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Just Another Teachin’ Tuesday: Brain Physiology (dry, but amazing)

Let’s discuss some brain physiology I believe will attract and sustain your attention. Can you tell I find this stuff fascinating? Kind of a geek, aren’t I? Um – sure.

Since the early 1950’s biological theory, and treatment, for mood and anxiety has focused upon neurotransmitters (chemicals that enable neurons to interconnect) in the brain. Now, it’s absolutely unfathomable to me that the human brain consists of some 100 billion neurons (nerve cells), and each and every one of these neurons generates 1 to 10,000 synapses (connections between neurons). Oh, by the way – if you do the math, that would mean the number of potential synaptic connections in the brain is knocking on the door of 40,000,000,000,000,000. That’s forty quadrillion. Astounding.

Well, then – it’s obvious the neurons within this three-pound mass we call “brain” are interconnected, allowing messages to travel along them much like electricity speeds along a wire. Indeed, the messages travel from neuron to neuron in the form of electrical potential. And to maintain this interconnectivity, during synapse, these messages jump a one-millionth of a centimeter gap known as a synaptic cleft. Oh, and by the way – messages travel within the neuron at up to 260 miles-per-hour.

Neurotransmitters are chemicals that are employed by the brain to relay, amplify, and modulate the electrical signals involved in a synapse; and they’re stored in small vesicles gathered at the tip of a neuron’s messenger arm, the axon. Neurotransmitters are activated upon the arrival of electrical action potential, which causes some of the synaptic vesicles to shift to the very end of the axon and release their contents into the synaptic cleft. It’s at this point that neurotransmitters pour out and spread across the cleft, causing ion channels on the cell to open. Oh – ion channels are specific protein types that help establish and control the small electrical characteristics that exist across the plasma membrane of all living cells.

Once in the cleft, neurotransmitters are active for only a short time, between .5 and 1 milliseconds. In this incredibly brief timeframe the neurotransmitters cross the cleft, binding to receptor molecules on a dendrite of the receiving neuron. The dendrite then conducts the electrical signal into the body of the neuron. Now, after all of the action takes place, neurotransmitters have several potential fates – destruction by enzymes in the synaptic cleft, being allowed to pour out of the cleft and spread, or re-absorption by the molecular transporter of a pre-synaptic neuron, a process known as reuptake.

Now, this reuptake business is of great relevance to us because, though much is still to be learned about the workings of neurons and neurotransmitters, modern theory suggests the presence of specific neurotransmitters is a little suspect in the brains of folks like us. It seems they just don’t stick around long enough, as reuptake ensues and they get sucked back into the originating neuron. Theoretically, this dynamic impairs the full and correct transmission of a neuron-to-neuron message, leading to mental and emotional distress.

Here are a few additional neurochemical tidbits I find interesting. Neurotransmitter secreting neurons – this is pre-synapse, now – have what are called autoreceptors assigned to specific neurotransmitters. These autoreceptors monitor the amount of neurotransmitter manufactured and secreted. An agonist is any chemical compound that replicates the action of a neurotransmitter, and an antagonist is a chemical compound that either totally blocks, or inhibits, the action of a neurotransmitter.

Don’t know about you, but I find all of what I just shared incredibly awe-inspiring. And to know it happens trillions upon trillions of times is beyond my comprehension. Is it any wonder why the human brain is thought to be the most complicated three-pound mass in the universe?

Not bad for a Teachin’ Tuesday, huh!

So what do you think chipur readers? Amazing stuff? Why not comment?

  • Marianne

    I really have to wonder what this medicine called keppra is doing in my brain. I assume that it is an antagonist. Medicines like these are suppose to slow down the overfiring of electrical impulses. So far no doctor has seen any overactivity that they can record in my brain. I have never been diagnosed as having epiIepsy. have heard that some kinds of seizures happen near the center of the brain and cannot be seen withut the right equipment. Regardless, keppra has stopped the shaking and jerking that was happening every time I layed down to sleep in the last few months. I suppose I am going to become a science project. :-)

    • Well, and I’m sure a very pleasant and (somewhat) willing project at that. From Wikipedia: The exact mechanism by which levetiracetam (Keppra) acts to treat epilepsy is unknown. However, the drug binds to a synaptic vesicle glycoprotein, SV2A, and inhibits presynaptic calcium channels. This is believed to impede impulse conduction across synapses.
      Bill