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The system you already have, mapped.

You have an endocannabinoid system whether or not you ever meet the plant. This is where it is.

what is acting

Assembling the body…

Which targets to draw

nothing added

Your own system

Nothing added. This is where the receptors and enzymes are in a body that has taken nothing at all — the system you have whether or not you ever meet the plant.

how good is the evidence

Percentages are shares of what is currently drawn, by weight — turn the weaker two off and what remains is what is actually settled.

look at one place

This map says where things act. It does not say what to take, how much, or for what — those are questions for a clinician who can see you.

Nothing here draws a body. Points are placed where receptors and enzymes are expressed, as densely as they are expressed there — and a human shape appears because that is where the system is. The colour says which target; the density says how much; and the blur says how certain anyone actually is.

How to read the figure

Blur is not a style. It is the confidence interval.

Density is expression

A region with twice the receptor rank gets twice the points. The brightest places are the places the system genuinely concentrates — and the dark places are as informative.

Sharpness is certainty

An established finding sits within millimetres of its anatomical home. A single-study, non-human one is scattered across a neighbourhood, because that is how well it is actually located.

Confidence flows downhill

A rock-solid receptor map acted on by a weak finding is drawn as the weak finding. Strong anatomy is never allowed to launder a thin claim — which is the usual way these pictures mislead.

Two things worth trying

Select CBD and watch the gold stay dark. Nearly everyone believes cannabidiol works at the cannabinoid receptor; its affinity there is very low, and the map shows you where it actually goes instead.

Then find the brainstem — the notch at the top of the spine that never lights up for THC. That is where breathing is controlled, and CB1 is scarce there. It is why cannabis does not suppress respiration the way opioids do. It is not a claim that cannabis is harmless; the harms are real, and they are elsewhere.

The whole map, in writing

Every point in the figure comes from one of the rows below, and every row carries the source it rests on and the weight that source can bear. Read it instead of the figure if you prefer — it is the same map, and it is the version that works without a graphics card.

Where the system is, region by region

Ordered by how much of the system sits there. “Rank” is ordinal — how prominent a target is here relative to where it is most prominent — and deliberately not a concentration, because the underlying measurements are not in comparable units.

Cerebral cortex

The outer sheet of the brain, where deliberate thought, perception and judgement are organised.

  • CB1 receptorrank 0.80human · autoradiographyWidespread across the cortex, heaviest in frontal regions — judgement, planning and the sense of time.
  • FAAHrank 0.80human · immunohistochemistryFAAH is abundant on the receiving side of the synapse, destroying anandamide within seconds of its release.
  • MAGLrank 0.80human · immunohistochemistryMAGL sits on the *sending* side, which is the elegant part: 2-AG travels backwards across the synapse and is destroyed at the terminal it was aimed at.
  • 5-HT1A receptorrank 0.70human · autoradiographyWidespread cortical expression.
  • CB2 receptorrank 0.12rodent · mrnaSparse, largely on microglia rather than neurons, and rising under inflammation.

Hippocampus

A pair of curved structures deep in the temporal lobes, central to laying down new memories.

  • CB1 receptorrank 0.90human · autoradiographyHigh density, and the direct explanation for the effect on forming new memories while intoxicated.
  • 5-HT1A receptorrank 0.80human · autoradiographyHigh density. This receptor is on the map because cannabidiol acts at it, not because it belongs to the cannabinoid system.
  • FAAHrank 0.80human · immunohistochemistryHigh, matching the density of the signalling it terminates.
  • MAGLrank 0.70human · immunohistochemistryHigh.

Cerebellum

The dense structure at the back and base of the brain, coordinating movement and balance.

  • CB1 receptorrank 0.90human · autoradiographyVery high density. Coordination and timing are cerebellar functions, and both are measurably affected.
  • MAGLrank 0.80human · immunohistochemistryHigh, alongside the CB1 it regulates.
  • FAAHrank 0.70human · immunohistochemistryHigh in the cerebellum.

Gut and enteric nervous system

The digestive tract and its own nerve net — enough neurons to be called a second brain, and it behaves like one.

