Neurons, synapses, and neural communication

Something small and fast. A neuron, a nerve cell that sends and receives signals, took in messages from its neighbors, added them up, and fired. The signal ran down the cell as a brief electrical pulse. At the far end it became a chemical message that crossed a tiny gap and nudged the next neuron (Spielman et al., 2020).

Memory, as psychologists use the word, is a construct. We infer it from what people say and do. The pulses and chemicals in this lesson are the biological events underneath. This lesson walks through them in order, one part at a time.

Your nervous system is built from two kinds of cells. Neurons carry the signals. Glial cells (glia) support them: they hold neurons in place, bring nutrients, clear waste, and wrap some axons in insulation (Spielman et al., 2020; Betts et al., 2022). There are also different jobs among neurons. Sensory neurons carry information in from the eyes, ears, and skin. Motor neurons carry commands out to muscles. Interneurons connect the two (National Institute of Neurological Disorders and Stroke [NINDS], n.d.).

Most neurons share the same basic parts. Read Figure 3.1 from left to right, the same direction the signal travels.

Receiving: dendrites and the cell body

Dendrites are the tree-like branches of a neuron. They are the input side. Other neurons connect to them and pass messages in. The dendrites feed into the cell body, also called the soma. The cell body holds the nucleus, which contains the cell's genetic material and directs its work (NINDS, n.d.).

Deciding: the axon hillock

The cell body narrows into a cone called the axon hillock. This is where the neuron "decides." All the small incoming signals add up here. If the total is strong enough, the neuron fires. Together with the first stretch of the axon, this region is called the trigger zone (Betts et al., 2022).

Sending: the axon, myelin, and nodes

The axon is a single long fiber that carries the signal away from the cell body. Some axons are a fraction of an inch long. Others run for several feet (Spielman et al., 2020). Many axons are wrapped in a myelin sheath, a fatty coating made by glial cells. In the brain and spinal cord, cells called oligodendrocytes make it. In the rest of the body, Schwann cells do (Betts et al., 2022). Myelin works like the plastic on an electrical cord. It insulates the axon and makes the signal travel faster.

The myelin is not one continuous tube. It comes in segments with small bare gaps between them. Each gap is a node of Ranvier. As you will see below, those gaps are where the signal is renewed.

Passing it on: terminals and the synapse

At its far end the axon branches into axon terminals. Each ends in a small bulb (textbooks also call it a terminal button). Inside are vesicles, tiny sacs filled with chemical messengers (Spielman et al., 2020). The place where a terminal meets the next cell is the synapse. The two cells do not quite touch. A very narrow space, the synaptic cleft, lies between them.

A neuron at rest is like a stretched rubber band, ready to snap (Spielman et al., 2020). The "stretch" is electrical. Charged particles called ions are spread unevenly across the cell's outer membrane. Sodium ions (Na⁺) are about ten times more concentrated outside the cell than inside. Potassium ions (K⁺) are more concentrated inside (Betts et al., 2022).

That uneven spread creates a small voltage across the membrane, the membrane potential. When the neuron is quiet, the inside sits at about -70 millivolts (mV) compared with the outside. This quiet state is the resting potential. The exact number varies from cell to cell, but -70 mV is the standard textbook value (Betts et al., 2022).

Keeping that charge takes work. A protein in the membrane, the sodium-potassium pump, pushes three sodium ions out for every two potassium ions it brings in (Spielman et al., 2020). It runs on the cell's energy supply, ATP (Betts et al., 2022).

Each message that arrives at a dendrite shifts the voltage a little. Some push it up toward firing. These are excitatory. Others push it down, away from firing. These are inhibitory. These shifts are small and local, and their size depends on the strength of the input (Betts et al., 2022).

At the axon hillock, all these shifts are added together. This adding up is called summation. It can come from many inputs arriving at once, or from one input firing again and again in quick succession (Betts et al., 2022).

If the total reaches the threshold, about -55 mV, the neuron fires an action potential, a brief electrical spike that runs down the axon (Betts et al., 2022). It happens in a set order:

• Depolarization. Gates in the membrane called voltage-gated sodium channels swing open. Sodium rushes in. The inside of the cell swings from negative to about +30 mV.
• Repolarization. The sodium channels shut and potassium channels open. Potassium flows out, and the voltage falls back down.
• Hyperpolarization. The potassium channels close a little late, so the voltage briefly dips below -70 mV. Then it settles back to rest.

