Chapter 9: Hearing, Balance, Taste & Smell

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Welcome back to The Deep End.

Today, we are tuning out the noise, or rather, we're figuring out how we tune into the noise.

We're looking at the actual machinery of perception itself.

It is a fascinating place to be.

You know, we often walk around treating our senses, seeing, hearing, tasting like they're just simple open windows.

Right, like the world just comes in.

The world comes in, we experience it, end of story.

But the reality, as we're going to see today, is that these senses are complex, messy mechanical and chemical filters.

And we are working off Chapter 9 of Behavioral Neuroscience, the 8th edition by Breedlove and Watson.

And the mission is to unpack hearing, balance, taste and smell.

These are the sensory systems that let us monitor signals from a distance like hearing a predator snap a twig, and the systems that tell us where our body is in space or, you know, what we're about to swallow.

It's all about survival, really.

It's ultimately a story about survival.

Exactly.

So to kick things off, I want to introduce you to a guy named Tony.

Ah, yes.

The case study from the text, the man with no ear for music.

Exactly.

And I want to linger on Tony for a minute because his experience really, um, it sets the stage for how weird and specific this biology can be.

It really does.

So the text describes Tony as a guy with perfectly normal intelligence.

He's sharp, his cognitive functioning is totally fine.

He functions in society without any issues.

But music.

To him, it's just noise.

A complete foreign language.

And we're not talking about someone who just has bad taste or doesn't like pop songs.

No, this is much deeper.

Yeah.

It's a fundamental inability to process the core components of music.

Yes.

He cannot tell the difference between musical tones.

If you sat him down at a piano and played a high C and then a low C, he might look at you and say, they sound exactly the same.

Wow.

The text even mentions that he can't recognize happy birthday, which is arguably the most ubiquitous song on the planet.

Right.

I mean, unless people are singing the lyrics, happy birthday to you.

He has no idea what the melody is.

It's just the sequence of sounds to him.

And he tries to sing, I believe.

Oh, he does.

And the best part is he sings completely off key, but because he can't perceive pitch, he has no realization that he's doing it.

He thinks he sounds perfectly fine.

He thinks he sounds like Pavarotti, but his friends are, you know, wincing.

And this condition is known as amusia.

And what makes it so interesting for neuroscientists is that Tony isn't deaf.

Not at all.

Right.

And that's the twist.

He can hear speech perfectly fine.

If you ask him a question, he hears the rising intonation at the end of the sentence.

He knows you're asking, not telling.

So his brain can process pitch in the context of language.

That sharp rise of a question mark.

But it fails completely when that same pitch information is used in a musical context.

It just goes to show that hearing isn't one single process.

It's a bundle of different, very specific skills.

And Tony isn't alone in this.

The text lists some surprisingly heavy hitters who likely had amusia.

It's quite the list.

Pope Francis, Che Guevara, Theodore Roosevelt, and the economist Milton Friedman.

I'm just picturing Che Guevara trying to hum a revolutionary anthem and everyone around him just politely looking away.

It's a strange image, but it really challenges our assumption about talent versus biology.

We tend to think being tone deaf is just a lack of practice.

But for people with amusia, it's a hardware or software issue in the brain.

It launches us perfectly into the theme of this deep dive.

How do we get from physical energy, a vibration in the air, to a perception in the mind?

So let's start with that physical energy.

Before we get into the biology, we have to talk about the physics of sound.

Because to me, sound feels like an experience.

It feels emotional.

But physically,

it's just air moving.

That's it.

Physically, sound is described as pressure waves in the air.

Picture a loudspeaker cone.

When it pushes out, it shoves the air molecules together.

That's compression.

When it pulls back, it creates space.

That's expansion or rarefaction.

That alternating pattern of squished air and spread out air travels away from the speaker.

Like ripples in a pond.

Similar to ripples, yes.

But ripples are 2D.

Sound is a 3D sphere of pressure expanding at about, what, 700 miles per hour?

And when we talk about pure tones, which are rare in nature but useful for science, we measure them in two basic ways.

The first is amplitude.

Which we perceive as loudness.

Correct.

So amplitude is intensity.

It's the force per unit area.

Basically, how hard are those air molecules hitting your eardrum?

And we measure this in decibels, or dB.

I've always found decibels confusing because the numbers don't seem to add up intuitively.

