jeopardy/

questions to know as well

classic NT

made in terminal cytoplasm THEN put into vesicles 

peptide neurotransmitters

made in cell body and directly put in vesicles, THEN travel down to terminal 

Which receptor(s) are mainly responsible for LTP?

AMPA and NMDA

What is the correct pathway of a GProtein Coupled Receptor?

Receptor -> G-protein -> Effector (adenylyl cyclase) -> 2nd messenger (cAMP) -> protein kinase (PKA) -> phosphorylation target 

Mnemonic: RGE2>PK>P TARGET

Voltage-clamp studies of ACh receptors producing EPCs demonstrated what?

The reversal potential of those receptors were not set at a specific equilibrium potential of any ion there the channels are permeable to more than one type of ion species. 

What kind of receptors are opioid receptors?

Metabotropic (inhibitory) 

What is the difference between classic neurotransmitters and peptide neurotransmitters?

Peptide = made in cell body and directly put in vesicles, THEN travel down to terminal 

Classic = made in terminal cytoplasm THEN put into vesicles 

How does habituation work?

As the mantle is repeatedly shocked, action potentials decrease which causes less calcium to enter the presynaptic cells. This results in less neurotransmitter release thus less depolarization of the postsynaptic membrane. 

What is sensitization? 

Shock a different part of the body like the tail causes future, innocuous stimulus to the mantle to elicit a very strong gill-siphon withdrawal.

What activates the alpha subunit in a g-protein?

GTP

What breaks down cAMP?

phosphodiesterase

Name a step in the GPCR pathway that causes amplification? 

Activating g-proteins, activating cAMP, PKA phosphorylating targets 

What kind of receptors utilize metabotropic signaling?

G-protein coupled receptor 

What kind of ion channel are Ionotropic receptors? 

Ligand-gated ion channels

Which direction do IPSPs drive the membrane potential?

Below the action potential threshold potential

What happened to the reversal potential of an ACh receptor when external Na+ was lowered?

The reversal potential decreased 

Input A into a neuron is excitatory, while Input B is inhibitory. Both are on the same dendrite but B is closer to the cell body than A. Is the neuron more or less likely to fire an action potential if both A and B fire at the same time?

less likely

Voltage-clamp studies of ACh receptors producing EPCs demonstrated what?

The reversal potential of those receptors were not set at a specific equilibrium potential of any ion there the channels are permeable to more than one type of ion species. 

Chlorpromazine is a drug used to treat schizophrenia symptoms by occupying the dopamine site on D2 receptors. Does this mean schizophrenia is due to too little to too much dopamine?

too much

What are the four types of stimulants? Give an example of each

Behavioral stimulants = cocaine and amphetamine 

Convulsants = strychnine 

General stimulants = caffeine 

Psychoactive drugs = LSD, THC 

What does Botulin Toxin do? How does it do this?

the toxin itself paralyzes. Prevents release of ACh by blocking interaction between the synaptic vesicles and the cell membrane that leads to ACh release. 

What is an agonist? 

What is an antagonists?

Agonists increase effectiveness of a given neurotransmitter 

Antagonists decrease effectiveness of a given neurotransmitter 

What kind of postsynaptic potential would be generated if glutamate was released onto a glutamate receptor?

Excitatory Postsynaptic Potential (EPSP)

What did Otto Loewi discover during his frog heart experiment? 

When the vagus nerve of one frog heart is stimulated, the heart rate of both that heart and a separate heart would slow. Chemical messengers (ACh) would be released from heart 1 and affect heart 2. 

starting materials of Ach (Acetycholine)

acetate + choline, choline acetyltransferase puts them together

breakdown enzyme + vesicular transporter

Vesicular ACh Transporter moves it into vesicles 

Acetylcholine Esterase breaks it up 

Which neurotransmitter is found in the locus coeruleus? 

norepinephrine

Four Stages of Neurotransmitter Function…(SSRI)

• S: Synthesis – Neurotransmitters are made (in the terminal or soma).

• S: Storage – Packaged into synaptic vesicles.

• R: Release – Ca²⁺ influx triggers vesicle fusion and neurotransmitter release.

• I: Inactivation – Neurotransmitters are removed or broken down.

Small vs. Peptide Neurotransmitters

Small: Synthesized at the terminal, stored in small vesicles, fast action.

Peptide: Synthesized in the cell body, transported in large vesicles, slower action.

