Chapter 13: Synaptic Transmission in the Nervous System

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Welcome to the Deep Dive.

We're here to cut through the complexity and get straight to the core ideas, those aha moments, you know.

Today we're tackling something pretty fundamental, actually happening inside your head right this second.

It's how those billions of neurons,

how they actually talk to each other.

It's amazing stuff.

Every thought, every memory, even just moving your finger, it all relies on this incredibly precise microscopic conversation.

Right, and our mission today is to really unpack this neural communication, what's called synaptic transmission.

Exactly.

We're drawing heavily from a classic text here, chapter 13 of Boron and Bull Peep's Medical Physiology.

It's a cornerstone for understanding this.

So the plan is to take these concepts, which can seem pretty dense, honestly, and make them clear, connect them to why they matter in medicine, in clinical practice.

And importantly, build it from the ground up, you know.

So it feels more like we're figuring it out together, even without diagrams in front of us.

By the end, you should really get how neurons communicate.

It's wild to think people like Sherrington and Ramoni Cajal figured out the basics way back before electron microscopes.

Totally.

Late 1800s, they deduced this synapse must exist a tiny gap.

Cajal's idea of contiguity, not continuity, that neurons touch but aren't fused.

That turned out to be spot on, only confirmed visually in the 50s, right?

Yeah, with the electron microscope finally showing that gap, that separation,

amazing foresight.

Okay, so let's dive into the main mechanism,

chemical synapses.

They're the most common type, the brain's primary way of sending signals.

And you might know the neuromuscular junction where nerves talk to muscles.

There are similarities, definitely.

Both use chemical messengers.

But the brain, it's just way more diverse, isn't it?

Not just one messenger, like at the muscle.

Oh, vastly more diverse.

It's like comparing a single instrument to a whole orchestra.

But the fundamental steps, the sequence of events at a chemical synapse, that's remarkably conserved.

Think of it like a seven -step process happening incredibly fast.

Okay, step one.

First, the neurotransmitters, the chemical signals, they get packaged into tiny membrane bubbles called vesicles.

These vesicles then get positioned, sort of docked, right at the edge of the presynaptic terminal that's the sending end.

Got it, ready to go.

What triggers the release?

An electrical signal.

The presynaptic membrane gets depolarized, its electrical charge rapidly shifts.

Usually, this is from an action potential arriving down the neuron's axon.

So that electrical jolt is the key.

It opens specific gates.

Exactly, voltage -gated calcium channels.

And when they open, calcium ions, K2 +, flood into the terminal from the outside.

A big rush of calcium.

Right, and the sudden spike in internal calcium is the immediate trigger.

It makes those docked vesicles fuse with the presynaptic membrane.

Use and release their contents.

How fast is this?

Incredibly fast.

We're talking fractions of a millisecond for each vesicle fusion event, this exocytosis.

It's thought a protein called synaptotagmin plays a key role in this speed.

Okay, so transmitters are released.

Where do they go?

They're released in these distinct packets, quantized amounts, into that tiny gap, the synaptic cleft.

Then they just diffuse across, passive movement.

Straight across to the receiving neuron.

Yep.

They bump into and bind to specific receptor proteins on the postsynaptic membrane, the receiver.

Binding is like a key in a lock.

And that unlocks, what, an action in the receiving cell?

It initiates some kind of event.

Could be opening an ion channel directly, changing the receiver's electrical state, or maybe starting a more complex chain reaction inside the cell, a G protein pathway, for instance.

Okay, message delivered.

But it can't just hang around, right?

No, gotta clear the signal.

The transmitters diffuse away from the receptors, and then they're removed either by just drifting away, getting broken down by enzymes right there in the cleft, or being actively pumped back into cells.

Like a cleanup crew.

Exactly.

And the presynaptic neuron also takes back the vesicle membrane through endocytosis, recycling it to make new vesicles.

It's a very efficient cycle.

And this whole machinery, these steps, they're ancient, right, evolutionarily speaking.

Absolutely.

Many parts are based on fundamental processes found in almost all eukaryotic cells.

Which also highlights why understanding each step is so crucial clinically.

If anything goes wrong here, packaging, release, binding, clearances, you can get serious neurological issues.

It's a finely turned system.

You mentioned the huge diversity of neurotransmitters in the brain, compared to the neuromuscular junctions, acetylcholine.

