Chapter 5: Days to Months Before

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Welcome to a deep dive into one of the most, well, profound questions about us.

Yeah.

Our human behavior.

Why did I just do that?

Or maybe, why do I feel this way?

We've previously explored how immediate things, you know, like a sudden sound or rush of hormones, how they shape our actions right in the moment.

But today, we're going even further back.

We're looking at changes that unfold over days to months.

Yeah, it's a really fascinating shift in perspective.

Okay, so let's unpack this a bit.

Our mission for this deep dive is to explore how these deeper, often invisible changes literally reshape our brains and, by extension, our actions and reactions.

We're drawing our insights from a brilliant chapter, it's titled Days to Months Before, from Robert M.

Sapolsky's incredible book, Behave.

Behave, yeah, an amazing book.

It really is.

So this is a journey into understanding the very architecture that underpins who we are.

And what's truly fascinating here is just how far back the roots of our behavior can stretch.

It shows just how much our brains adapt over time.

We're talking about neural plasticity, not just, you know, over hours, but over weeks and months.

This can lead to actual structural alterations in the brain itself.

Structural alterations, wow.

This isn't just about fleeting thoughts.

It's about the very foundation, the very wiring of our being.

So how do these long -term changes actually happen?

How can something that happened months ago result in a brain connection, a synapse that's fundamentally altered today?

I mean, how do our synapses even remember things?

For a long time, the scientific community really grappled with this, didn't they?

They really did.

Those early ideas suggesting maybe every new memory meant growing brand new neurons or new branches.

Well, they were largely tossed aside for a while.

Right.

So imagine your brain isn't just like static after birth, but it's constantly rewriting itself.

For decades, the big question was, how exactly?

And then in 1949, this Canadian neurobiologist, Donald Hebb.

Oh, the bobblehead guy.

Yeah.

Yeah, apparently.

He gave us this profound answer.

He proposed it's not necessarily about making entirely new connections for every single memory, but about strengthening the ones we already have.

Ah, the famous mantra, neurons that fire together wire together.

Exactly.

That simple phrase, it really unlocked a whole universe of understanding about how we learn, how we adapt.

Okay.

So strengthening.

What does that mean, like, technically?

Right.

So strengthening means that when neuron A talks or synapses onto neuron B, an action potential in A becomes much more likely to trigger one in B.

They become more tightly coupled.

That wave of excitation, it spreads farther within the receiving end, the dendritic spine, getting closer to the part that decides whether to fire the axon hillock.

Neuron B basically becomes a better listener.

A better listener.

I like that.

So how does a connection actually get stronger?

You mentioned glutamate.

Yeah, glutamate is often the key player here.

Most synapses work in a fairly standard way, but many glutamate synapses have this, well, this clever two -part lock and key system on the receiving neuron, neuron B.

Two parts.

Like, two different doorbells.

Kind of.

Think of it like a normal doorbell.

That's your non -NMDA receptor.

When glutamate hits it, you get a little blip of excitation.

Pretty standard.

But then there's a second special doorbell, the NMDA receptor.

And this one is usually, let's say, jammed or blocked.

Jammed.

So it doesn't usually ring.

Right.

It needs a really strong or a really repeated signal via those non -NMDA receptors to finally unstick it, to pop the block out.

Okay, I think I'm following.

It's a bit like maybe a lecturer says something and it just goes in one ear and out the other.

They repeat it.

Same thing.

Annoying, maybe.

But then they repeat it enough times where maybe you shout it and suddenly, aha,

the light bulb goes on.

You finally get it.

That's a great analogy.

At the synaptic level, that repeated droning on or that really strong signal builds up enough excitation through the regular non -NMDA receptors.

And that buildup is what finally kicks the block out of the NMDA receptor, activating it.

And that's when you get this big rush, this explosion of excitation, the synapse finally gets it.

Okay.

That aha moment is great.

But, you know, getting it in the middle of a lecture doesn't mean I'll remember it for the final exam.