  • CB2 receptorrank 0.50human · immunohistochemistryOn gut immune tissue, and upregulated where there is inflammation.
  • CB1 receptorrank 0.40human · immunohistochemistryOn enteric neurons, slowing motility — the same mechanism behind both the appetite change and the constipation.
  • TRPV1 channelrank 0.40human · immunohistochemistryOn gut sensory fibres, relevant to visceral pain.
  • FAAHrank 0.40human · mrnaPresent in the gut wall.

Liver

The body's chemical works: most of what is swallowed is processed here before it reaches the rest of you.

  • FAAHrank 0.60human · mrnaSubstantial — the liver clears endocannabinoids as it clears much else.
  • MAGLrank 0.40human · mrnaModerate.
  • CB1 receptorrank 0.20human · mrnaLow but functionally real, with a role in lipid handling.
  • CB2 receptorrank 0.20human · mrnaLow at rest and rising with injury: this receptor turns up where there is damage.

Peripheral nerves

The nerves running out to the limbs and organs — where sensation arrives and movement leaves.

  • TRPV1 channelrank 0.90human · immunohistochemistryDense on sensory nerve endings. This is the channel that answers to chilli heat, and anandamide acts at it too.
  • CB1 receptorrank 0.35human · immunohistochemistryOn peripheral nerve terminals, which is part of why effects are not purely central.

Amygdala

Paired almond-shaped nuclei involved in threat appraisal and emotional salience.

  • CB1 receptorrank 0.60human · autoradiographyModerate density in the threat-appraisal circuitry. Relevant to why the same dose can calm one person and frighten another.
  • 5-HT1A receptorrank 0.60human · autoradiographyPresent in the threat circuitry, and the most plausible route for an anxiolytic effect that does not go through CB1 at all.

Skin

The largest organ, and the boundary — nerve endings, immune cells and glands all in one sheet.

  • TRPV1 channelrank 0.60human · immunohistochemistryIn the skin's sensory endings and keratinocytes.
  • CB2 receptorrank 0.35human · immunohistochemistryOn skin immune cells, which is the basis of most topical claims — and the reason those claims are about the skin rather than the whole body.
  • CB1 receptorrank 0.25human · immunohistochemistryIn nerve fibres, glands and keratinocytes. The largest organ is not exempt from the system.

Spinal cord

The main cable between brain and body, and the first place pain signals are gated.

  • TRPV1 channelrank 0.70human · immunohistochemistryOn incoming pain fibres at the dorsal horn.
  • CB1 receptorrank 0.40human · autoradiographyPresent in the dorsal horn, where incoming pain signals are first gated.

Basal ganglia

Deep nuclei — including the globus pallidus and substantia nigra — that shape movement and habit.

  • CB1 receptorrank 1.00human · autoradiographyThe densest CB1 territory in the brain — globus pallidus and substantia nigra especially, which is why movement is among the first things cannabis alters.

Spleen

An immune organ behind the stomach, dense with the white cells that patrol the blood.

  • CB2 receptorrank 1.00human · mrnaThe densest CB2 tissue. The receptor was found by looking in the periphery precisely because it is so abundant here.

Brainstem

The stalk joining brain to spinal cord. It runs breathing and heart rate without asking.

  • 5-HT1A receptorrank 0.70human · autoradiographyDense in the raphe nuclei, the brainstem's own serotonin source — one of the few places on this map where the brainstem is bright.
  • CB2 receptorrank 0.15rodent · functionalCB2 in the brain was denied for years and is now accepted, chiefly on microglia. How much is there, and when, is still argued — so it is drawn as the uncertain thing it is.
  • CB1 receptorrank 0.10human · autoradiographyStrikingly sparse. The brainstem runs breathing, and the near-absence of CB1 here is why cannabis does not suppress respiration the way opioids do. It is not a claim that cannabis is harmless — the harms are real and are elsewhere.

Circulating immune cells

White cells moving through blood and lymph, so this one has no fixed address — it is everywhere at once.

  • CB2 receptorrank 0.95human · mrnaOn leukocytes throughout blood and lymph — which is why this row has no fixed address on the figure. Immune cells are not in a place.

Adipose tissue

Body fat, which is not inert storage but an active endocrine tissue.