Can you elaborate on that?

What kinds are there?

Sure, we can go with them broadly.

You've got small molecule transmitters.

These include amino acids like glutamate and aspartate.

They're the main excitatory ones tending to make neurons fire.

And the inhibitory ones?

That's mainly GABA, amylobutyric acid, and glycine.

They quiet things down.

Then there are simple amines like acetylcholine itself, but also norepinephrine, serotonin, histamine.

Even ATP, the energy molecule, acts as a transmitter in some places.

Interesting, and then there are bigger ones.

Yeah, the neuropeptides.

These are actual proteins or bits of proteins like endorphins or enkephalins, the brain's natural opioids.

Their production is different too.

They start as larger precursors, get processed in the Golgi apparatus, and are packaged into larger vesicles called dense core vesicles.

Can a single neuron use more than one type?

Oh, definitely.

That's called co -localization.

Many neurons package both a small molecule transmitter, maybe in small clear vesicles, and a neuropeptide in those larger dense core vesicles, all in the same terminal.

Why do that?

It allows for more complex signaling.

Low frequency firing might only release the small transmitter for fast effects, but a high frequency burst of action potentials could release both, adding the slower, perhaps more modulatory, effects of the neuropeptide.

It adds another layer of control based on activity patterns.

Fascinating.

Are there any really weird messengers, ones that break the rules?

Absolutely.

Nitric oxide, NO, is a great example.

It's a gas.

It's not stored in vesicles.

It's made on demand.

And because it's a small, uncharged gas, it just diffuses right through membranes.

So it can go anywhere, even backwards.

Potentially, yes.

It can act as a retrograde messenger flowing from the postsynaptic side back to the presynaptic terminal to influence further release.

It's quite unusual.

Any others?

Endocannabinoids are another interesting class.

These are lipid molecules, like anandamide, that our brain makes.

They act on cannabinoid receptors, the same ones THC from marijuana acts on.

And we have a lot of those receptors.

More cannabinoid receptors, specifically CB1 type, than any other G protein coupled receptor in the brain.

Suggests a really widespread role, probably modulating things like pain, appetite, memory.

We're still figuring it all out.

They're also retrograde messengers, typically suppressing transmitter release.

Okay, shifting from the messengers to the structure, where do these connections actually happen on a neuron?

Pretty much anywhere on the receiving neuron.

Presynaptic terminals, often called bouton terminals, can synapse onto dendrites, axodendritic, the cell body or soma, axosomatic, even onto another axon terminal, exoaxonic.

So lots of possibilities for connection points, right.

And many excitatory synapses, especially in areas like the cortex and hippocampus, occur on these tiny little protrusions from the dendrites, called dendritic spines.

Spines, why have those?

That's a great question, still debated.

One leading idea is they create tiny biochemical compartments.

They might help isolate the effects of calcium influx at that specific synapse.

And calcium is key for?

For synaptic plasticity.

The ability of synapses to change their strength, which is thought to underlie learning and memory.

So these spines could be critical little micro domains for learning rules.

You also mentioned synapses are polarized.

Yeah, they have a clear directionality.

The presynaptic side has these active zones where the vesicles cluster, ready for release.

The postsynaptic side has a corresponding postsynaptic density, which is packed with neurotransmitter receptors and associated proteins, perfectly positioned to receive the signal.

It's highly organized.

So far we've focused on these very specific point -to -point connections, but you mentioned the brain also needs broader changes, like for mood or alertness.

Exactly.

Think about falling asleep or waking up or feeling generally anxious or focused.

That's not just one synapse talking to another.

It's a global shift in brain state.

How does the brain manage that?

Through what are called diffuse modulatory systems.

These are really remarkable.

They typically originate from small clusters of neurons, maybe just thousands, often deep in the brain stem.

Small numbers, but big reach.

Huge reach.

Their axons branch incredibly widely, potentially influencing hundreds of thousands of postsynaptic neurons all across the brain cortex, thalamus, hippocampus, everywhere.

And how do they signal?

Is it the same fast, precise way?

Often, no.

They sometimes release their neurotransmitter more diffusely into the extracellular fluid, baiting large regions rather than just targeting a single synaptic cleft.

And critically, they predominantly act via G protein -coupled receptors, also called metapotropic receptors.

Which means their effects are?