A sound of 60 dB doesn't sound twice as loud as 30 dB.

It doesn't.

And that's because it's a logarithmic scale.

This is crucial to understand.

It's not a linear ladder like one, two, three.

Each step up is a huge multiplication of intensity.

Can you give a sense of that scale?

What are we talking about?

Sure.

The text compares the threshold of human hearing, a faint whisper, which is about 20 dBs, to a jet airliner flying 500 feet overhead.

That's about 120 dB.

Okay, so 20 to 120.

Mathematically, 120 is only six times larger than 20.

But I know for a fact a jet is more than six times louder than a whisper.

A lot more.

In terms of physical pressure, that 120 dB jet is about a million times more intense than the whisper.

A million.

Wow.

Our ears are incredibly versatile instruments to be able to handle that range without just exploding.

Okay, so that's loudness.

The second measure is frequency.

Right.

Frequency is the number of cycles per second.

How fast are those waves hitting you?

We measure this in hertz or hertz.

And this correlates to our perception of pitch.

Exactly.

Low frequency is a bass rumble.

High frequency is a squeak or a whistle.

And the text gives a musical reference, middle A on a piano.

Yes, that's 440 hertz.

That means the string is vibrating back and forth 440 times every single second.

But here's where my brain starts to hurt a little.

If I play middle A on a piano and then I play middle A on a violin, they're both 440 hertz.

They're the same pitch.

I can tell they're the same note, but they sound completely different.

A piano doesn't sound like a violin.

Why?

And that brings us to the concept of timbre.

It's because real world sounds are almost never purer sine waves.

They're messy.

When that piano string vibrates at 440 hertz, which we call the fundamental frequency,

it is also vibrating at multiples of that speed.

Multiples?

Like what?

Yes.

It's also vibrating at 880 hertz, 3820 hertz, 1760 hertz, and so on.

Just quieter.

These are called harmonics or overtones.

So every single note is actually a hidden chord of invisible notes stacked on top.

Precisely.

And the reason the violin sounds different from the piano is that the violin might be really loud at the 880 hertz harmonic but quiet at the 1320 hertz one, while the piano has a completely different recipe of those harmonics.

So the flavor of the sound, the timbre, is determined by the relative intensity of those harmonics.

That's it.

It's the unique recipe of fundamental plus harmonics.

The book mentions something called Fourier analysis here.

It sounds like high -level calculus.

It is math, but the concept is beautiful.

Imagine you make a smoothie.

You throw in strawberries, bananas, yogurt, and kale, and you blend it into a, well, a green sludge.

Okay, I'm with you.

A complex wave.

That sludge is a complex wave.

Fourier analysis is a machine that can take a sip of that sludge and mathematically unblend it.

It would say this contains 40 % strawberry, 30 % banana, etc.

It breaks the complex mix back down into its pure ingredients.

It does.

And our ear is a biological Fourier analyzer.

It takes the complex pressure wave of a symphony orchestra hitting your head, and it breaks it down into individual frequencies so your brain can process violin, drum, and flute separately.

That is incredible processing power.

Okay, so let's track the sound wave.

It's traveled through the air.

It's a complex mix of frequencies, and now it hits the side of my head, the outer ear.

We start with the peanut.

That's the fleshy, wrinkly wing on the side of your head.

Which, I have to be honest, looks kind of ridiculous.

The text jokes that for humans, it's mostly used for hanging jewelry.

Compared to other mammals, ours are pretty static.

We don't have the mobile ears of a cat or a bat.

We can't really swivel them to catch a sound.

But they're not useless.

Not at all.

Those ridges and valleys aren't just for show.

They act as a filter.

They call it spectral filtering.

How does a ridge filter sound?

It physically modifies the shape of the sound wave depending on where it comes from.

The sound bounces around in those little folds.

And the specific shape of the human ear enhances frequencies between 2000 and 5000 hertz.

Is that a random range?

Not at all.

That frequency range is exactly where the important information in human speech lives.

The consonants, the things that give speech clarity.

So evolution has shaped our ears to be perfectly tuned to the voices of other humans.

It's a speech detector.

So the pinna funnels the sound into the ear canal, and then we hit the end of the line, the eardrum.

The tympanic membrane.

This seals the end of the ear canal.

And this is where we cross the border from the outer ear to the middle ear.

And inside, we find an engineering marvel.