  • MAGLrank 0.50human · mrnaPresent in fat tissue, where MAGL also participates in ordinary lipid handling — a reminder that these enzymes had other jobs before we named them after cannabis.
  • CB1 receptorrank 0.30human · mrnaPresent in fat tissue, where the system participates in energy balance rather than merely reflecting it.

Bone and marrow

The skeleton and the marrow inside it, where blood and immune cells are made.

  • CB2 receptorrank 0.60human · mrnaWhere immune cells are made, and where bone itself is remodelled.

Hypothalamus

A small central hub governing appetite, temperature, sleep and hormone release.

  • CB1 receptorrank 0.45human · autoradiographyModerate, and the appetite effect lives partly here.

Reproductive tissue

The gonads and associated tissue, which carry the system in both sexes.

  • CB1 receptorrank 0.30human · mrnaPresent in reproductive tissue, with roles in fertility that are still being characterised.

Heart and vessels

The pump and the pipework, including the vessel walls that set blood pressure.

  • CB1 receptorrank 0.20human · functionalIn the heart and vessel walls, contributing to blood-pressure regulation.

Lungs

Where breath meets blood — and, for anything inhaled, the first tissue it touches.

  • CB1 receptorrank 0.15human · mrnaLow. Worth noticing that the tissue most exposed by smoking is not the tissue most receptive to the drug.

What acts on it, and where

The pharmacology the figure re-weights by. Note the direction: an enzyme inhibitor raises the signal it touches, because the enzyme’s job was to end it.

THC

from the plant

Δ9-tetrahydrocannabinol, the plant molecule responsible for intoxication. A partial agonist at CB1 — it turns the receptor on, but not fully.

Usually got wrong — THC is a partial agonist, not a full one. That single fact is why the receptor's own messengers can be displaced by it, and part of why tolerance builds the way it does.

  • CB1 receptorpartial agonist · uphumanThe interaction that makes cannabis cannabis. Partial rather than full agonism: it turns CB1 on, but never as hard as the receptor can go.
  • CB2 receptorpartial agonist · uphumanTHC acts at CB2 as well. Because CB2 sits on immune cells rather than neurons, this arm of its activity is not what is felt.

CBD

from the plant

Cannabidiol. Not intoxicating, and — this is the part that surprises people — barely active at CB1 at all.

Usually got wrong — CBD is not 'the calm one at the same receptor'. Its affinity for CB1 is very low; what it does happens largely elsewhere. Watch how little of the gold lights up, and where the map moves instead.

  • CB1 receptornegative allosteric · downin-vitroNot an agonist. Cannabidiol binds CB1 at a different site and changes how *other* things act there — which is close to the opposite of what it is usually said to do, and is why the gold barely lifts.
  • TRPV1 channelagonist · upin-vitroCannabidiol activates the vanilloid channel — the chilli-heat receptor. A large part of what it does happens on nerve endings, not in the brain's cannabinoid system.
  • 5-HT1A receptoragonist · upin-vitroActivity at a serotonin receptor. If cannabidiol calms anything, this is a more plausible route than CB1 — and it is a serotonergic story, not a cannabinoid one.
  • FAAHenzyme inhibitor · upin-vitroSlowing the enzyme that destroys anandamide raises your own anandamide. Note the direction: the signal goes *up* because its off-switch was slowed.

Anandamide

made by your body

One of the two messengers your body makes for this system. Named from ānanda, the Sanskrit for bliss — an unusually candid piece of naming for a molecule.

Usually got wrong — It is made on demand and destroyed within seconds by FAAH, never stored. Your own signalling is local and brief; an inhaled agonist is neither.

  • CB1 receptorpartial agonist · uphumanThe endogenous ligand CB1 was found to have. Made on demand, acting locally, gone in seconds.
  • TRPV1 channelagonist · upin-vitroAnandamide also acts at TRPV1, which is why the body's own cannabinoid is not a tidy one-receptor molecule either.
  • FAAHenzyme inhibitor · downhumanShown here as the relationship it is: FAAH is what ends anandamide. Where FAAH is dense, anandamide is brief.

2-AG

made by your body

The other endogenous messenger, and the more abundant of the two. Ended by MAGL rather than FAAH.

Usually got wrong — Two messengers with two different off-switches is not redundancy — they are released in different circumstances and reach different distances.

