BIO 2140 Exam 4 studying

Axon Diameter

• fast nerve

• Larger diameter axon provides less resistance to flow of ions

• Membrane reaches threshold faster so impulse travel faster

Degree of Myelination

• slow nerve

• Myelinated nerves AP’s are generated next to each other, one after another (this is called continuous conduction)

• Myelinated nerves AP’s occur only at node of Ranvier

• There are no Na+ channels under myelin

• The current flow under myelin from node to node, so nerve conduction impulses is faster (saltatory conduction)

Group A

• fastest neurons

• Somatic sensory + motor fibers serving

• In the skin, skeletal muscle, and joints

• Have larger diameter thick myelin sheaths

• Speed up to 150m/s or 300 mph

Group B

• autonomic nervous system sensory + motor fibers

• Small somatic sensory fibers

• Are medium diameter

• Lightly myelinated

• Speed of 40 mph

Multiple Sclerosis

• demyelination of your motor nerves

• Immune system makes antibodies to myelin → destruction of myelin sheaths → slow impulse conduction.

• Leakage + short-circuiting of electrical current

Eventually the impulse stops

Amyotrophic Lateral Sclerosis (ALS)

• means no muscle electrical current flow

• Lou Gehrigs disease, motor neuron disease

• Degeneration of motor nerves- sporadic 90-95% of cases- familial 5-10% cases

• Familial cases have mutation in gene for SOD1- no protection from free radicals (too many waste products)

Electrical to chemical signaling

• nerve impulses travel along motor neurons

• The end of the axon branches form a neuromuscular junction (NMJ) with a single muscle fiber

• NMJ consists of a motor nerve ending (terminal), the synaptic cleft, and at the motor end plate.

Nerve Terminal

• contains synaptic vesicles (sacs containing a neurotransmitter)

• A neurotransmitter is a chemical message (NT)

• At the NMJ the NT is the Acetylcholine (Ach)

Synaptic Cleft

The gap between the nerve terminal and sarcolemma

Motor end plate

• dimple in the sarcolemma

• Junctional folds of sarcolemma

• Many Ach receptors, called nicotonic acetylcholine receptors or nAchR.

Nicotonic acetylcholine receptors (nAchR)

Transmit chemical signal into electrical signal

1st step of the neuromuscular junction (NMJ)

Nerve impulse travels down axon

2nd step of the neuromuscular junction (NMJ)

Impulse reaches nerve terminal

3rd step of the neuromuscular junction (NMJ)

Voltage gated Ca²+ channels open

4th step of the neuromuscular junction (NMJ)

Ca²+ flows into nerve terminal

5th step of the neuromuscular junction ( NMJ)

Ca²+ fuses with the synaptic vesicles

6th step of the neuromuscular junction (NMJ)

Synaptic vesicles fuse with terminal membrane (presynaptic membrane)

7th step of the neuromuscular junction (NMJ)

Exocytosis of Ach into synaptic cleft

8th step of the neuromuscular junction (NMJ)

Ach diffuses across synaptic cleft

9th step of the neuromuscular junction (NMJ)

Ach attaches to nAch receptors on postsynaptic membrane

10th step of the neuromuscular junction (NMJ)

nAch receptors trigger depolarization of sarcolemma

11th step of the neuromuscular junction ( NMJ)

Depolarization spreads to T-tubules

12th step of the neuromuscular junction (NMJ)

Causes Ca²+ binds troponin…etc

How is signal terminated?

1. Decrease nerve impulses, but it’s slow

2. Acetylcholinesterase ( AchE) located in the synaptic cleft degrades Ach.

   • most rapid mechanism

   • Life time of Ach in synaptic cleft- 200 microseconds (.0002 seconds)

   • Destroys Ache very quickly