The ossicles.

These are the three smallest bones in the human body.

The malleus, the incus, and the stapes, or as they're commonly known from their shapes.

The hammer, the anvil, and the stirrup.

Because that's exactly what they look like.

It is.

They form a little mechanical chain.

The eardrum vibrates, which shakes the hammer.

The hammer hits the anvil, and the anvil pushes the stirrup.

But why?

This seems like such a Rube Goldberg machine.

Why do we need this chain of tiny wobbly bones?

Why not just have the eardrum vibrate the inner ear directly?

That's a great question.

And it comes down to physics again.

The problem is something called impedance matching.

You see, the inner ear isn't filled with air.

It's filled with fluid.

It's filled with fluid.

Have you ever been swimming underwater and tried to hear someone shouting at you from the pool deck?

Yeah, it sounds all muffled and far away.

You can barely hear anything.

Right.

That's because air is light and compressible, while water is heavy and dense.

When sound waves in the air hit the surface of the water, something like 99 .9 % of that energy just bounces off.

It reflects.

It can't push the heavy water.

It can't.

So if our eardrum was connected directly to the fluid -filled inner ear, we'd be effectively deaf.

The sound would just bounce off our heads.

So we need an amplifier.

We need a serious amplifier.

The ossicles act as a mechanical lever system.

They take the vibration from the large surface area of the eardrum, and they concentrate all of that force onto a tiny spot called the oval window.

It's like a woman in stiletto heels stepping on your foot versus a woman in sneakers.

Same person, same weight.

But the heel concentrates the force into a tiny, painful point.

That's a perfect analogy.

By concentrating the force, the ossicles amplify the pressure by about 20 times.

Just enough to shove the heavy fluid in the inner ear and get it moving.

They bridge the gap between air and water.

But the text mentions they aren't just dumb levers.

They have a kind of safety feature built in.

They do.

Attached to these tiny bones are tiny muscles.

The tensor tympani and the stapedius.

The smallest muscles in the body attach to the smallest bones.

When the brain detects a really loud sound,

these muscles instantly contract.

They pull on the bones and stiffen the entire chain.

And stiffening them makes them vibrate less.

Exactly.

It dampens the vibration.

It's like an internal volume knob that turns down automatically to protect the delicate machinery of the inner ear from being overloaded.

That is incredibly smart.

It is, but it has a flaw.

It's not instantaneous.

It takes about 200 milliseconds to kick in.

That's pretty fast, but...

It's fast enough to protect you from the roar of a jet engine building up or a rock concert.

But it is not fast enough to protect you from a sudden explosive sound like a gunshot.

The damage from the gunshot happens before the muscles can even wake up and react.

That explains why sudden bangs are so dangerous for long -term hearing.

Okay, we've moved the bones.

We've pushed on the oval window.

Now we are entering the inner ear, the cochlea.

The cochlea, from the Greek word for snail, which describes it perfectly.

It's a coiled, fluid -filled tube embedded in the temporal bone of the skull.

It's tiny, about the size of a pea.

And inside this pea -sized snail shell is where the magic happens.

This is where physical motion turns into a neural signal, the moment of transduction.

This is the holy grail of sensory science right here.

The interior of the cochlea is divided into three parallel canals.

But the main event, the actual business end, is the organ of corti.

And the key players, the workers doing the conversion, are the hair cells.

The hair cells.

They sit on a flexible structure called the basal or membrane.

Now we have two types of hair cells here, and they have very, very different jobs.

We have inner hair cells and outer hair cells.

Break those down for us.

The inner hair cells, you can think of them as the artists.

There's just a single row of them, about 3 ,500 in total.

They are the primary sensors.

They are the ones that actually send the sound information to the brain.

So they do all the talking.

They do 95 % of the talking to the brain.

Now the outer hair cells,

there are way more of them, about 12 ,000 in three rows.

But curiously, they don't send much information to the brain.

So what are they doing?

They are the roadies.

They're the technicians.

They receive signals from the brain.

And get this, they physically change their length.

They get shorter and longer, almost like they're dancing to the music.

Wait, the cell itself moves.

It elongates and contracts.

Yes.

They use a special motor protein called Preston.

And by expanding and contracting with incredible speed, they physically stiffen or relapse the basal or membrane in that specific spot.

They are a cochlear amplifier.

What's the point of that?