Slower to start, longer lasting, and often more about modulating the cell's overall excitability or responsiveness to other inputs, rather than directly causing it to fire or be inhibited immediately.

And these systems are really important clinically, right?

Interestingly important.

Many psychoactive drugs, medications for depression, anxiety, schizophrenia, Parkinson's.

They often target one or more of these diffuse modulatory systems.

Understanding them is key to neuropsychiatry.

Can you give some examples of these systems?

Sure.

Let's take norepinephrine.

Its neurons are mainly in a tiny spot in the brainstem called the locus coeruleus, but they project almost everywhere.

This system is vital for attention, arousal, sleep -wake cycles, learning, mood, anxiety.

It seems particularly activated by new, unexpected, or potentially salient stimuli.

Okay, who else?

Serotonin.

Mostly from the rofe nuclei and other set of clusters along the brainstem midline.

Again, very diffuse projections.

Crucial for regulating sleep -wake cycles, and especially mood.

This is the system targeted by many antidepressants, like SSRIs, selective serotonin reuptake inhibitors, and also involved in the action of drugs like LSD.

What about dopamine?

Dopamine has a couple of major pathways.

One originates in the substantia nigra and projects to the striatum, essential for initiating voluntary movement.

Degeneration here causes Parkinson's disease.

And the other pathway.

Originates in the ventral tegmental area, VTA, projecting to the prefrontal cortex and limbic areas.

This pathway is heavily involved in reward, motivation, reinforcement learning.

And it's implicated in drug addiction and schizophrenia.

Many antipsychotics block dopamine receptors in this system.

And acetylcholine.

We know it from the muscle junction.

Acetylcholine also has central modulatory roles.

There are clusters in the basal forebrain projecting to the hippocampus and cortex, and another group in the brainstem projecting to the thalamus.

They're involved in arousal, sleep -wake, attention, and likely learning and memory.

Alzheimer's disease involves significant loss of these cholinergic neurons.

So even though these systems have relatively few neurons, their widespread connections give them enormous influence over our overall brain state and behavior.

Precisely.

They act like master regulators, setting the tone for everything else.

Okay, this raises a really interesting question.

We briefly mentioned electrical synapses, gap junctions, which are super fast.

Why did the brain predominantly go with these more complex, seemingly slower chemical synapses?

It feels a bit backward.

It does seem like a paradox at first glance,

but chemical synapses offer some massive advantages.

First, amplification.

An electrical synapse just passes the signal along, maybe even making it smaller.

But with a chemical synapse, one vesicle releasing a few thousand transmitter molecules can trigger a cascade involving G proteins and second messengers that ultimately affects many ion channels or enzymes.

You get signal gain.

A small input can have a big effect.

What else?

Inhibition.

It's very easy for chemical synapses to be inhibitory.

They just need to open channels for ions like chloride, which makes the neuron less likely to fire.

Doing that effectively with just electrical connections is much harder.

Makes sense.

Third, the time domain.

Chemical synapses can mediate effects that last anywhere from milliseconds with direct ion channel opening to seconds, minutes, hours, or even longer through these G protein cascades and changes in gene expression.

Electrical synapses are basically locked to the duration of the presynactic event.

And maybe the biggest one.

Plasticity.

Chemical synapses are incredibly adaptable.

Their strength can change based on past activity.

This ability to modify connections is fundamental for learning, memory, and development.

Electrical synapses are generally much less plastic.

So flexibility and control seem to be the key trade -offs for speed.

That's a good way to put it.

Okay, so when a chemical synapse does act, what kinds of effects can it have?

We can broadly say excitatory, inhibitory, or modulatory.

Excitatory makes the next neuron more likely to fire.

In the brain, most fast excitation uses glutamate or aspartate.

They bind to receptors that open channels letting positive ions, mainly sodium, flow in.

This causes a small depolarization called an EPSP excitatory postsynaptic potential.

Small.

So one EPSP usually isn't enough.

Almost never in the CNS.

You need summation.

Many EPSPs arriving close together in time and space have to add up to push the postsynaptic neuron's membrane potential all the way to its action potential threshold.

It's like collecting votes.

And inhibition does the opposite.

GABA and glycine are the main inhibitory players.

They typically bind to receptors that are channel selective for chloride ions, CL.

When CL flows in or sometimes stabilizes the membrane near the resting potential, it makes the inside more negative or harder to depolarize.

