How Neurons Communicate - Sept. 27, 2000

Announcements:

READINGS THIS WEEK: Ch. 2 & 3 (up to p. 71)
Yalda's OH - Wed. 4:30-5:30 (CSB 102)

Notes:

Today's topic: synapses (how neurons talk to one another).
          -a neuron by itself is "pretty stupid"

REVIEW: Reminder of terms from last time:
Carlson, p. 47

There are more NA+ and Cl- ions outside of the cell than K-, and vice versa.

There are pumps on the membrane to keep sodium out of the cell. Sodium has a tendency to go into the cell (forced in by diffusion and electrostatic pressure). The other two ions have a balance of forces.

The action potential is the language the neurons have to talk to each other.

TODAY'S TOPIC: Now we have this neuron that is "talking" (generating action potential) -How is this translated for another neuron to understand?
          -SYNAPSE

What does a synapse look like?

Some terms to get straight:

The synapse is a place! It's a gap filled with water and ions between the neurons! This gap is also called the synaptic cleft.

Carlson, p. 46Where do you find synapses?
3 places:

  1. in between terminal buttons and dendrites (on spines or not).
  2. directly on the cell body (skips the dendrite altogether)
  3. in some weird cases, the synapse happens to be on another axon.

How do synapses work?/How are signals produced?           Steps in the basic mechanism:

  1. action potential generated near the soma. Travels very fast down the axon.
  2. vesicles fuse with the pre-synaptic membrane. As they fuse, they release their contents (neurotransmitters).
  3. Neurotransmitters flow into the synaptic cleft. If the synaptic cleft looks the same on both sides, it's a symmetric synapse. If the sides look different, it's an asymmetric synapse.
  4. Now you have a neurotransmitter free in the synaptic cleft. On the other side are receptors in the membrane. They're like keyholes. They let ions through if and only if neurotransmitters are bound to them! The neurotransmitter binds to the "keyhole" and lets ions through.

So, the steps in generating action potential:

  1. - action potential generated.
  2. - vesicle fuses to pre-synaptic membrane.
  3. - release of neurotransmitters.
  4. - neurotransmitters bind to receptors.
  5. - ions flow through the open receptor.

There is another type of receptor - metabotrophic receptor.
This type binds the neurotransmitter like the ionotrophic receptor. But instead of letting ions go through directly, the metabotropic receptor activates the second messenger. This messenger goes to open the ion channels.

The metabotrophic mechanism is slower than the ionotrophic one, but it's very diffused.
          -it will activate ion channels far away from the binding site.

The ionotrophic mechanism is very quick, but very local (only lets ions through right where the neurotransmitter is located).

Carlson, p. 50 What is happening when ions are going through the membrane?

If the neurotransmitter binds to a sodium channel (NA+):

What happens is you have a different neurotransmitter that "opens the keyhole" of a potassium channel?

Sodium depolarizes, potassium hyperpolarizes - What about chloride?

The final polarization the neurotransmitter creates depends on the type of channel it activates.

This process starts with electrical and ends with electrical signals. In between, there are chemical signals.
          action potential > vesicle fusion > neurotransmitter release > receptor opening > ion flow > EPSP/IPSP

Why not just "glue" together neurons?

Drugs work in the chemical stages (talk about that in Ch.4)

For the postsynaptic neuron to generate an action potential, it needs to receive a stimulus to bring it above the threshold of excitation. It needs a sum of stimuli. (two movies about this on the web)

After neurotransmitters bind to receptors in the synaptic cleft, what happens to them?

What happens with EPSPs/IPSPs?

There are 2 kinds of summation:

  1. spatial
  2. temporal

In review, spatial summation involves many synapses at one time, and temporal summation involves one synapse at many times.
In real life, both types of summation are involved with the transmission of action potentials.

To summarize today's lecture:
          The axon tries to reach the dendrite. Axons are filled with microtubules. On these are vesicles, which travel from the soma to the terminal button. The vesicles sit in the terminal button until an action potential is generated. In vesicles are neurotransmitters. a neuron can have only one kind of neurotransmitter. When action potential is reached, vesicles dock with the presynaptic membrane and fuse with it. They release neurotransmitters into the synaptic cleft. These neurotransmitters bind to receptors on the postsynaptic site. If the postsynaptic cell's receptors are ionotrophic, they allow ions to enter the postsynaptic cell directly. If they're metabotrophic, they activate second messengers to open ion channels. The postsynaptic neuron sums al the action potentials it receives and generates its own action potential on it's own axon, if the voltage of the summed pulses is greater than the threshold of excitation.

The symmetric and asymmetric synapses have different shapes and neurotransmitters.

Carlson, p. 51

Neurotransmitter molecules are recycled back into the presynaptic site or destroyed by chemicals.
But sometimes, you have receptors in the presynaptic site. These are autoreceptors. The goal of autoreceptors is to modulate the production of neurotransmitters on the presynaptic side.

If there are too many vesicles, they'll be destroyed. If there are too few vesicles, the neuron won't talk.

All illustrations copied from
Foundations of Physiological Psychology,
by Neil R. Carlson.