They're sharpening the tuning.

They allow us to discriminate between very, very similar frequencies.

They turn a muddy signal into a sharp one.

So the brain isn't just passively listening.

It's actively reaching back into the ear and tuning the instrument while it plays.

That is a beautiful way to put it.

It's an active dynamic process.

OK, I want to slow down and really visualize this magic moment of transduction.

We have these hair cells.

They have little stiff hairs on top called stereocilia.

What happens when a sound wave hits?

OK, let's zoom in.

The sound has been turned into a vibration in the fluid of the cochlea

that causes the basilar membrane, the floor the cells are standing on, to ripple up and down.

Like shaking out a long rug.

Exactly like that.

As the floor ripples, the hair cells riding on top of it rock back and forth.

Now, above these hairs is a kind of gelatinous roof called the tectorial membrane.

The tips of the tallest hairs are nestled into this roof.

So the floor moves, the cells rock, and the hairs get bent against the roof.

They get sheared back and forth.

Now, here's the mechanism, and it's shockingly simple.

The tips of these tiny hairs are connected to each other by microscopic threads.

The text calls them tip links.

Like little guy wires connecting the tops of the hairs.

Exactly.

Now imagine a tiny little trap door on the tip of each hair.

That's an ion channel.

The tip link is like a string tied from the top of its taller neighbor to that trap door.

I think I see where this is going.

When the hair bends, the string gets pulled tight.

It physically pops the trap door open.

It's surprisingly low tech.

It's literally a string pulling a door open.

It is brilliantly mechanical.

The door opens, and because of the unique chemistry of the fluid in that part of the ear, potassium and calcium ions rush into the cell.

And since ions carry an electrical charge.

The cell instantly depolarizes.

It goes from resting to active.

This causes the cell to release neurotransmitters, glutamate, in this case onto the auditory nerve fiber connected to its base, and boom, the brain hears a sound.

Why it's so important that this is mechanical?

Why not use a chemical receptor like we do for taste or smell?

Speed.

Chemical reactions take time.

They're relatively slow.

If hearing relied on a chemical binding to a receptor, we couldn't hear high frequencies.

We couldn't hear 20 ,000 hertz.

Because the chemistry couldn't reset itself fast enough to fire 20 ,000 times a second.

Exactly.

But a string pulling a door, that's instantaneous.

You can do that tens of thousands of times a second.

The mechanical nature of hearing is what gives us our incredible temporal resolution.

That is just mind blowing.

OK, so the door opens, the nerve fires.

But how does the brain know what the sound is?

How does it know a high pitch from a low pitch?

The nerve signal, the action potential, it looks the same either way.

This is the other brilliant part.

The cochlea uses two main coding strategies.

The first and most dominant is blaze coating.

Blaze coating.

Remember the basilar membrane, the floor.

It's not uniform.

At the base of the cochlea near the oval window, the membrane is narrow and stiff.

OK.

At the apex, the far end of the snail shell, it's wide and floppy.

Like the difference between a guitar's high E string and its low E string.

Stiff and thin versus thick and floppy.

An excellent analogy.

High frequencies, fast, energetic waves have a lot of energy, but they burn out quickly.

They cause the stiff base of the membrane to vibrate.

They don't have the oomph to move the floppy end.

And low frequencies.

Low frequencies are these long, slow, powerful waves.

They travel all the way down the tube and they vibrate the wide, floppy apex.

So the brain knows the pitch simply by checking the address.

Precisely.

It's all about where?

Oh, the nerve connected to the bass is firing.

Must be a high note.

The nerve at the apex is firing.

Must be a bass note.

It's a literal map of the piano keys unrolled inside your head.

That's exactly what it is.

This is called the tonotopic organization.

But for really low frequencies below about 200 hertz, this place coding gets a bit fuzzy.

The whole floppy end kind of vibrates together.

So we need another strategy.

So we use strategy number two.

Temporal coding.

Which is?

For those low notes, it's about direct timing.

If a sound is 200 hertz, the auditory nerve fires 200 times a second.

It locks its firing rate to the frequency of the sound.

The brain just counts the beats.

Okay, so the signal is encoded.

Now we are on the highway to the brain, the auditory pathway.

It's quite a relay race.

The auditory nerve leaves the cochlea and its first stop is the cochlear nuclei in the brainstem.

