mod 7

1. Key Terms & Definitions

Drug Effects on Neurotransmission

• Agonist – A substance that mimics or enhances neurotransmitter action (e.g., nicotine for ACh).

• Antagonist – A substance that blocks neurotransmitter action (e.g., curare blocks ACh).

• Botulin Toxin – Blocks ACh release, leading to paralysis (used in Botox).

• Curare – Blocks nicotinic ACh receptors, leading to paralysis.

• Nicotine – ACh agonist at nicotinic receptors, leading to increased stimulation.

• Barbiturates – GABA agonists, cause sedation; can be deadly when combined with benzodiazepines.

• Benzodiazepines – GABA agonists, used for anxiety; enhance inhibitory effects.

• Anticonvulsants – Reduce seizure activity by enhancing GABA or blocking excitatory signals.

• Amphetamine – Increases dopamine & norepinephrine by blocking reuptake and stimulating release.

• Cocaine – Blocks dopamine reuptake, increasing dopamine effects in the brain.

Drugs Affecting Monoamines & Psychedelics

• Monoamine oxidase inhibitor (MAOI) – Prevents breakdown of serotonin, dopamine, norepinephrine, increasing their levels.

• Selective serotonin reuptake inhibitor (SSRI) – Blocks serotonin reuptake, increasing serotonin availability (e.g., Prozac).

• Psychedelics – Alter perception & consciousness (e.g., LSD, psilocybin).

• PCP (Phencyclidine) – Blocks NMDA receptors, mimicking schizophrenia-like symptoms.

• THC (Tetrahydrocannabinol) – Active ingredient in marijuana; binds cannabinoid receptors, altering mood & memory.

Opiates & Learning Mechanisms

• Opiate/Opioid – Pain-relieving drugs (e.g., morphine, heroin).

• Morphine – Natural opioid; strong painkiller.

• Heroin – Synthetic opioid; highly addictive, converts to morphine in the brain.

• Codeine – Milder opioid, used in cough medicine.

Aplysia & Learning

• Aplysia californica – A sea slug used to study learning & memory.

• Gill-siphon withdrawal reflex – Simple reflex used to study habituation & sensitization.

• Habituation – Reduced response to repeated stimulation.

• Sensitization – Increased response after a strong stimulus.

• Long-term potentiation (LTP) – Strengthening of synapses; basis of learning & memory.

• NMDA channel – Allows Ca²⁺ entry, crucial for LTP induction.

• LTP induction – Requires NMDA receptor activation & Ca²⁺ influx.

• LTP Maintenance – Strengthened synapse through AMPA receptor insertion.

2. Mnemonics for Memorization

A. Seven Stages of Neurotransmitter Action (Modified by Drugs)

"S-S-R-B-R-P-D"

1. Synthesis (drug can block neurotransmitter production).

2. Storage (drug can affect vesicle packaging).

3. Release (e.g., botulinum toxin blocks ACh release).

4. Binding (agonists or antagonists act here).

5. Reuptake (e.g., cocaine blocks dopamine reuptake).

6. Postsynaptic signaling (e.g., PCP blocks NMDA receptors).

7. Degradation (e.g., MAOIs block breakdown of monoamines).

B. Nicotine vs. Curare

"Same Target, Opposite Effects"

• Both act on nicotinic ACh receptors.

• Nicotine = agonist (activates).

• Curare = antagonist (blocks, causing paralysis).

C. Glutamate Hypothesis of Schizophrenia

"Less Glutamate, More Symptoms"

• Low glutamate causes cognitive & psychotic symptoms.

• PCP blocks NMDA receptors, mimicking schizophrenia.

3. Table: Effects of Common Drugs

4. Answers to the Questions

1. Name 7 stages of neurotransmitter action that can be modified by psychotropic drugs.

✅ Synthesis, Storage, Release, Binding, Reuptake, Post-synaptic effect, Degradation (Use S-S-R-B-R-P-D mnemonic).

2. How are nicotine and curare the same in action? How are they different?

✅ Same: Both act on nicotinic ACh receptors.
✅ Different: Nicotine is an agonist, while Curare is an antagonist (causes paralysis).

3. Why shouldn’t you take barbiturates and benzodiazepines at the same time?

✅ Both increase GABA activity, leading to dangerous CNS depression (slowed breathing, coma).

4. How does caffeine affect the nervous system?

✅ Blocks adenosine receptors, increasing alertness.

5. What is the glutamate hypothesis of schizophrenia? Why does PCP induce schizophrenic-like symptoms?

✅ Low glutamate activity → cognitive & psychotic symptoms.
✅ PCP blocks NMDA receptors, mimicking symptoms.

6. Name 2 effects of opioid drugs on the body.

✅ Pain relief, euphoria, respiratory depression.

7. Why is Aplysia a good model for studying learning & memory?

✅ Simple nervous system, easy to track neuronal changes in learning.

8. How many types of neurons are involved in habituation of the gill-siphon withdrawal reflex in Aplysia?

✅ Two (sensory & motor neurons).

9. How many types of neurons are involved in sensitization of the gill-siphon withdrawal reflex in Aplysia?

✅ Three (sensory, motor, interneuron).

10. Steps of Sensitization in the GSW Reflex

✅ Strong stimulus → interneuron releases serotonin → enhances sensory neuron response → stronger withdrawal reflex.

11. Extra Steps for Long-Term Facilitation in GSW Reflex

✅ Repeated sensitization → activates CREB → gene transcription → structural changes in synapse.

12. How is LTP induced?

✅ High-frequency stimulation → NMDA receptor activation → Ca²⁺ influx.

13. NMDA receptor’s role in inducing LTP

✅ Detects coincidence of presynaptic glutamate & postsynaptic depolarization.
✅ Allows Ca²⁺ entry, triggering LTP.

14. AMPA receptor’s role in maintaining LTP

✅ More AMPA receptors inserted into synapse, strengthening the signal.