QUESTIONS

1. Know the following areas on a neuron:
   
   a) Soma
   b) Axon
   c)  Dendrites
   d) End Bulb
   e) Axon Hillock
    
2. When an action potential is travelling down the axon & finally gets to the end bulb, little vesicles of neurotransmitters must be made to exocytose. Another cation is involved here & without this cation there can be no neurotransmitter release. What is the cation?
    
3. What is the synaptic problem that occurs in myasthenia gravis?
    
4. What is the synaptic problem in Botulism?
    
5. Same question for tick paralysis?
    
6. Explain Renshaw inhibition (hint:  it is a type of recurrent inhibition.)
   
   
   
   
    

ANSWERS

1. a) Soma = the cell body of the neuron
   
   b) Axon is the long fiber of the neuron transmitting info away from the cell body
   
   c) Dendrites are little branches coming off the soma transmitting info toward the cell body.
   
   d) The end bulb at the end of the axon & is where synapse with effector occurs
   
   e) Axon Hillock is the area where the axon comes off the cell body.
   
   
   
   
    
2. The cation needed for release of neurotransmitters is calcium.
   
   
   
   
    
3. There is a reduction in nicotinic receptors at muscle end plates in myasthenia gravis. ACH is released but can't bind to enough places. We treat w/cholinesterase inhibitors to prolong the action of the ACH that does manage to bind.
   
   
   
   
    
4. In Botulism the Clostridium spore casing blocks the release of ACH from presynaptic nerve terminals.
   
   
   
   
    
5. Tick venom inhibits choline acetylase which prevents ACH synthesis from occuring normally.  This occurs at the neuromuscular junction. It only takes one female engorged tick (this is not a dose related phenomenon).
   
   
   
   
    
6. Imagine an afferent fiber, and interneuron, & an efferent fiber.  The interneuron is inhibiting the efferent fiber.  Now imagine another fiber coming off the efferent fiber & inhibiting the interneuron. This is recurrent inhibition.  If the efferent fiber is a lower motor neuron, then this is Renshaw inhibition.  The interneuron is then said to be a "renshaw cell."  In strychnine poisoning, strychnine competes with glycine (an inhibitory neurotransmitter) thus undoing Renshaw inhibition.  No wonder you get seizures.  In tetanus, the tetanus toxin interferes w/the release of glycine & the same thing happens.