But let's jump to the next stop because it's a really crucial one.

The superior olivary nuclei.

The superior olive.

Why is this stop so important?

This is the first place in the entire system where information from both ears comes together.

It's the brain's mixing board.

And this is where we figure out where sound is coming from.

This is where sound localization begins.

This is something I take for granted every second of the day.

If someone snaps their fingers on my left, I look left.

I don't even think about it.

But how do I know?

We use something called the duplex theory.

Which basically means we use two different clues depending on the pitch of the sound.

Okay, clue number one.

Intensity differences.

This works great for high frequencies.

If a bird tweets on your right side, the sound hits your right ear directly in a full volume.

But your head is a big, dense, sound -absorbing object.

It gets in the way.

It gets in the way.

It casts a sound shadow.

By the time the sound gets to your left ear, it's physically quieter.

So the brain just compares the volume levels.

Louder on the right.

The sound must be on the right.

Simple.

Simple.

But this doesn't work for low frequencies.

Why not?

Physics again.

Low frequency waves are really long.

They can be many feet long.

They just wrap right around obstacles like your head, like it's not even there.

There is no sound shadow for a day's note.

Okay, so what do we do for the low notes?

Clue number two.

Latency differences.

Or timing differences.

The sound arrives at your right ear a tiny fraction of a millisecond before it hits your left ear.

And the brain can detect that tiny, tiny gap.

It is incredibly precise at it.

The text details the Jeffress model to explain how this might work based on studies in birds.

It's fascinating.

Imagine a series of neurons inside your brain stem.

I'm picturing it.

Each of these neurons is a coincidence detector.

It will only fire if it gets a signal from the left ear and the right ear at the exact same moment.

Okay, a perfect collision.

Right.

Now imagine the nerve fibers are like runners on a track leading to these detectors.

If a sound comes from the right, the signal from the right ear starts this journey early.

The signal from the left ear starts late.

So the right runner gets a head start.

It does.

But what if the track for the right ear is physically longer?

What if it has to take a little detour?

Then the left runner has a chance to catch up.

Ah, so the brain has a whole array of these coincidence detectors, each with different path lengths from each ear.

Exactly.

And if detector B fires, the one with a medium length delay for the right ear, the brain knows, aha, the sound must have started on the right to make the timing work out perfectly here.

It converts a difference in time into a difference in place.

It builds a map.

It builds a physical map of auditory space using biological delay lines.

Some serious neural engineering.

From there, the signal goes up to the inferior colliculi in the midbrain, then the thalamus.

The medial geniculate nucleus of the thalamus, yes.

And finally to the auditory cortex in the temporal lobe.

And that tonotopic map is preserved the whole way.

All the way up.

The piano is still unrolled, even in the cortex.

Now we talked about Tony at the start, amusia.

This implies that the brain's auditory system isn't fixed.

It can be different from person to person.

Absolutely.

The auditory cortex is incredibly plastic.

It is shaped by experience.

The text highlights professional musicians as a prime example.

I'm assuming their brains look different.

Significantly different.

MRI studies show that an area called Heschel's gyrus, a primary part of the auditory cortex, is up to 130 % larger in professional musicians compared to non -musicians.

130%.

Wait, does the brain physically grow new cells?

Or does it just steal real estate from neighboring areas?

It's more about the density and connectivity.

The neurons there become more robust, with more connections, more synapses.

And the big question is always, were they born that way, which is why they became musicians?

Nature versus nurture.

Or did years of musical training make them that way?

The evidence points strongly to nurture.

The younger a musician starts training, the larger that area becomes.

Experience shapes the brain.

And for Tony, the man with amusia, what does his brain show?

For people with congenital amusia, MRI studies show fewer connections in a fiber tract called the arcuate fasciculus.

The arcuate fasciculus.

It's a massive neural highway that connects the temporal lobe where you hear sound to the frontal lobe where you make sense of it.

In Tony's brain, that highway is missing a few lanes.

The signal gets lost in traffic.

Before we leave hearing, we have to touch on when it breaks.

Hearing loss and deafness.

The text puts this into three main buckets.

Right.

The first one is conduction deafness.

This is basically a plumbing problem.

A plumbing problem?

Yeah.

The outer or middle ear is blocked or damaged.

Maybe you have fluid from an ear infection or maybe the ossicles have fused together from a condition called otosclerosis.

