.
5. Brain’s Survival Game — Neural Darwinism
Babies’ brains overproduce synapses.
Synapses fight for survival:
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Winners = kept
●
Losers = pruned
Targets release NGF and BDNF.
If a neuron doesn’t get enough → apoptosis (self-destruct).
6. The Developing Brain Is Fragile
Things that damage it:
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alcohol
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toxins
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infections
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malnutrition
Fetal Alcohol Syndrome:
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hyperactivity
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attention problems
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thinner cortex
→ because alcohol increases GABA and decreases glutamate → neurons die from lack
of stimulation.
7. Brain Plasticity — your brain adapting like clay
Experiences shape dendrites throughout life.
Examples:
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enriched environment → more branching
●
blind individuals → visual cortex used for touch/hearing
●
musicians → thicker cortex in auditory/motor areas
BUT too much practice → focal hand dystonia (cramp)
8. Adolescence & Old Age
Adolescents take risks not because their PFC is “immature,”
but because their reward system wants excitement (especially around peers).
Old age:
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some shrinkage
●
memory declines
●
but exercise helps preserve cognition