How do we make that burst of understanding actually stick long term?

Ah, yes.

Excellent question.

That's where the concept of long -term potentiation, or LTP, becomes absolutely critical.

LTP.

Go away.

Precisely.

First demonstrated way back in 1966, LTP explains how that initial powerful NMDA receptor activation leads to a prolonged increase in the synapse's excitability.

It makes the connection last.

And the crucial detail here is what rushes in when those NMDA receptors finally open wide.

It's not just the usual sodium ions.

It's calcium.

Calcium.

Like in milk.

Well, yes.

The element calcium.

But here, it acts like a powerful internal messenger inside the neuron.

This influx of calcium triggers a whole cascade of changes within that receiving neuron B.

Okay.

So what does this calcium messenger do?

Imagine it as a calcium tidal wave.

This wave causes several really important things to happen almost simultaneously.

First, more of those regular glutamate receptors, the non -NMDA ones, are quickly inserted into the receiving neuron's membrane, making it even more receptive to future signals.

So more ears listening.

Exactly.

And the existing receptors often become more sensitive too.

But then there's this remarkable twist.

The receiving neuron, the postsynaptic one, actually synthesizes these peculiar signals, neurotransmitters, that travel backward across the synapse.

Backward.

Wait, they go back to the sender?

Yeah.

They go back to the axon terminal, the sender, and essentially tell it to release more glutamate next time it fires.

Wow.

So the whole connection gets upgraded.

Totally.

In essence, with LTP, the sending neuron, the presynaptic axon terminal, learns to yell glutamate more loudly, and the receiving neuron, the postsynaptic dendritic spine, learns to listen more attentively.

That's how the connection strengthens and lasts.

That's amazing.

Yeah, but it can't all be about boosting signals, right?

Sometimes we need to prune things back.

Or maybe forget stuff that isn't important.

Absolutely spot on.

It's not always about amplification.

There's also a process called long -term depression, or LTD.

LTD.

Makes sense.

And as the name suggests, it decreases synaptic excitability.

But it's not just like generic forgetting or decay.

LTD actually helps sharpen signals by actively erasing what's extraneous or irrelevant.

Think of it like fine -tuning a radio dial, getting rid of the static to focus on the clear channel.

So it helps us learn what not to pay attention to.

Precisely.

It's just as important for learning and memory as LTP is.

Okay.

And this LTP and LTD stuff, it's not just happening in, say, the hippocampus when I'm trying to learn a phone number, is it?

Oh, not at all.

LTP occurs throughout your nervous system.

It's a fundamental mechanism.

For example, fear conditioning.

That primal learning of what to be afraid of involves LTP happening specifically in the basolateral amygdala, often called the brain's fear center.

The amygdala, right.

And then your frontal cortex, the part involved in control and decision -making, actually learns to regulate or control that fear response.

Also through LTP.

It learns to inhibit the amygdala.

It's also how our brain's reward pathways, the dopaminergic systems, learn to associate a particular stimulus with a reward.

Ah, like you mentioned with addiction.

Exactly.

That explains, for instance, how an addict comes to associate a specific location or maybe even certain paraphernalia with their drug, driving that intense craving.

That's LTP at work in the reward circuit.

This all ties back to behavior so clearly.

Now, you mentioned stress earlier.

How does stress fit into this intricate dance of synapses, strengthening and weakening?

Right.

Stress is a huge factor.

And it's complex.

What's fascinating, maybe even counterintuitive, is that moderate transient stress, the kind that might feel stimulating, like before a performance, can actually promote LTP in the hippocampus.

So a little bit of stress can be good for learning.

It seems so, yes.

It can improve cognition in the short term.

This is a big but prolonged severe stress does the opposite.

It disrupts that beneficial hippocampal LTP and actually promotes LTD instead.

Ah, so that's why my brain feels like mush when I'm under chronic pressure.

That's a key biological reason, yes.

We see this classic inverted U concept of stress playing out right there at your synapses.