This is an IPSP inhibitory postsynaptic potential.

It counteracts excitation.

Okay, excite, inhibit.

What about modulate?

Modulatory synapses often don't cause big voltage swings themselves.

Instead, they tweak the neuron's properties, changing how it responds to other excitatory or inhibitory inputs.

We mentioned norepinephrine before it can act via beta adrenergic receptors, and it can't be cascaded to close certain potassium channels.

What does closing potassium channels do?

It makes the neurons slightly more depolarized and, importantly, less leaky to potassium.

This can make the neuron more excitable, more likely to fire in response to an EPSP, and less able to adapt or slow its firing during prolonged stimulation.

So norepinephrine isn't directly exciting it, but it's changing its responsiveness, tuning the instrument.

And these modulatory effects often involve those G protein pathways you mentioned.

Very often.

There are two main flavors.

Some G proteins act directly on ion channels nearby in the membrane that's relatively fast and localized, called membrane -delimited pathways, like acetylcholine slowing the heart by opening potassium channels.

And the other flavor.

Involves second messengers.

The G protein activates an enzyme, like adenyl cyclase, which then produces lots of small messenger molecules like cyclic AMP, CMP, inside the cell.

These messengers can diffuse widely and activate other enzymes like protein kinases, which then phosphorylate target proteins like ion channels, changing their function.

That sounds slower, but allows for more spread and amplification.

Exactly.

And you need ways to turn it off too.

So cells have protein phosphatases that remove those phosphate groups, reversing the effects.

It's a constant push and pull.

This seems incredibly complex.

Does one transmitter always do the same thing?

Not necessarily.

That's where divergence and convergence come in.

Divergence means one neurotransmitter can bind to multiple different types of receptors, triggering different effects in different cells or even different parts of the same cell.

And convergence.

Convergence is when multiple different neurotransmitters, each binding to its own receptor, might ultimately influence the same downstream target, like a single type of ion channel or second messenger system.

It allows integration of different signals.

Okay, let's focus on the real workhorses.

Glutamate and GABA synapses, they handle most of the fast info processing, right?

Absolutely.

Let's start with glutamate, the main excitatory one.

When glutamate binds, the resulting EPSP often has two parts, if you look closely, a fast part and a slower part.

What causes the fast part?

That's primarily mediated by AMPA receptors.

These are ligand -gated ion channels that, when glutamate binds,

open quickly and let sodium neoplus in and potassium K plus out, causing rapid depolarization.

They generally don't let much calcium through.

Okay, fast excitation via AMPA.

What about the slower component?

That's where NMDA receptors come in.

These are really special.

There are also glutamate -gated channels permeable to Na plus and K plus.

But crucially, they're also highly permeable to calcium, CO2 plus.

And calcium influx is a big deal inside the cell.

A very big deal.

But there's a catch with NMDA receptors.

At the normal resting membrane potential, around negative 70 millivolts, the channel pore is actually blocked by a magnesium ion, Mg2 plus.

Blocked, so glutamate binding isn't enough.

Nope, to open the channel and let ions flow, including that important calcium, you need two things.

Glutamate has to bind, and the postsynaptic membrane needs to be sufficiently depolarized, usually above about negative 60 millivie, to physically push the magnesium ion out of the way.

Ah, so it needs prior activity, maybe from those AMPA receptors, to relieve the block?

Precisely.

It acts like a coincidence detector.

It only opens significantly when there's both glutamate release and strong postsynaptic depolarization happening at the same time.

And the resulting calcium influx through the NMDA receptor.

That's a critical trigger signal.

It can activate enzymes, change channel properties, influence gene expression.

It's absolutely central to many forms of synaptic plasticity, like LTP, which we'll get to.

But too much K2 plus influx through NMDA receptors can also be toxic, leading to cell death, excited toxicity.

Wow, okay, so AMPA for fast sap, NMDA for a slower calcium -dependent signal that requires coincident activity.

You got it.

There are also kinate receptors for glutamate, less well understood, but they likely contribute too.

Now let's switch to the main inhibitor, GABA.

Right, GABA primarily acts on GABA receptors.

These are ionotropic receptors, meaning they are the ion channel, and they're selective for chloride ions, CL.

So when GABA binds, chloride flows through.

Usually into the cell, making the inside more negative, leading to inhibition or stabilization near rest.

Controlling inhibition is vital.

