This Module covers:

• Synaptic Transmission
• Muscles: Anatomy, Contraction Physiology, Excitation of, Actin & Myosin
• Halteres

 

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Synaptic Transmission (Chemical Synapses) & the role of Ca++

In order for one neuron to communicate with another at a chemical synapse (the most common type of synapse), neurotransmitter must be released from one cell and bind to receptors on another cell. Therefore, synaptic transmission is very important.

Neurotransmitter release is directly dependent on a few crucial changes occuring in the axon terminal or synaptic region of the presynaptic neuron:

1. depolarization
2. influx of Ca++

These two requirements are interdependent. It is the depolarization that opens voltage-gated channels in the axon terminal and this allows Ca++ to flow in down its concentration gradient. It is the Ca++ that causes the synaptic vesicles to exocytose their contents (i.e., release neurotransmitter into the synapse). In this manner, the release of neurotransmitter is graded relative to the amount of depolarization that the axon terminal experiences AND the amount of Ca++ that comes into the axon term. Synaptic transmission is graded. In neurons that use an AP to trigger the release of neurotransmitter, higher frequency APs trigger a large of amount of neurotransmitter to be released, whereas lower frequency APs trigger a smaller amount of neurotransmitter to be released. It's all related to the level of depolarization and the related influx of Ca++. It is very important that you understand this connection because it is the basis for how learning and memory are thought to occurr. We will discuss this later in the quarter.

The depolarization of the axon terminal is usually only triggered by an AP. This is because the axon terminal in most neurons lies so far away from the stimulus initiation site that a simple graded EPSP or receptor potential would die out ong before it reached the axon terminal. However, in some neurons where the axon terminal is not so far away and the neuron's passive electrical properties are such that an EPSP or receptor potential can travel to the terminal without significant degradation, then a simple EPSP or receptor potential can trigger neurotransmitter release without the propagation of an AP. All that matters is that the axon terminal be depolarized enough to open voltage-gated Ca++ channels. It doesn't matter what causes the depol.

Neurons in which a graded potential can propagate with less degradation are said to have a very large "space constant". This is a calculated # that is related to the membrane being not very leaky to charge (hi Membrane Resistance) and the cytoplasm being a good conductor (low Internal Resistance). An example of this is seen in the nematode Ascaris, which does not use APs but still communicates across a chemical synapse by relying on a simple EPSP or receptor potential to trigger neurotransmitter release instead of an AP.

A small note for understanding experimental procedures:
Certain questions that neurobiologists need answered involves examining synapses and what happens if you block communication across a particular synapse. This can be achieved experimentally by removing all the Ca++ out of the neuron's external medium and replacing it with Mg++.
since neurotransmitter release is directly related to the influx of Ca++ into the axon terminal, if you remove Ca++ from the external environment, then you won't get any neurotransmitter release even though the AP or EPSP/receptor potential has depolarized the terminal.

Mg++ is very similar to Ca++, both are divalent cations and are about the same size. BUT Mg++ influx does not trigger neurotransmitter release. So if you replace the ext. medium of a neuron with Mg++ and no Ca++ then you block that synapse. Now you can see what downstream effects blocking the synapse has and maybe even see a behavioral effect.

Notice: Mg++ is not normally used in synaptic transmission, it is only used experimentally to block a synapse.

 

 

Muscle Anatomy & Contraction Physiology

Instead of writing my own description of muscles and muscle contraction physiology, I've searched the web and found a few really excellent sites that were written by muscle experts. This sites do a much better job than I would have in describing the anatomy and excitation-contraction coupling mechanisms.

Please check out the sites I've linked to below. They are short, well written, have excellent diagrams and pictures, and present material that is appropriate to the level of this course.

• An introduction to muscles
  
  
• Muscle Anatomy: the breakdown from the whole anatomical muscle to the muscle fibers and their myofibrils (great diagrams!)
  
  
• Excitation-Contraction Coupling Mechanisms: how a motor axon triggers contraction in a muscle, includes figures of muscle fibers and their associated t-tubules and sarcoplasmic reticulum.
  
  
• Molecular Components of Contraction: Actin and myosin: what they are, where they are inside a muscle fiber, and how they work.
  Visit this other page for a photograph of an actual skeletal muscle stretched and contracted so you can see the changes that take place in the sarcomeres--how actin and myosin work together to contract a muscle.
  
  
• Length-Tension Relationship of Muscles: a Fundamental property of all muscles, helps in the understanding of how the crayfish controls its muscles and the asynchronous flight muscles in insects.

 

 

 

Halteres: the flight stabilizers for the Dipterans See Syllabus p. 46

Remember halteres are only found in dipterans.

The insect in the picture below does not have halteres. How do I know this? How many pairs of wings does it have? If it has more than 1 pair then it must not have halteres, becuase halteres are only found in insects that have a reduced 2nd pair of wings that have evolved into sense organs that detect changes in the insect's orientation = halteres.

Halteres are sensory structures that detect a change in the orientation of an insect in flight. The halteres can detect a change in orientation in the lift, pitch and yaw planes (see diagram below). When the halteres detect a change they trigger motor neurons to correct for the change and thus stabilize the insect while in flight.

Halteres have mechanoreceptors to detect the change in orientation.