Too little or too much stress is bad for hippocampal function, but there's a sweet spot.

And what's more, sustained stress does something different in the amygdala.

It actually enhances LTP there.

Enhances it in the fear center.

That sounds bad.

It contributes to boosting fear conditioning, making you learn fearful associations more readily.

And at the same time, that sustained stress tends to suppress LTP in the frontal cortex.

So less control, more fear.

Pretty much.

Which can contribute to things like impulsivity and poor emotional regulation.

It's a double whammy under chronic stress.

OK, so we've got strengthening existing connections with LTP, weakening them with LTD.

And that seemed like the whole story for a long time.

It really dominated the field, yeah.

But didn't you say earlier that an old, discarded idea made a comeback?

Something about new connections.

Ah, yes.

Get ready for this.

That idea that was initially tossed aside, the idea that memories might actually require the formation of entirely new synapses has been dramatically, and I mean dramatically resuscitated.

Really?

So the brain can build new connections from scratch?

It turns out, yes.

There were studies on rats, for example, that showed if you housed them in a really rich stimulating environment, lots of toys, other rats, things to explore.

The enriched environment.

Exactly.

Those rats actually showed an increase in the number of synapses in their hippocampus compared to rats in standard boring cages.

So it wasn't just making the existing connections stronger, but actually building more of them.

Precisely.

Building new infrastructure, not just reinforcing the old roads.

That's incredible.

How do we know this?

Can we actually see it happen?

Well, now we can, thanks to some profoundly fancy imaging techniques.

Scientists can literally watch a single dendritic branch, the receiving end of a neuron, in a living rat as it learns something new.

And astonishingly, over minutes to hours, they can see a new little nub emerge a new dendritic spine.

A new spine pops up.

Yeah.

And then an axon terminal, the sending end of another neuron, kind of hovers nearby.

And then over the following days to weeks, they actually form a functioning synapse together.

Wow.

You can watch a memory being physically built.

Essentially, yes.

This process is called activity -dependent synaptogenesis, new synapse formation triggered by neural activity.

And get this, it's even coupled to LTP.

How so?

Remember that calcium tidal wave that rushes in during LTP?

Well, that calcium can actually diffuse a short distance within the dendrite and trigger the formation of a new spine nearby.

So LTP can help seed new connections.

That is just wild.

And these new synapses, are they only forming in the hippocampus from memory?

Nope.

They form all over the brain.

You see them in the motor cortex when you learn a new physical task, like juggling or playing piano.

You see them in the visual cortex after lots of visual stimulation.

Sapolsky even mentioned studies with rats where lots of whisker stimulation leads to new synapses in their whisker cortex.

So wherever the brain is getting a workout, it might be building new connections.

That seems to be the case.

It's a truly widespread phenomenon showing this incredible capacity for structural adaptation based on experience.

Okay, and I'm guessing stress messes with this too.

You bet.

And again, it's complicated and depends on context.

Just like with LTP, moderate short -term stress can actually increase the number of these dendritic spines in the hippocampus, maybe helping you adapt quickly.

But same patterns sustain stress or conditions like major depression tend to reduce spine density in the hippocampus.

This is often linked to decreased levels of a key brain growth factor called BDNF, brain derived neurotrophic factor.

BDNF.

So chronic stress starves the hippocampus of connections and growth factors.

That seems to be part of the picture, yeah.

And conversely, sustained stress can actually increase the number of dendrites and spines in the amygdala.

Again, with the amygdala getting beefed up by stress.

Exactly.

Leading to persistently boosted anxiety and fear conditioning.

But here's that wonderful context dependency again.

The same amount of stress hormones, glucocorticoids, might cause dendrites in the hippocampus to shrink if the rat is, say, terrified and immobilized.

But if the rat is experiencing those same hormone levels while voluntarily running on a wheel, something it enjoys, the dendrites might actually expand.

So the brain's interpretation of the stressor really matters, whether it's perceived as controllable or uncontrollable.

