(5) neural communication II & drug properties (midterm 1)

Question 1

What are the two basic types of receptors? Why have both?

Answer 1

ionotropic (channels):

• AKA ligand-gated ion channels
• excitatory (depolarise)
• inhibitory (hyperpolarise)
• fast, transient effect

metabotropic (signalling proteins):

• AKA g-protein-coupled receptors
• modulate cell & signals
• slow, longer lasting effect
• causes signal cascades

Question 2

What is the relationship between receptor location and its function?

Answer 2

• postsynaptic: typically dendrite w/ receptors
• presynaptic: releases NTs
  1. autoreceptors
  2. heteroceptors

Question 3

What are autoreceptors?

Answer 3

receptors that bind to same NT being released from neuron

• negative feedback mechanism
  
  • inhibit axon when enough NTs released
  • ensure presynaptic axon isn’t releasing more NT than needed
• found on edges of synapse

Question 4

What are heteroreceptors?

Answer 4

receptors that bind to different NTs not part of synapse

• found on edges of synapse
• suggests another synapse/axon is releasing NTs
• volume signal: turn up/down (modify) a signal, causing more/less NT to be released on subsequent APs

Question 5

What are the 3 types of NT clean-up?

Answer 5

Diffusion: float out into extracellular space

Enzymatic degradation: enzymes break down NT into molecules that will no longer activate receptors

Re-uptake: transporters bring NTs back
- pre-synaptic: back to neurons
- astrocytes: back to astrocytes, then back to vessicles

Question 6

What are the major groups of NTs and some examples within each group?

Answer 6

1. Agonist: drug that increases function of NT system
2. Antagonist: drug that decreases function of NT system
3. Other - e.g.
   
   • transporter blocker/reuptake inhibitor (prevent reuptake of NT)
   • enzyme inhibitor (prevent degradation of NT)

Question 7

What are the two primary types of drug action?

Answer 7

1. Agonists: activate NT receptor
2. Antagonists: block NT receptor
   
   • competitive: binds to same location as NT, blocks activity of receptor
   • noncompetitive: binds somewhere else on receptor & causes receptor to fail to be activated
3. Partial agonists/antagonists: have lowered ability to activate receptor
4. Allosteric regulators: no effect on its own, influence effects of NT
   
   • positive modulators: increases ability for NT to activate receptor
   • negative modulator: decreases ability for NT to activate receptor

Question 8

What is the role of glutamate?

Answer 8

• primary excitatory NT
• used thruout brain
• ionotropic: AMPAR (AMPA receptor), NMDAR (NMDA receptor), Kainate receptor
• metabotropic: mGluR (metabotropic glutamate receptor)
• not great target for drugs: can’t target specific system in brain

Question 9

What is the role of GABA?

Answer 9

• aka gamma-Aminobutyric acid
• primary inhibitory NT
• used thruout brain
• ionotropic & metabotropic
• not great target for drugs

Question 10

What are GABA agonists?

Answer 10

Similar to glutamate antagonists

- Benzodiazepines
- Ethanol
- Chloroform
- Ether

Question 11

What is the role of norepinephrine?

Answer 11

• originates in locus coeruleus
• released when startled, stressed
• causes heterosynaptic facilitation
• enhancement of memory by stress/emotion
• evolutionary useful

Question 12

What is heterosynaptic facilitation?

Answer 12

binds to heteroreceptors & increases subsequent release from other synapses

Question 13

What is propranolol?

Answer 13

norepinephrine/noradrenergic receptor antagonist

• beta-blockers
• affects brain & heart
• potential PTSD treatment via reconsolidation
  
  • reconsolidation: take memory from long term to working
  • decrease emotional response to traumatic event

Question 14

What are glutamate antagonists?

Answer 14

• Barbiturates
• Nitrous oxide
• Ketamine
• Ethanol