The whole spike lasts about 2 milliseconds (Betts et al., 2022). During and just after it, the neuron cannot fire again, or needs a stronger push to do so. That short pause is the refractory period.

By how often the neuron fires. The action potential is all-or-none. If threshold is reached, the full spike happens. If not, nothing happens. There is no half spike, and every spike peaks at about the same voltage. A stronger stimulus does not make a bigger spike. It makes more spikes, closer together (Betts et al., 2022).

This also explains why a stubbed toe hurts as much as a bumped nose, even though the toe is much farther from the brain. The spike is rebuilt at full strength along the way. It does not fade over distance, like the lit fuse of a firecracker (Spielman et al., 2020).

When sodium enters at one spot, it spreads a little way along the inside of the axon. That raises the voltage of the next patch of membrane past threshold, so channels there open too. The spike is rebuilt, patch by patch, all the way down (Betts et al., 2022).

It only moves forward. The patch it just left is still in its refractory period, so the spike cannot turn back (Betts et al., 2022).

On a myelinated axon, the channels sit mostly at the nodes of Ranvier. The spike appears to leap from node to node. This is called saltatory conduction, from the Latin word for "to leap," and it is much faster than rebuilding the spike along every bit of membrane. Wider axons also carry signals faster (Betts et al., 2022).

Myelin matters for health. In multiple sclerosis (MS), the immune system damages myelin in the brain and spinal cord. Signals slow down or fail, which can bring fatigue, dizziness, and trouble with movement (Spielman et al., 2020; Betts et al., 2022).

Figure 3.2 puts the whole sequence in motion, from rest to the synapse. Play it through once, then step through it slowly.

The electrical signal becomes a chemical one. When the spike arrives at an axon terminal, calcium channels open and calcium ions (Ca²⁺) flow in. Calcium helps the vesicles fuse with the terminal's outer membrane. They open and release their contents into the synaptic cleft (Betts et al., 2022). A single vesicle holds about 10,000 molecules of neurotransmitter (Spielman et al., 2020).

A neurotransmitter is a chemical messenger that carries the signal across the synapse. The molecules drift across the cleft and attach to receptors, proteins on the surface of the next cell. Each receptor has a shape that fits only certain neurotransmitters, like a key in a lock (Spielman et al., 2020; Betts et al., 2022).

What happens next depends on the receptor, not only on the chemical. Some receptors open channels that push the next neuron toward threshold. Others push it away. Glutamate is usually excitatory. GABA and glycine are usually inhibitory (Betts et al., 2022). The receiving neuron adds up all these pushes at its own axon hillock, and the cycle can start again.

A few synapses skip the chemistry. At an electrical synapse, two cells are joined directly and current passes straight through. These are much less common in the brain, but faster (Spielman et al., 2020).

If neurotransmitter stayed in the cleft, the signal would never end. So it is cleared in three ways (Spielman et al., 2020; Betts et al., 2022):

• Reuptake. Pumps on the sending neuron pull the molecules back inside to be reused.
• Breakdown. Enzymes split the molecules into inactive pieces. For example, acetylcholinesterase breaks down acetylcholine.
• Drifting away. Some molecules simply diffuse out of the cleft.

Clearing the cleft gives each signal a clear start and a clear end (Spielman et al., 2020).

Because many drugs act at the synapse, and they change behavior and experience. Psychologists sort them by what they do there (Spielman et al., 2020):

• An agonist mimics a neurotransmitter at its receptor. Dopamine agonists are one treatment for Parkinson's disease, in which dopamine-producing neurons are lost (NINDS, n.d.; Spielman et al., 2020).
• An antagonist blocks a receptor without activating it. Some antipsychotic medications block dopamine receptors.
• A reuptake inhibitor slows reuptake, so the neurotransmitter stays in the cleft longer. Selective serotonin reuptake inhibitors (SSRIs), used to treat depression, work this way.

These medications are not instant fixes. They often take several weeks to help, people respond to them very differently, and they can have side effects. Some research suggests that medication combined with therapy works better than either one alone (Spielman et al., 2020). If you have questions about a medication, a doctor or pharmacist is the right person to ask.

Now try the model in Figure 3.4. Turn it, zoom in on the synapse, and tap each part until you can name it without looking.

So, back to the name that came back to mind. Behind it were many neurons adding up their inputs, firing all-or-none spikes, and passing chemical messages across thousands of synapses. Psychologists study the memory. Neurons are part of how it happens.