It seems profoundly important, yes.

It's not just the hormone level, but the psychological context.

Okay, we've covered strengthening synapses, weakening them, even growing new ones.

What else can change over days to months?

We've talked about the receiving end, the dendrites and spines.

What about the sending end?

The axons?

Ugh, good question.

The plasticity extends there too.

Axons, those long fibers that transmit signals, aren't static either.

They can actually sprout offshoots, little branches that head off in novel directions.

This can lead to completely remapping parts of our brain's circuitry over time.

Remapping, like changing the brain's internal map.

Exactly.

Think about this amazing example.

When a person who is blind reads Braille, you see activity in their tactile cortex, the part processing touch from their fingertips.

That makes sense.

But uniquely, you also see activation in their visual cortex.

Visual cortex?

But they aren't seeing anything.

Great.

It seems that neurons that typically send axons carrying touch information from the fingertips have somehow rerouted, gone miles off course anatomically, to connect with the now unused visual cortex.

The brain is repurposing that cortical real estate.

That's incredible repurposing.

It really is.

And it's why someone who is deaf and fluent in American Sign Language often activates their auditory cortex when they watch someone signing.

The brain regions are being reallocated based on sensory input and experience.

Does this remapping also happen after, say, an injury?

Yes, definitely.

If someone has stroke damage, for instance, to the part of their cortex that normally receives sensation from their hand, sometimes axons carrying signals from the hand can sprout into neighboring cortical regions.

Over time, this can slowly bring back some sense of touch as that neighboring area learns to interpret the hand signals.

Wow.

The brain is trying to rewire around the damage.

It is.

And it can happen surprisingly quickly.

There was a study where people were blindfolded for just five days.

Only five days.

Yep.

And in that short time, auditory signals actually started to remap into their visual cortex.

And fascinatingly, when the blindfolds came off, those projections were tracked again.

It's quite dynamic.

Very dynamic.

It shows how quickly the brain tries to adapt and compensate, almost like it's constantly checking if its resources are being used efficiently.

That's incredible how the brain adapts to injury or sensory loss.

But what about positive experiences?

Does this remapping happen when we learn something new and challenging, not just when we're compensating for a deficit?

Oh, absolutely.

It's not just for injury or deficits.

Think about musicians.

They typically have a larger auditory cortical representation of musical sounds compared to non -musicians.

To a sense.

And it's often particularly enlarged for the specific frequencies of their own instrument.

And the earlier they start playing, the stronger this remapping effect tends to be.

So practice literally expands the brain map for that skill.

It appears so.

Alvaro Pascual -Leone at Harvard did some famous studies.

He had non -musicians practice a simple five -finger piano exercise daily.

And sure enough, their cortical map for finger control expanded.

But here's the really wild part.

He had another group who just spent two hours a day imagining playing the exercise.

Just imagining.

He's vividly imagining.

And their cortical maps also remapped.

No way.

Just thinking about it changed the brain structure.

It seems mental practice can drive physical changes in brain maps, too.

Other examples Sapolsky gives include mothers showing an expansion of the tactile map around their nipples after giving birth, presumably due to nursing.

And people who learned to juggle showed expansion in cortical areas, processing visual motion after just three months of practice.

Experience, whether physical or mental, truly sculpts our brain's physical connections, literally changing its geography over weeks and months.

OK, this is all mind -blowing.

Synapses, strengthening, weakening, new synapses, axons, remapping.

But you mentioned something earlier that sounded like the biggest bombshell of all.

Something about new neurons.

Ah, yes.

The final and perhaps most revolutionary form of plasticity over this time scale.

For decades, I mean decades, the central dogma in neuroscience was crystal clear.

Adult brains don't make new neurons.

Right, I always heard you get all your brain cells pretty early on and then it's just downhill from there.

Lose them but never gain them.

That was the firm belief.

Any evidence to the contrary was often dismissed or ignored.

But get ready.

The biggest revolution in neuroscience in years, arguably, is this.