The vibration physically can't get through to the cochlea.

Is that fixable?

Often.

Yes.

You can drain the fluid or surgeons can even replace the ossicles with tiny prosthetics.

Okay.

Bucket two.

Sensor neural deafness.

This is the more common type of hearing loss.

This is a hardware failure.

The hair cells are dead.

And what kills them?

All sorts of things.

Genetics, infections, certain drugs called ototoxic drugs.

Even high doses of aspirin can be damaging.

But the big one is noise pollution.

Loud sounds physically shear the stereocilia off the hair cells.

And once they're gone?

In mammals, they're gone for good.

They don't grow back.

This is also often associated with tinnitus, that persistent ringing in the ears.

And this is where cochlear implants come in.

Yes.

These devices are miraculous because they bypass the damage entirely.

If the hair cells are dead, the implant ignores them.

It threads a wire with a series of electrodes into the cochlea and uses it to zap the auditory nerve directly.

It translates sound from a microphone into a pattern of electrical pulses, skipping the entire biological part.

It learns to speak the brain's language directly.

It's a true neural prosthesis.

And the third bucket.

Central deafness.

This is when the ear is fine, the nerve is fine, but the brain itself is damaged.

A stroke or tumor in the auditory cortex can lead to things like word deafness.

It's a terrifying condition where you can hear that someone is speaking.

You can tell their tone of voice, but the words themselves sound like a foreign language or just meaningless noise.

You've lost the ability to decode speech.

Wow.

Okay, let's pivot.

We are staying in the area anatomically, but we are leaving sound behind.

We're talking about the sense that keeps us upright.

The vestibular system.

The unsung hero of the senses.

We barely notice it until it fails.

And then you get vertigo, nausea.

You can't even stand up.

And this system is the cochlea's next door neighbor, right?

It's part of the same continuous hollow structure in the temporal bone, the labyrinth.

And it has two main components.

First, the semicircular canals.

Those are the three loops we always see in diagrams of the ear.

Yes.

They're oriented in three planes, like the X, Y, and Z axes on a graph.

They're designed to track rotation.

Notting your head yes, shaking it no, and tilting it side to side.

How do they do that?

Fluid again.

It's all about fluid and inertia.

Inside each canal is a swelling called the ampulla.

Inside that is a gelatinous sail -like structure called the cupula.

When you turn your head to the left, the bony canal moves left.

But the fluid inside lags behind for a split second.

Exactly.

The fluid lags behind, pushing against the cupula sail and bending the hair cells embedded within it.

That signal tells your brain we're rotating left.

Okay, so the canals handle rotation.

What about going up in an elevator or accelerating forward in a car?

That's not rotation.

That's the job of the other component, the utricle and the saccule.

These are two little sacs that detect linear acceleration and static position.

Your relationship to gravity.

And how do they work?

Inside them, the hair cells are covered by a layer of jelly.

And sitting on top of that jelly are tiny dense crystals.

They're called otoliths.

Otoliths.

Literally ear stones.

Literally.

They are heavy calcium carbonate crystals.

When you're sitting still, gravity pulls them straight down.

When you accelerate forward in a car, your body moves forward.

But the heavy stones want to stay put.

They lag behind, pulling on the jelly, which bends the hair cells.

So we literally have little rocks in our heads that tell us which way is down and how fast we're moving.

We do.

And this system is hardwired to our eyes in a way that is absolutely vital for survival.

It's called the vestibulo -ocular reflex,

or VOR.

Is this the trick where you can shake your head back and forth, but your eyes stay locked on a single point?

It is.

But don't think of it as a trick.

Think of it as a biological steadicam.

If you're running away from a predator through a forest, your head is bobby and weaving all over the place.

Without the VOR, your vision would be a blurry, chaotic mess.

You wouldn't be able to see the branch you're about to run into.

The VOR takes the signal from the vestibular system, and uses it to drive your eye muscles in the exact opposite direction, instantly stabilizing your gaze.

And it has to be incredibly fast to work.

It is one of the fastest reflexes in the human body.

The signal goes from ear to brain stem to eye muscles.

It bypasses the thinking part of your brain entirely.

Okay, let's leave the complex mechanics of the ear and head to the face.

The chemical senses.

Taste and smell.

These are our oldest, most primal senses.

Even a single -celled bacterium has chemical senses.