Too little can cause seizures.

Too much can cause coma.

Then this is where certain drugs come in.

Exactly.

The GABA receptor has binding sites for other molecules besides GABA.

Benzodiazepines like Valium or Xanax bind to one site.

Barbiturates, like phenobarbital, bind to another.

What do they do there?

They don't open the channel themselves, but they enhance the effect of GABA when it binds.

Benzodiazkenes increase the frequency of channel openings.

Barbiturates increase the duration the channel stays open.

So both effectively boost the inhibitory chloride current.

Yes, leading to stronger IPSPs, more inhibition, and the resulting sedative anti -anxiety or anti -convulsant effects.

It highlights how modulating these natural systems pharmacologically can have powerful behavioral effects.

Interestingly, these GABA receptors, along with acetylcholine nicotinic, serotonin 5 -HT3, and glycine receptors, they all belong to one big structural family, right?

Yeah, the cis -loop or pentameric ligand -gated ion channel superfamily, they share a common blueprint of five subunits surrounding a central pore.

It's a great example of evolutionary adaptation of a core structure.

Now, one last point comparing brain synapses to the neuromuscular junction,

the reliability of release.

Big difference.

The NMJ is fail -safe.

One nerve impulse triggers a huge release of acetylcholine, generating a massive EPSP that always triggers a muscle action potential every time.

But not in the brain.

Generally, no.

Most CNS synapses are much less reliable, and action potential arriving at a presynaptic terminal might only release one vesicle, or often, no vesicles at all.

The probability of release can be quite low.

So how does anything happen?

Summation again.

You typically need the near simultaneous activity of many synapses, maybe tens or even a hundred, converging onto a single postsynaptic neuron to provide enough summed EPSPs to reach a threshold and make it fire.

It makes the neuron an integrator of many inputs, not just a slave to one.

Okay, integration is key.

This leads perfectly into the final topic.

How synapses change.

Plasticity.

Learning and memory.

Arguably the brain's most incredible feat.

And the overwhelming evidence points to synapses as the physical location where memories are stored, or at least initiated.

Synaptic strength isn't fixed.

It changes based on experience and activity.

That's plasticity.

There are short -term changes.

Yes, short -term plasticity lasts seconds to minutes.

Things like facilitation, augmentation, potentiation, where repeated stimulation briefly makes the synapse stronger.

Or depression, habituation where it gets weaker.

What causes these short -term changes?

Usually changes in the presynaptic side, specifically in the amount of neurotransmitter release per action potential.

A leading idea for strengthening, like facilitation, is the residual calcium hypothesis.

High frequency firing leaves some extra calcium lingering in the terminal.

Exactly, so the total calcium peak gets higher, triggering more vesicle fusion and more transmitter release.

For depression, it might be temporary depletion of readily releasable vesicles.

But for long -term memory, we need something more lasting.

That's where long -term potentiation LTP comes in.

First discovered in the hippocampus, a brain area critical for forming new declarative memories, LTP is a long -lasting increase in synaptic strength, potentially lasting days, weeks, or longer.

It's a prime candidate for a memory mechanism.

How do you trigger LTP?

Typically with a brief burst of high -frequency stimulation to the presynaptic axons.

Or, importantly, by pairing relatively weak presynaptic stimulation with strong depolarization of the postsynaptic cell.

What makes LTP such a good candidate for memory?

It has key properties.

One is input specificity.

Only the synapses that were active during the induction get strengthened, not inactive synapses nearby on the same cell.

Specificity is crucial for storing distinct information.

Makes sense, what else?

Cooperativity or associativity.

LTP usually requires the simultaneous activation of multiple inputs onto the postsynaptic cell to depolarize it sufficiently.

This allows for associations to be formed.

Can you give an example of associativity?

Sure, imagine trying to learn someone's name associated with their face.

Seeing the face activates one set of synapses, hearing the name activates another.

If these happen close together in time and strongly enough to trigger LTP at both sets of synapses onto a common neuron.

Then later, just seeing the face might be enough to activate the name representation more strongly.

Exactly, the connection is strengthened through simultaneous activity.

This fits well with associative learning principles.

What's happening at the molecular level during LTP in the hippocampus?

The classic form heavily involves those NMDA receptors.

Remember, they need both glutamate and strong postsynaptic depolarization to open and let calcium in.