Adult brains, including aged human brains, do make new neurons.

Olvan, adult neurogenesis.

It actually happens.

It actually happens.

This finding is truly epic and the story of its discovery is quite dramatic too.

You mentioned it was a struggle to get this accepted.

Oh, a huge struggle.

It really started seriously with a researcher named Joseph Altman back in 1965.

He used radioactive tagging techniques and found convincing evidence for new neurons in adult rats.

His work was initially well received, but then the tide turned.

The field largely rejected his findings.

He reportedly lost tenure, lost funding.

It was tough.

Wow, punch for being ahead of his time.

Seems that way.

And then a decade later, Michael Kaplan found similar evidence, also faced crushing rejection.

Established figures like the highly respected Pasko Rekic publicly dismissed his work.

Kaplan eventually left research altogether.

That's heartbreaking.

So how did the idea ever come back?

It took someone with immense scientific clout.

Fernando Nottebohm, a very highly esteemed neuroscientist at Rockefeller University, was studying bird song.

He demonstrated convincingly that adult birds make new neurons, particularly when they're learning new songs in the spring.

His prestige was such that people had to take it seriously.

Okay, so birds do it.

Right, but then the skepticism just shifted.

Okay, fine, birds are weird, but mammals,

especially primates, no way.

Moving the goalposts.

Then came researchers like Elizabeth Gould, then at Princeton, and Fred Rusty Gage at the Salk Institute.

Using newer, more sophisticated techniques, they conclusively showed adult neurogenesis was happening in adult rats and mice, particularly in the hippocampus.

Even Rackage, the former skeptic, eventually found evidence in his own lab with monkeys, though he initially downplayed its significance.

Only a few.

Maybe they don't live long, maybe not in the cortex, probably not in primates.

Still hedging.

Still hedging.

But the evidence kept mounting.

It was shown more robustly in monkeys.

And finally, using clever techniques looking at brain tissue from deceased cancer patients who'd received a special marker drug, it was shown unequivocally in humans.

Adult humans make new neurons.

Wow.

So it's actually true.

Where does this happen?

And how much?

The most significant and well -established site is the hippocampus, crucial for learning and memory.

Estimates suggest about 3 % of the neurons there might be replaced monthly in adult humans.

3 % a month.

That's substantial.

It really is.

There's also evidence for some neurogenesis occurring in parts of the cortex, although that's perhaps more debated regarding its extent and function.

But it happens throughout adult life, even into old age.

And what influence of it?

Can we boost it?

Yes.

Lots of things influence the rate.

Things like learning new things, physical exercise,

environmental enrichment.

Like those rats with the toys.

Exactly.

Also, estrogen seems to promote it, as do some antidepressants, interestingly.

Even recovery after a brain injury can enhance it.

And the flip side?

What slows it down?

Predictably, various stressors tend to inhibit neurogenesis.

Chronic stress, glucocorticoids, aging to some extent.

They can all put the brakes on the birth of new neurons.

Okay, stepping back.

What do these new neurons actually do?

Why is it important that we make new ones in the hippocampus?

That's the million dollar question, and it's a super hot area of research right now.

These new hippocampal neurons seem to migrate into place, integrate into the existing circuits, and become functional.

One leading idea is that they play a crucial role in something called pattern separation.

Pattern separation?

Yeah.

It's the ability to distinguish between two similar memories or experiences, helping you learn that two things you previously might have lumped together are, in fact, distinct.

Like learning the difference between dolphins and porpoises, or maybe telling apart Zooey Deschanel and Katy Perry, as Sapolsky humorously puts it.

These new neurons might help make those fine distinctions.

So they help refine our memories and understanding.

That seems to be a key function.

It's genuinely one of the trendiest, most exciting topics in neuroscience today.

Figuring out exactly how these new neurons contribute to learning, memory, mood, and maybe even mental health.

So all these different kinds of plasticity, we've talked about the LTPLTD, the new synapses, the axonal remapping, and now adult neurogenesis, can they add up?

