# Neurotransmitters

Psychology I · Behavioral Biology · https://tryals.app/learn/psychology-i/neurotransmitters

## The Brain's Chemical Messengers

Different neurotransmitters specialize in distinct jobs to keep your mind and body running.

**Acetylcholine (ACh)** activates skeletal muscle and supports memory; its loss is linked to Alzheimer's disease. **Dopamine** drives reward and motivation. Too little in the substantia nigra causes Parkinson's disease, while excess triggers schizophrenia symptoms.

**Serotonin** regulates mood, sleep, and appetite, and is targeted by SSRIs for depression. **Norepinephrine** promotes arousal and alertness for the fight-or-flight response.

## Excitatory vs Inhibitory Traffic

**Glutamate** is the main **excitatory** transmitter essential for learning. **GABA** is the main **inhibitory** transmitter that dampens neural excitability. **Endorphins** act as natural opioid painkillers.

| Term | Effect on Receptor | Example |
| --- | --- | --- |
| **Agonist** | Mimics or enhances effect | Nicotine mimics ACh |
| **Antagonist** | Blocks or reduces effect | Curare blocks ACh |

**Pitfall:** Never assume an **antagonist** does nothing. Blocking a receptor has dramatic effects, like naloxone reversing an overdose.

## Practice questions

5 of this lesson's 12 practice questions, with answers. The full set is in the app.

### 1. GABA is the brain's main inhibitory transmitter, so it DECREASES excitability. Why does the brain need a dedicated brake?

A. Because excitatory transmitters would otherwise be depleted
B. Because unchecked excitation runs away without active inhibition
C. Because inhibition is needed to conserve the brain's energy supply
D. Because inhibition is how memories are erased

**Answer:** B. Because unchecked excitation runs away without active inhibition

**Why:** Excitation alone is unstable. Benzodiazepines enhance GABA and calm; GABA antagonists convulse, the brake is as load-bearing as the accelerator.

Page: https://tryals.app/practice/psychology-i/neurotransmitters/gaba-is-the-brains-main-inhibitory-transmitter-so-it-decreases

### 2. An SSRI blocks the transporter that pulls serotonin back into the presynaptic terminal. It does not make any neuron release a single extra molecule of serotonin. Why does blocking reuptake nevertheless increase serotonin signalling at the synapse?

A. Because reuptake is how serotonin is cleared from the cleft.
B. Because blocked transporters are recycled into receptors.
C. Because the drug carries serotonin of its own.
D. Because the transporter normally suppresses release.

**Answer:** A. Because reuptake is how serotonin is cleared from the cleft.

**Why:** Cleft concentration is set by what arrives and what leaves; the drug does nothing to the first and everything to the second, so the same release produces more binding for longer. Cocaine does this to dopamine, a large share of psychoactive drugs act on clearance rather than on release.

Page: https://tryals.app/practice/psychology-i/neurotransmitters/an-ssri-blocks-the-transporter-that-pulls-serotonin-back-into-the

### 3. Parkinson's disease is a shortage of dopamine, yet patients are given **L-DOPA** rather than dopamine itself. Why prescribe the precursor?

A. Because dopamine cannot cross the blood-brain barrier and L-DOPA can
B. Because dopamine breaks down too quickly to be manufactured as a drug
C. Because L-DOPA treats the cause while dopamine would only mask symptoms
D. Because L-DOPA is more potent than dopamine at the same receptors

**Answer:** A. Because dopamine cannot cross the blood-brain barrier and L-DOPA can

**Why:** The barrier decides the prescription. Dopamine is exactly what is missing and cannot get in; L-DOPA is carried across and converted on arrival. Half of neuropharmacology is this problem, the right molecule is useless if it cannot reach the tissue, so drugs are designed around the door as much as the lock.

Page: https://tryals.app/practice/psychology-i/neurotransmitters/parkinsons-disease-is-a-shortage-of-dopamine-yet-patients-are-given

### 4. Because naloxone only blocks opioid receptors and never activates them, giving it to a patient in an opioid overdose should have no meaningful effect.

**Answer:** False

**Why:** False. An antagonist has a powerful effect precisely by removing the opioid's action - naloxone can reverse life-threatening respiratory depression within seconds. Equating 'does not activate the receptor' with 'no effect' is the classic antagonist pitfall.

Page: https://tryals.app/practice/psychology-i/neurotransmitters/because-naloxone-only-blocks-opioid-receptors-and-never-activates

### 5. Sort each drug action as an agonist (enhances the transmitter's effect) or an antagonist (reduces it).

**Answer:**

- Agonist: Nicotine binds and activates ACh receptors, An SSRI blocks serotonin reuptake, leaving more serotonin in the cleft, A drug that mimics GABA and opens its channel
- Antagonist: Curare occupies ACh receptors without activating them, causing paralysis, Naloxone occupies opioid receptors and blocks endorphins

**Why:** Agonists enhance a transmitter's effect - directly (nicotine, GABA-mimic) or indirectly (an SSRI blocks reuptake, boosting serotonin). Antagonists occupy the receptor without activating it (curare, naloxone). The SSRI is the classic trap: 'blocks' a process yet ENHANCES the transmitter, so it is an agonist.

Page: https://tryals.app/practice/psychology-i/neurotransmitters/sort-each-drug-action-as-an-agonist-enhances-the-transmitters