The main neurotransmitters !

Table to know
Exam priority: medium

Neurons talk with a small set of chemicals; each one has its own jobs, its source nuclei and the diseases that follow when it fails.

Updated 2026-11-01

Also called: Neuromodulators, Neuropeptides

Key points

Glutamate acts on AMPA and NMDA receptors; NMDA needs glycine as co-agonist and depolarization to expel its Mg²⁺ plug. Excess glutamate kills neurons (excitotoxicity) in stroke and seizures.
GABA_A is a Cl⁻ channel and the site of action of benzodiazepines, barbiturates and alcohol; GABA_B is a G protein receptor.
Glycine inhibits in the cord and brainstem; tetanus toxin and strychnine block it, causing spasms.
Source nuclei: dopamine – substantia nigra and ventral tegmental area; norepinephrine – locus coeruleus; serotonin – raphe; acetylcholine – nucleus basalis of Meynert; histamine – tuberomammillary nucleus.
Alzheimer disease: early loss of cholinergic neurons of the nucleus basalis; Parkinson disease: loss of nigral dopamine.
Synthesis: dopamine and norepinephrine from tyrosine (tyrosine hydroxylase is rate-limiting); serotonin from tryptophan; GABA from glutamate by glutamate decarboxylase (needs vitamin B6).

What it is

Small-molecule transmitters (acetylcholine, amines, amino acids) are made in the terminal and act fast; neuropeptides are made in the cell body, released in small amounts and act slowly and for longer. Glutamate is the main excitatory transmitter of the brain, GABA the main inhibitory one and glycine the inhibitory one of the spinal cord and brainstem. The monoamines (dopamine, norepinephrine, serotonin, histamine) come from small brainstem and hypothalamic nuclei that project widely and set arousal, mood and motivation.

Transmitters, sources and receptors

Transmitter	Main source	Receptors	Role and disorders
Glutamate	Widespread (cortex, hippocampus)	AMPA, NMDA, kainate, mGluR	Excitation, memory (LTP); excitotoxicity in stroke
GABA	Interneurons, striatum, cerebellar Purkinje cells	GABA_A (Cl⁻), GABA_B	Inhibition; too little favours seizures
Glycine	Cord and brainstem interneurons	Glycine receptor (Cl⁻)	Inhibition; blocked by tetanus toxin and strychnine
Acetylcholine	Nucleus basalis, motor and autonomic neurons	Nicotinic, muscarinic	Attention, memory, muscle; lost early in Alzheimer disease
Dopamine	Substantia nigra, ventral tegmental area, hypothalamus	D1–D5	Movement, reward; inhibits prolactin; lost in Parkinson disease
Norepinephrine	Locus coeruleus, sympathetic postganglionic neurons	α, β	Arousal, attention; implicated in depression
Serotonin	Raphe nuclei	5-HT1 to 5-HT7	Mood, sleep, appetite, pain modulation
Histamine	Tuberomammillary nucleus (hypothalamus)	H1–H3	Wakefulness; first-generation antihistamines sedate
Neuropeptides (substance P, enkephalins, endorphins)	Dorsal horn, hypothalamus, periaqueductal gray	NK1; μ, δ, κ opioid	Pain transmission and its modulation

Clinical notes

Tetanus (Clostridium tetani toxin) blocks glycine and GABA release in the cord: trismus, opisthotonus, painful spasms.
Alcohol or benzodiazepine withdrawal leaves glutamate unopposed: tremor, agitation and seizures.
Antipsychotics that block D2 receptors cause parkinsonism (striatum) and high prolactin (pituitary).

Test yourself

Think of the answer, then tap the question to see it.

Why does the NMDA receptor act as a coincidence detector in memory formation?

It opens only when glutamate is bound and the membrane is already depolarized enough to expel its Mg²⁺ plug. Then Ca²⁺ enters and triggers long-term potentiation.

Why do D2-blocking drugs raise prolactin?

Hypothalamic dopamine reaches the pituitary through portal blood and inhibits lactotrophs through D2 receptors. Blocking them removes the brake, so prolactin rises (galactorrhea, amenorrhea).

Benzodiazepines and alcohol both enhance GABA. Why is stopping them suddenly dangerous?

Chronic use reduces GABA_A function and increases glutamate signalling. Abrupt withdrawal leaves excitation unopposed, causing tremor, agitation and seizures.

Why do first-generation antihistamines cause drowsiness?

They cross the blood–brain barrier and block H1 receptors of the tuberomammillary histamine neurons, which keep the cortex awake.

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 12.5 Communication Between Neurons (OpenStax (Rice University), 2022); Parkinson Disease (StatPearls (NCBI Bookshelf), 2023); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 46). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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