It's the most fundamental way to identify what's food, what's poison, and what's a potential mate.

Let's start with taste or gestation.

First, we need to clear up a common misconception that the book points out.

Flavor and taste are not the same thing.

Not at all.

Taste is strictly what the tongue detects.

And for a long time, we've settled on five basic tastes.

Salt, sweet, bitter, sour, and umami.

And flavor.

Flavor is the brain's integrated experience of taste plus smell.

The text mentions the classic nose pinch test.

You should try it at home.

Hold your nose tightly and eat a strawberry and jelly bean.

All you will get is sweet, maybe a little sour.

You won't get strawberry until you let go of your nose and the aromatic molecules travel up the back of your throat to your nasal cavity.

Anatomy time.

The bumps on my tongue, those are taste buds, right?

Incorrect.

That's another common mistake.

The bumps you can see and feel are called papillae.

The taste buds are microscopic clusters of 50 to 150 cells and they're buried in the trenches on the sides of those papillae.

They're hidden away.

They're hidden away for protection.

So how do they work?

It turns out not all tastes are created equal.

They use very different mechanisms.

Okay.

Salt and sour are the simple ones.

They're ionic.

Meaning?

To taste salt, you are literally detecting sodium ions.

Nah plus gay.

The sodium from your precator chip flows directly into the taste cell through an open ion channel.

It's a direct entry.

It changes the voltage of the cell.

Done.

And sour?

Sour is the taste of acid, which is defined by hydrogen ions H plus assy.

Same deal.

The H plus ions enter the cell or affect other ion channels.

It's direct and fast.

But then we get to the complex ones.

Sweet, bitter, and umami.

These don't use simple open doors.

They use a much more sophisticated lock and key system called G protein -coupled receptors.

The sugar molecule, the key, has to fit perfectly into a receptor, the lock on the outside of the cell.

And that triggers a signal inside.

That triggers a complex cascade of chemical reactions inside the cell, which eventually leads to it sending a signal.

It's a much more indirect process.

Why the extra complexity?

Likely because we need to be much more specific.

We need to identify specific complex organic molecules, not just simple ions.

Take sweetness.

It uses a receptor made of two different proteins combined T1R2 and T1R3.

Heterodimer.

It's a fancy word for two different parts working together.

And here's where genetics tells a great story, which the text highlights.

Let's talk about cats.

Yes, the fact that cats don't care about sweets.

And they don't just not care.

They are physically incapable of tasting them.

Yeah.

All cats, from your house cat to a lion, have a deletion in the gene that codes for the T1R2 protein.

They're missing half of the sweet receptor lock.

So if a cat eats ice cream.

They are enjoying the fat and the protein.

They have absolutely no idea it's sweet.

And there's a similar story for pandas, but with a different taste.

Yes, pandas have a broken gene for T1R1.

That's part of the umami receptor, the one that detects savory meaty amino acids.

Since pandas evolved to eat only bamboo over millions of years, they lost the ability to taste the meat they no longer ate.

Use it or lose it at a genetic level.

Exactly.

Then there's bitter.

The text says we have a huge family of bitter receptors.

The T2R family, like dozens of them.

Why so many?

Because in nature, bitter usually means poison.

There are thousands of different toxic alkaloids in plants.

We need a broad spectrum warning system.

We don't need to know which specific praising it is, just that it is a potential poison.

So all these different T2R receptors trigger the same universal yuck, spit it out.

Exactly.

It's our primary chemical defense system.

There's a big debate mentioned in the chapter about how the brain actually reads these signals, labeled lines versus pattern coding.

This is a classic neuroscience fight.

The labeled line theory says that each taste has its own dedicated private cable to the brain.

There is a sweet wire, a salt wire, and so on.

If you were to zap that sweet wire with an electrode, you would taste candy, even if there was nothing in your mouth.

And pattern coding.

That theory is a bit more complex.

It suggests the brain isn't listening to single lines, it's listening to the whole orchestra.

It analyzes the ratio of activity across all the lines to figure out the taste.

A specific food might activate the sweet line a lot, the sour line a little, and the salt line not at all.

That overall pattern is the taste.

Who's winning the debate?

Right now, the evidence is leaning pretty strongly towards labeled lines, at least for the five basic tastes.

Experiments where they knock out only the sweet receptor cells show that animals lose sweet taste completely, but the others are totally unaffected.