Can they be so significant that they actually change the size of entire brain regions over time?

Absolutely.

When these changes accumulate over days, weeks, and months, you can sometimes detect macroscopic changes in brain volume.

Like what?

Can you give some examples?

Sure.

For instance, studies have shown that postmenopausal women receiving estrogen treatment can show an increase in the size of their hippocampus.

So hormones can influence brain size.

Definitely.

And conversely, conditions associated with prolonged stress like chronic depression, some chronic pain syndromes, or Cushing's syndrome where glucocorticoid levels are very high, these are often associated with hippocampal atrophy.

The hippocampus actually shrinks.

And that would explain the cognitive problems often seen in those conditions.

Exactly.

It links the structural change to the functional deficit.

And think about PTSD, post -traumatic stress disorder, that's often associated with an increased volume and hyperreactivity in the amygdala.

The fear center gets bigger and overactive again.

Paired often with that hippocampal shrinkage we just mentioned, it's a nasty combination structurally.

You also mentioned taxi drivers earlier.

Ah, yes.

The classic London taxi driver study.

It's a fantastic example.

To get licensed, they have to memorize the knowledge.

This incredibly complex map of London streets.

It takes years.

And researchers found that the posterior, or back part, of their hippocampus, a region strongly implicated in spatial memory and navigation, was significantly enlarged compared to controls.

So navigating those complex routes literally grew part of their brain.

It appears so.

And a follow -up study was even cooler.

They scanned trainees during the multi -year training process.

They found that enlargement happened progressively during training, but only in those individuals who actually went on to pass the grueling test.

Wow.

So success was correlated with the brain change.

Maybe I should start practicing complicated routes if I want to remember where I parked.

Couldn't hurt, right?

But it really highlights how sustained experience, health status, hormones, they can physically sculpt your brain structure over months.

And beyond just the structure, the size of regions, experience can also cause lasting changes in the numbers of receptors for specific neurotransmitters.

Oh, right.

You mentioned that with stress and dopamine.

Exactly.

Chronic stress can lead to a depletion of certain dopamine receptors in the brain's reward circuitry, the nucleus accumbens.

This might make rewards feel less rewarding, biasing someone towards depression, towards anhedonia.

Or, conversely, studies in animals show that winning a fight can lead to long -lasting increases in receptors for testosterone and pleasure centers, which might enhance the rewarding effects of testosterone and aggression in the future.

Experiences change brain chemistry sensitivity, too.

They do.

Even, get this, parasites can do it.

There's a parasite called Toxoplasma gondii, often carried by cats.

Oh, I've heard of that.

If it infects the brain of a rat, over weeks to months it can subtly alter brain circuits, making the rat less fearful of cats, which is obviously beneficial for the parasite's life cycle.

Makes the rat easier prey for the cat, so the parasite gets back into the cat.

Clever if creepy.

Very.

And there's even controversial research suggesting subtle effects in infected humans, maybe making them slightly less fearful or more impulsive.

It shows how even external biological agents can induce these slow plastic changes.

That's quite something.

Now, with all these changes, brain size, receptors, connections,

are they permanent?

Or can things change back?

Ah, that's an incredibly important point, and generally the news is hopeful.

Most measurable changes in the nervous system that occur in response to some sustained stimulus or environmental condition are often reversible if the environment changes back.

So if the stress stops,

the hippocampus might recover.

If the enrichment goes away, the extra synapses might prune back.

Largely, yes.

The brain retains a remarkable capacity for plasticity in both directions throughout life.

Things aren't necessarily set in stone.

This reversibility offers a lot of hope, for instance, in recovering from the neurological effects of chronic stress or trauma.

Okay, so wrapping this all up, what does this whole picture mean for us?

The discovery of adult neurogenesis, especially, sounds revolutionary.

And this whole topic of neuroplasticity over days to months seems immensely important.

It really is, and it radiates a certain kind of optimism, doesn't it?