So the high frequency stimulation or pairing provides that strong depolarization needed to unblock the NMDA receptors.

Precisely, and the critical event for inducing LTP is a large rapid rise in postsynaptic intracellular calcium concentration lasting maybe a second or two, coming mainly through those NMDA receptors.

What does the calcium do then?

It activates several key intracellular enzymes, especially protein kinases.

A really important one is CAMKI,

calcium calmodulin -dependent protein kinase II.

Activating CAMKII seems essential for LTP induction.

And how does this make the synapse stronger long -term?

What actually changes?

The expression of LTP, the reason the synapse stays stronger, seems to be primarily postsynaptic.

A major mechanism involves increasing the number and or the effectiveness, like conductance, of NMPA receptors in the postsynaptic membrane.

More NMPA receptors mean a bigger response to the same amount of glutamate release.

So, more listeners for the same shout, is there any change on the presynaptic side too?

That's been debated for decades.

There's evidence suggesting sometimes presynaptic release might also increase long -term, possibly triggered by a retrograde messenger sent from the postsynaptic side back to the presynaptic terminal.

But the identity of such a messenger is still not fully settled.

Okay, so LTP strengthens connections, but we must need to weaken them too, right?

To forget or refine memories.

Absolutely.

And the brain has mechanisms for that too, called long -term depression, LTD.

It's a long -lasting decrease in synaptic strength.

Can it happen at the same synapses as LTP?

Yes, often at the very same synapses in the hippocampus.

What determines whether you get LTP or LTD often depends on the pattern of activity.

High frequency stimulation tends to cause LTP.

And LTD?

Lower frequency stimulation, say around one hertz for several minutes,

often induces LTD.

It's also input specific.

What's the mechanism?

Is it just the reverse of LTP?

In the hippocampus, it's intriguingly similar in some ways, but crucially different.

It also often requires NMDA receptor activation and a rise in postsynaptic calcium.

Wait, calcium causes both strengthening and weakening.

How?

It seems to depend on the amount and dynamics of the calcium signal.

A large, fast calcium rise, like in LTP, preferentially activates protein kinases, like CAM -CAMII, but a smaller, slower, more modest rise in calcium, like during low frequency stimulation for LTD, seems to preferentially activate protein phosphatases.

Enzymes that do the opposite of kinases, they remove phosphate groups.

Exactly.

So kinases phosphorylate targets, like AMPA receptors, leading to LTP, while phosphatases dephosphorylate them, potentially leading to LTD, maybe by causing AMPA receptors to be removed from the synapse.

It's like the level of calcium sets a threshold determining which pathway dominates.

That's elegant.

Is LTD the same everywhere?

Not entirely.

For example, in the cerebellum, which is critical for motor learning, there's a very well -studied form of LTD at the synapses between parallel fibers and Purkinje cells.

It's crucial for adapting motor commands.

How is cerebellar LTD different?

It also requires postsynaptic calcium influx, but here, the calcium comes mainly through voltage -gated calcium channels opened by strong depolarization from another input, climbing fibers, not through NMDA receptors, which are less prominent in mature Purkinje cells.

But the end result is similar, a decrease in AMPA receptor effectiveness.

So LTP and LTD provide this bidirectional control over synaptic strength, driven by patterns of neural activity and calcium signals, the likely cellular basis for learning and memory.

That's the prevailing view, yes.

It provides a plausible mechanism for how experience can physically alter neural circuits.

Wow, okay, that was quite a journey.

From the basic steps of synaptic transmission through the diversity of messengers and modulatory systems,

right up to the potential cellular basis of memory itself.

It really covers a huge amount of ground, showing how these molecular details build up to explain incredibly complex brain functions.

It underscores the elegance and adaptability of the nervous system.

Absolutely,

and understanding these fundamentals, as we've discussed, directly links to understanding neurological disorders and how treatments might work.

It might seem daunting, but breaking it down step -by -step Makes it manageable.

You absolutely can grasp the stuff.

We hope this deep dive has helped clarify things.

Remember, you're part of the deep dive family, and you've totally got this.

Keep digging into it.

Definitely, and maybe leave you with a final thought to chew on if our experiences through LTP and LTD are constantly strengthening some connections and weakening others.

How much are we through our focus, our learning, our daily lives, actively sculpting the physical structure of our own brains, shaping who we become, quite literally synapse by synapse?

Something to think about.