EPSP vs. IPSP

"Na⁺ for excites, K⁺ or Cl⁻ for inhibits"**

• If a channel lets Na⁺ in, the cell is more likely to reach threshold (EPSP).

• If a channel lets K⁺ out or Cl⁻ in, the cell hyperpolarizes (IPSP).

The presence of which ion inside the presynaptic cell is important for neurotransmitter release?

• Calcium (Ca²⁺) influx triggers vesicle fusion with the membrane.

Name 2 differences in synthesis and storage of small-molecule neurotransmitters vs. peptide neurotransmitters.

• Small-molecule are synthesized in the axon terminal and stored in small vesicles; peptides are synthesized in the cell body and stored in large dense-core vesicles.

What happens if acetylcholine is dumped on an acetylcholine-gated sodium channel? What if dopamine is dumped on that channel?

• ACh on an ACh-gated Na⁺ channel → channel opens, Na⁺ flows in → EPSP.

• Dopamine on the same channel → no effect, because the channel is specific to ACh.

4 ways that a neurotransmitter’s action can be terminated. (ERDU)

• Enzymatic breakdown (e.g., AChE for ACh)

• Reuptake into presynaptic terminal (e.g., via transporters)

• Diffusion away from the synaptic cleft

• Uptake by glial cells (especially for glutamate, GABA)

How does the reversal potential of the ACh receptor at the neuromuscular junction show that these channels are permeable to more than one ion?

The reversal potential is between the equilibrium potentials for Na⁺ and K⁺, indicating both ions flow through the receptor.

Sodium’s reversal potential is higher than the threshold potential in most neurons. So a PSP caused by opening sodium channels is excitatory or inhibitory?

• Excitatory (EPSP), because Na⁺ flows in, depolarizing the cell toward threshold.

Potassium’s reversal potential is lower than the threshold potential in most neurons. So a PSP caused by opening potassium channels is excitatory or inhibitory?

• Inhibitory (IPSP), because K⁺ flows out, hyperpolarizing the cell away from threshold

Major Neurotransmitters

• Glutamate – Major excitatory neurotransmitter in the CNS.

• GABA – Major inhibitory neurotransmitter in the CNS.

• Glycine – Another inhibitory neurotransmitter, mainly in spinal cord.

Glutamate Receptors

• AMPA receptor – Fast ionotropic receptor for glutamate.

• NMDA receptor – Ionotropic glutamate receptor involved in LTP (learning & memory); requires Mg²⁺ removal for activation.

1. What is the difference between synaptic and endocrine signaling?

• Synaptic → Local, fast, neurotransmitters act on specific receptors.

• Endocrine → Systemic, slow, hormones travel via blood.

2. Is GTP associated with active or inactive G-proteins? What about GDP?

• GTP = Active

• GDP = Inactive

Correct Order of a Typical Signaling Pathway

✅ b → e → c → a → d

• (b) Neurotransmitter binds to metabotropic receptor.

• (e) G-protein activated.

• (c) Adenylyl cyclase activated.

• (a) cAMP generated.

• (d) PKA phosphorylates target.

4. Difference Between Phosphorylation & Transcription Factor Activation

• Phosphorylation → Short-term, modifies existing proteins (e.g., ion channels).

• Transcription factors → Long-term, alters gene expression (e.g., CREB activation)

5. Does adding acetylcholinesterase increase or decrease ACh action?

• Decrease, because AChE breaks down ACh in the synapse.

6. Does amphetamine increase or decrease dopamine’s effects?

• Increase, by blocking dopamine reuptake, prolonging its effect.

7. Neurotransmitter deficit in Parkinson’s disease & treatment?

• Dopamine deficit.

• Treatment → L-DOPA (converted to dopamine in the brain).

8. Why did early schizophrenia drugs cause Parkinson’s-like symptoms?

• They blocked dopamine receptors, reducing dopamine action (like in Parkinson’s).

A. Seven Stages of Neurotransmitter Action (Modified by Drugs) "S-S-R-B-R-P-D"

• Synthesis (drug can block neurotransmitter production).

• Storage (drug can affect vesicle packaging).

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

• Binding (agonists or antagonists act here).

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

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

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

C. Glutamate Hypothesis of Schizophrenia "Less Glutamate, More Symptoms"

• Low glutamate causes cognitive & psychotic symptoms.

• PCP blocks NMDA receptors, mimicking schizophrenia.

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).

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).

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.