You see popular science books with titles promising to help you rewire your brain, think your way to a better life, things like that.

Yeah, there's a lot of that rewire your brain talk.

And there's truth to it based on everything we've discussed, but we absolutely need to inject a few crucial cautionary notes here.

Okay, what are the caveats?

Well, first and foremost, neuroplasticity, like pretty much any biological process, is inherently value free.

It's not intrinsically good.

It's amazing, biologically fascinating, that a blind individual can remap their visual cortex for reading Braille, or that a London cab driver's hippocampus expands to hold the knowledge.

Those seem like positive adaptations, but it's utterly disastrous that trauma can enlarge the amygdala and atrophy the hippocampus, contributing to the symptoms of PTSD.

That's also neuroplasticity.

So it cuts both ways.

Exactly.

Similarly, expanding your motor cortex map for fine finger dexterity is wonderful if you're training to be a neurosurgeon, but it's arguably not a societal plus if that same plasticity allows someone to become a more skilled safecracker.

The biology doesn't care about the morality.

That's a really important point.

Plasticity isn't inherently virtuous.

Not at all.

And the second major caution is that the extent of neuroplasticity is definitely finite.

There are real limits.

They're not limitless potential.

Absolutely not.

If neuroplasticity were truly unlimited, then grievously injured brains or severed spinal cords would eventually fully heal themselves, and they generally don't beyond a certain point.

And, you know, if it were unlimited, we could all become Yo -Yo Mas or LeBron James's just by putting in a few thousand hours of practice.

Talent and innate predisposition still matter.

Practice helps massively, drives plasticity, but it doesn't overcome all biological constraints.

Right.

We can't just rewire ourselves into anything overnight.

Precisely.

There are boundaries.

OK.

Those are important cautions.

Yeah.

But despite those limits and the value -free nature, you still feel understanding neuroplasticity offers benefits.

Oh, immense psychological benefits, I think, especially in the realm of human behavior and potential for change.

What the science does is it makes the functional malleability of the brain tangible.

It provides concrete scientific evidence that brains do change in profound ways in response to experience, environment, and even just thought over weeks and months.

And our brains can change.

Then people can change.

Think about some of the profound transformations we see in individuals or even societies.

Sapolsky mentions historical examples like the shifts leading up to the Arab Spring or figures like Rosa Parks standing up to injustice or enemies like Sadat and Begin Making Peace or Nelson Mandela emerging from prison transformed.

The changes weren't just metaphorical shifts in attitude.

These transformations unfolding over months and years almost certainly involved corresponding changes in their brains,

changes in synaptic strengths, maybe new connections, altered receptor levels, remapped circuits.

Their ways of thinking, feeling, and reacting fundamentally shifted, and that implies a neurobiological shift.

So understanding the biology makes the possibility of change feel more real?

I think so.

If we connect this to the bigger picture, as Sapolsky suggests, a different world truly can make for a different worldview.

And a different worldview means, ultimately, a different brain.

And the more tangible, the more real the neurobiology underlying such profound change seems, perhaps the easier it becomes to imagine that it can happen again.

That positive transformation isn't just wishful thinking, but something rounded in the adaptive capacity of our own biology.

That's a powerful thought to end on.

The idea that change is built into our very neurobiology.

And that brings us to the end of this deep dive.

We've covered so much ground how events from days to months before literally sculpted our brains.

We explored the brilliant insights of Donald Hebb, the nuts and bolts of long -term potentiation and depression, the surprising comeback of new synapse formation, the incredible remapping of our axons, and that revolutionary discovery of adult neurogenesis.

And we saw how these changes can manifest in brain size and function and, importantly, why we need to understand both the incredibly hopeful side and the necessary cautions around neuroplasticity.

We really hope this exploration into the days to months before, drawing from Sapolsky's work, has given you some powerful new insights into the biology of human behavior.

Thank you so much for joining us on this journey of discovery.

Until next time, keep exploring, keep questioning, and keep learning.