Lab 6 SomaticMotorNeuron

LAB 6 Somatic Motor Neuron Pathway

Upcoming Schedule

• Sun 9/22: Postlab 5 quiz due by 11:59 pm

• Tue 9/24: Prelab 6 Quiz due (Honors) at 10:00 am

• Wed 9/25: Prelab 6 Quiz due by 11:59 pm

• Thu 9/26: Lab 6

• Sun 9/29: Postlab 6 quiz due by 11:59 pm

Somatic Motor Neurons

• Overview: In Lab 6, the focus will be on the somatic motor neuron pathway, utilizing drugs/toxins/diseases to enhance understanding of the physiological regulation of this pathway.

• Neuronal Pathway:

  • Upper motor neuron in the CNS innervates lower motor neuron, which exits CNS at the spinal cord.

  • The lower motor neuron innervates skeletal muscle cell.

Action Potential Propagation

• Propagation begins with the action potential moving down the axon of the upper motor neuron.

• Voltage-Gated Sodium Channels: Critical for action potential propagation; they ensure the action potential moves in the correct direction (from cell body to terminal).

• At the upper motor neuron terminal, the action potential triggers voltage-gated calcium channels to open, allowing calcium influx.

  • This influx causes vesicles to fuse to the membrane and release glutamate into the synaptic space (via exocytosis).

  • Glutamate binds to receptors on the lower motor neuron (ligand-gated sodium channels), leading to depolarization of the lower motor neuron.

• Termination of the glutamate signal occurs through reuptake into the upper motor neuron.

Lower Motor Neuron Action Potential

• An action potential is triggered in the lower motor neuron and propagates down its axon via voltage-gated sodium channels.

• As the axon approaches the muscle, it divides into multiple terminals, forming a neuromuscular junction.

• At the nerve terminal, when the action potential reaches it, voltage-gated calcium channels open again, leading to:

  • Influx of calcium causing vesicles containing acetylcholine (Ach) to fuse with the membrane (exocytosis).

  • Ach diffuses across the cleft and binds to nicotinic acetylcholine receptors (nAChR), which are also ligand-gated sodium channels.

Muscle Contraction Initiation

• The opening of nAChR allows sodium influx, raising the muscle cell membrane potential to threshold, triggering the opening of voltage-gated sodium channels.

• This results in an action potential that propagates down the T-tubule, initiating muscle contraction.

• Signal Termination: The action of Ach is terminated by acetylcholinesterase (AchE), which cleaves acetylcholine in the neuromuscular junction, stopping its action.

Review Questions

1. Sequence the steps of the somatic motor neuron pathway, from action potential down the axon of the lower motor neuron to signal termination at the neuromuscular junction.

2. Describe how polio virus affects the motor neuron to muscle pathway, detailing normal and altered steps.

3. Identify the target inhibited by organophosphates and explain the resultant effects on muscle function.

Lab 5 Review

Concept Understanding

• This model illustrates:

  1. Conversion of chemical signals (neurotransmitter) to electrical signals (depolarization).

  2. Propagation of action potential down the axon via sequential opening of voltage-gated sodium channels.

Lab 5 Study Questions

• Cell Polarization at Rest: A cell has a negative resting membrane potential (RMP); it can depolarize (become more positive) or hyperpolarize (become more negative).

• Reason for Negative RMP: Mainly due to leaky potassium channels causing the efflux of potassium (positive charges).

• Depolarization Factors: Caused by sodium influx (open ligand-gated or voltage-gated channels).

• Repolarization: Occurs when the inactivation gate of voltage-gated sodium channels closes (stopping sodium influx) and voltage-gated potassium channels open (causing potassium efflux).

• Typical Threshold for Sodium Channels: The threshold is approximately -55 mV.

Voltage-Gated Sodium Channels

Voltage Sensor Location

• Located intracellularly to detect membrane potential changes via electrostatic repulsion (positive charges).

Importance of Two Gates

• Two gates are necessary:

  • Activation gate opens at potentials above threshold.

  • The second gate is needed for inactivation to stop sodium influx and allow repolarization.

Refractory Periods

• Absolute Refractory Period: Occurs when the inactivation gate is closed; no action potential can be fired.

• Relative Refractory Period: The channel is closed; an action potential can be triggered, but a larger stimulus is needed to reach threshold.

Converting Action Potential to Chemical Signal

• Sequence of events:

  • Action potential reaches axon terminal of presynaptic neuron.

  • Voltage-gated calcium channels open.

  • Vesicles containing neurotransmitters fuse to membrane, leading to exocytosis.

  • Neurotransmitter binds to receptors on the postsynaptic cell.

Action Potential Sequence in Neuronal Cell

1. Depolarization until threshold is reached (-55 mV).

2. Activation gates of voltage-gated sodium channels open; further depolarization occurs.

3. At +30 mV:

   • Inactivation gate of voltage-gated sodium channels closes (channel inactivated).

   • Voltage-gated potassium channels open.

4. Repolarization begins/Absolute refractory phase.

5. Hyperpolarization (due to slow closing of potassium channels) and Relative refractory period occurs.

6. Return to resting membrane potential (-70 mV).