That implies dedicated pathways.

Okay, finally, let's move from the tongue to the nose.

Olfaction.

The sense of smell.

We often think humans are bad at this compared to dogs,

and, well, anatomically we are.

We have about 6 million olfactory receptor neurons.

A bloodhound has closer to 300 million.

But we're still pretty good.

We can distinguish thousands, maybe even a trillion, different odors.

And this all happens in the olfactory epithelium, a little patch of cells way up in the nose.

But there is something really weird about these neurons.

Something unique among all neurons in the brain.

They die.

They die and get replaced.

Constantly.

This is unique.

Olfactory neurons are the only neurons that regularly die and are replaced by new ones throughout our entire adult life.

Why would that be?

Think about where they are.

They are dangling directly into the open air of your nasal cavity.

They are exposed to every virus, bacterium, pollutant, and dust particle you breathe in.

They're on the front lines of a war zone.

So they get damaged and need to be replaced.

The body just replaces the whole garrison every few weeks.

And the wiring of the sense of smell is unique too.

Most senses, vision, hearing, touch, taste, go to the thalamus first, the brain's grand central relay station.

But smell, smell goes rogue.

Smell skips the line.

The olfactory bulb sends axons directly to the amygdala, which is the brain's emotion center, and to the hypothalamus.

This explains why smell is so potent, so emotional.

It explains everything.

A whiff of your grandmother's perfume or the smell of crayons can instantly transport you back to a childhood memory with a powerful emotional punch,

often before you even consciously realize what you're smelling.

The signal hits your memory and emotion centers before it hits your conscious analytical cortex.

It is raw and primal.

It's the only sense that does that.

No, we have to talk about pheromones.

This is always a hot topic.

Do humans have them?

It's controversial.

Many animals have a special separate organ called the vomeronasal organ, or VNO,

specifically to detect pheromones chemicals that signal things like sexual readiness.

In humans, the genes for the VNO receptors are mostly broken.

They're what we call pseudogenes.

So we don't have the hardware.

Well,

we don't have that specific hardware.

But more recently, scientists have discovered a new class of receptors in our main olfactory epithelium called TARS -trace amine -associated receptors.

We know mice use these to detect social cues from predators and potential mates.

And humans have them too.

So we might be sending and receiving chemical signals to each other, and we just don't know how the system works yet.

It is very possible.

The mystery of subconscious attraction might be hiding in the TARS.

The jury is still out.

One final mind -bender from the cutting -edge section of the text.

Taste receptors.

Not on the tongue, but in the lungs.

This one blew my mind when I first read about it.

Scientists have found T2R bitter receptors and even T1R sweet receptors in the lining of the lungs, the gut, the stomach.

So my lungs can taste bitter.

In a way.

But the signal doesn't go to your conscious brain.

You don't think, yuck, my lungs taste bitter.

Instead, the receptors trigger a local physiological reflex.

If the lung tastes a bitter toxin from something you've inhaled, it might trigger a coughing fit or cause the airways to constrict to keep the poison out.

If the gut tastes sugar, it might release hormones to prepare the body for digestion.

It redefines what a sense is.

It's not just for creating a conscious experience.

It's for regulating the body's internal environment.

Precisely.

We are sensing machines from top to bottom, from our tongue to our lungs.

We have covered a massive amount of ground today.

From the mechanical trapdoors in the ear to the chemical keys in the nose to rocks in our head telling us which way is down.

What's the big takeaway for you?

For me, it's the concept of the umwelt, the German word for the self -world or the surrounding world.

We walk around thinking we perceive reality as it is, but we don't.

We perceive the tiny slice of reality that we have evolved the specific receptors for.

We're locked into our own sensory bubble.

A completely bespoke sensory bubble.

We don't hear the ultrasonic calls of a bat.

We don't see in the ultraviolet spectrum like a bee.

We're living in a world defined entirely by the limits of our biology.

It makes you wonder what is filling this room right now?

What signals?

What energies?

What chemicals that we are completely utterly oblivious to simply because we lack the hardware to detect them.

And that is the ultimate humbling question, isn't it?

A humbling thought to end on.

Thank you for listening to this deep dive into sense and sensitivity.

It's been a real pleasure.

This is the Last Minute Lecture Team signing off.

Keep listening.

And keep wondering.