  • CB1 receptoragonist · uphumanThe more abundant of the two endogenous messengers, and a full agonist where anandamide is partial.
  • CB2 receptoragonist · uphumanActive at CB2 as well, which is part of how the immune arm of the system is spoken to from inside.
  • MAGLenzyme inhibitor · downhumanMAGL is 2-AG's off-switch, sitting on the terminal the signal was aimed at.

Exercise

a behaviour

Sustained aerobic effort raises circulating endocannabinoids. Not a molecule you take — a state you can put yourself in.

Usually got wrong — The 'runner's high' was attributed to endorphins for decades. Endorphins are large molecules that cross into the brain poorly; endocannabinoids do not have that problem.

  • CB1 receptorraises endogenous · uphumanSustained aerobic effort raises circulating endocannabinoids in humans. Not a molecule taken — a state entered, acting through the system already there.
  • CB2 receptorraises endogenous · uprodentThe 'runner's high' was shown to depend on cannabinoid receptors — in mice. Real, suggestive, and not a human result, so it is drawn as the haze it is.

The six targets

  • CB1 receptorreceptor

    The receptor THC acts at, and among the most abundant of its type in the brain. Where it is dense, cannabis is felt; where it is sparse, cannabis largely is not.

  • CB2 receptorreceptor

    Concentrated on immune cells rather than neurons. Activating it does not produce intoxication, which is why it is the target most drug development aims at.

  • TRPV1 channelreceptor

    The channel that also answers to capsaicin — the heat in chilli. Anandamide and cannabidiol both act here, which is part of why neither behaves like a simple cannabinoid.

  • 5-HT1A receptorreceptor

    A serotonin receptor, and nothing to do with cannabinoids by name. It is on this map because cannabidiol acts at it, which is a large part of what cannabidiol actually does.

  • FAAHenzyme

    Fatty acid amide hydrolase: the enzyme that destroys anandamide. Because the signal is set by how fast it is ended, this is as much part of the system as any receptor.

  • MAGLenzyme

    Monoacylglycerol lipase, which does for 2-AG what FAAH does for anandamide. Two messengers, two off-switches, and they are not interchangeable.

Every source this rests on

Nothing on this page is drawn from a source that is not on this list. If a row could not be cited, it was not plotted.

  1. Devane, W. A. et al. (1992). Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science, 258(5090), 1946–1949.
  2. Di Marzo, V., Bifulco, M. & De Petrocellis, L. (2004). The endocannabinoid system and its therapeutic exploitation. Nature Reviews Drug Discovery, 3, 771–784.
  3. Fuss, J. et al. (2015). A runner's high depends on cannabinoid receptors in mice. Proceedings of the National Academy of Sciences, 112(42), 13105–13108.
  4. Gaoni, Y. & Mechoulam, R. (1964). Isolation, Structure, and Partial Synthesis of an Active Constituent of Hashish. Journal of the American Chemical Society, 86(8), 1646–1647.
  5. Laprairie, R. B. et al. (2015). Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor. British Journal of Pharmacology, 172(20), 4790–4805.
  6. Lu, H.-C. & Mackie, K. (2016). An Introduction to the Endogenous Cannabinoid System. Biological Psychiatry, 79(7), 516–525.
  7. Mechoulam, R. et al. (1995). Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors. Biochemical Pharmacology, 50(1), 83–90.
  8. Munro, S., Thomas, K. L. & Abu-Shaar, M. (1993). Molecular characterization of a peripheral receptor for cannabinoids. Nature, 365, 61–65.
  9. Raichlen, D. A. et al. (2012). Wired to run: exercise-induced endocannabinoid signaling in humans and cursorial mammals. Journal of Experimental Biology, 215(8), 1331–1336.
  10. Russo, E. B. (2011). Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects. British Journal of Pharmacology, 163(7), 1344–1364.

The written course behind this map — six lessons, free and complete — covers the discovery, the parts list, the clinical ledger including the harms, and what the system does with no plant involved at all.

This is a map of pharmacology, not advice. It shows where molecules act in a body; it does not say what to take, how much, whether it is legal where you are, or whether it is right for you — and no map can. Cannabis and cannabinoids carry real risks, including to people with a personal or family history of psychosis, in pregnancy, and in adolescence. Talk to a clinician who can see you. Read the full disclaimer.