WEEK 7 REVIEW

Explain the four key steps associated with neurotransmitter systems.

• Synthesis: Neurotransmitters (NTs) are synthesized in the presynaptic neuron. Small-molecule NTs are synthesized at the axon terminal, while peptides are synthesized in the soma and transported.

• Storage & Release: NTs are stored in vesicles and released when Ca²⁺ enters the presynaptic terminal in response to an action potential.

• Receptor Binding: NTs bind to receptors (ionotropic or metabotropic) on the postsynaptic cell, leading to changes in membrane potential.

• Termination: NTs are removed from the synaptic cleft via reuptake, enzymatic degradation, or diffusion to stop the signal.
  
  

What are the three main classes of neurotransmitters? Provide examples of each class.

• Amino Acids: Glutamate (excitatory), GABA (inhibitory), Glycine (inhibitory).

• Amines: Acetylcholine (ACh), Norepinephrine (NE), Dopamine (DA), Serotonin (5-HT).

• Peptides: Substance P (pain), Endorphins (pain relief), Oxytocin (bonding).
  
  

Define Dale’s Principle and explain its relevance to neurotransmitter release.

• Dale’s Principle: Initially stated that a neuron releases only one neurotransmitter.

• Modern View: Many neurons release co-transmitters (e.g., an amino acid/amine + a peptide). Some neurons violate Dale’s Principle, especially peptide-releasing neurons.
  
  

Outline the process of neurotransmitter synthesis and describe the enzymes involved.

• Amino Acid NTs: Synthesized from precursors via specific enzymes.

  • Glutamate → GABA (via glutamic acid decarboxylase, GAD).

• Amines: Synthesized from amino acid precursors.

  • Tyrosine hydroxylase (TH) converts tyrosine → L-DOPA → dopamine → norepinephrine.

• Acetylcholine (ACh): Synthesized from choline and acetyl-CoA by choline acetyltransferase (ChAT).

• Peptides: Synthesized in the soma, processed by ribosomes, and transported to terminals.
  
  

What are agonists and antagonists? Provide examples and explain their roles in modulating neurotransmitter systems.

• Agonists: Mimic or enhance neurotransmitter effects.

  • Nicotine (agonist at nicotinic ACh receptors).

  • Opioids (agonists of endorphin receptors).

• Antagonists: Block neurotransmitter effects.

  • Curare (blocks nicotinic ACh receptors, causing paralysis).

  • Atropine (blocks muscarinic ACh receptors).
    
    

Discuss the process of neurotransmitter reuptake and its importance in terminating synaptic transmission.

• Reuptake: NTs are taken back into the presynaptic neuron via transporters (e.g., serotonin transporter, SERT).

• Prevents prolonged signaling and recycles NTs.

• SSRIs (Selective Serotonin Reuptake Inhibitors) block reuptake to increase serotonin levels (e.g., Prozac).
  
  

Describe the role of acetylcholine (ACh) in the NMJ and its interaction with nicotinic receptors.

• ACh is released at the neuromuscular junction (NMJ) and binds to nicotinic ACh receptors (nAChRs).

• This causes Na⁺ influx, leading to muscle contraction.
  
  

Describe the structure and function of the NMJ.

• Structure:

  • Presynaptic motor neuron terminal (releases ACh).

  • Synaptic cleft (contains AChE to break down ACh).

  • Postsynaptic muscle fiber (has nAChRs).

• Function: Converts neural signals into muscle contraction via ACh release.
  
  

What is the role of AChE in terminating synaptic transmission at the NMJ?

• Acetylcholinesterase (AChE) breaks down ACh into choline and acetate, stopping the signal and allowing the muscle to relax.

• AChE inhibitors (e.g., sarin gas, nerve agents) prevent breakdown, leading to excessive muscle contraction (paralysis).
  
  

Describe the process of acetylcholine synthesis in presynaptic neurons, including the role of ChAT and acetyl-CoA.

Explain how the availability of choline affects acetylcholine synthesis, and how this process is regulated in the presynaptic terminal.

How does the reversal potential of nAChR relate to the direction of ion flow when acetylcholine binds to the receptor? Explain what happens when the membrane potential is more negative or positive than the reversal potential.