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[Physiology](https://durgical.com/en/physiology/) · [Cell and membrane](https://durgical.com/en/physiology/#s-cell)

# Endocytosis, exocytosis and vesicles

- Mechanism
- For completeness

Cells wrap particles in little membrane bags to bring them in (endocytosis) or to release their contents (exocytosis).

Updated 2026-11-01

Also called: Phagocytosis, Receptor-mediated endocytosis

## Key points

- Receptor-mediated endocytosis: receptors cluster in clathrin-coated pits (LDL, transferrin-bound iron).
- Familial hypercholesterolaemia: a faulty LDL receptor; LDL cannot enter the liver and plasma cholesterol is high from childhood.
- Regulated exocytosis: Ca²⁺ entry triggers fusion mediated by SNARE proteins.
- Botulinum toxin cleaves SNAREs: it blocks acetylcholine release and causes flaccid paralysis.

## What it is

Molecules too large for channels or carriers cross the membrane inside vesicles. In endocytosis the membrane folds in and closes around the material; in exocytosis a vesicle fuses with the membrane and empties its contents outside. Both use energy and depend on the cytoskeleton. Ca²⁺-regulated exocytosis is how neurotransmitters, hormones and digestive enzymes are released.

## How it works, step by step

- A ligand binds its membrane receptor and the complexes gather in a clathrin-coated pit.
- The pit folds inwards and dynamin pinches it off: a vesicle forms inside the cell.
- The vesicle sheds its clathrin and fuses with an endosome, whose acidic pH separates ligand from receptor.
- The receptor returns to the membrane for reuse; the ligand goes on to the lysosome, where hydrolases break it down.
- In the reverse route, Golgi vesicles dock at the membrane through SNAREs and, on a Ca²⁺ signal, fuse and release their contents.

## Vesicular transport processes

| Process | What it moves | Example |
| --- | --- | --- |
| Phagocytosis | Large particles (bacteria, dead cells) | Neutrophils and macrophages |
| Pinocytosis | Extracellular fluid with solutes | Almost all cells |
| [Receptor-mediated endocytosis](https://durgical.com/en/conditions/familial-hypercholesterolemia/) | Specific ligands | LDL into hepatocytes; transferrin |
| Transcytosis | Molecules across an epithelium | IgA into the gut lumen; IgG across the placenta |
| Regulated exocytosis | Granule contents, on demand | Neurotransmitters, insulin, pancreatic enzymes |

## Clinical notes

- Familial hypercholesterolaemia: tendon xanthomas and early coronary disease; heterozygotes are fairly common.
- I-cell disease: enzymes miss their mannose-6-phosphate tag, are secreted out of the cell and the lysosome fills with undegraded material.
- Botulism: symmetric descending paralysis with dilated pupils, from failed acetylcholine exocytosis.

## Memory aid

Clathrin to come in, SNAREs and calcium to go out.

## Test yourself

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

## Why is plasma cholesterol high in familial hypercholesterolaemia even though the liver works?

Without a working LDL receptor, receptor-mediated endocytosis fails: LDL cannot enter hepatocytes, stays in plasma, and the liver keeps making cholesterol.

## Which step of exocytosis does botulinum toxin block, and what does it cause?

It cleaves SNARE proteins and prevents fusion of acetylcholine vesicles; the result is descending flaccid paralysis.

## Why can the LDL receptor be used many times?

The endosome's acidic pH releases LDL from its receptor; the receptor returns to the membrane while LDL goes to the lysosome.

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## Related topics

- [Synaptic transmission](https://durgical.com/en/physiology/synaptic-transmission/)
- [The neuromuscular junction](https://durgical.com/en/physiology/the-neuromuscular-junction/)
- [Membrane transport: diffusion, channels and carriers](https://durgical.com/en/physiology/membrane-transport-diffusion-channels-and-carriers/)
- [Cell signaling for physiology](https://durgical.com/en/physiology/cell-signaling-for-physiology/)

## Related conditions

- [Familial hypercholesterolemia](https://durgical.com/en/conditions/familial-hypercholesterolemia/)
- [I-cell disease (mucolipidosis II)](https://durgical.com/en/conditions/i-cell-disease/)

## In Biochemistry

- [Cell organelles and their metabolism](https://durgical.com/en/biochemistry/topics/cell-organelles-and-their-metabolism/)
- [LDL receptor](https://durgical.com/en/biochemistry/enzymes/ldl-receptor/)
- [LDL (low-density lipoprotein)](https://durgical.com/en/biochemistry/topics/ldl/)
- [Mannose 6-phosphate tagging (sending enzymes to the lysosome)](https://durgical.com/en/biochemistry/topics/mannose-6-phosphate-tagging/)

[← All of physiology](https://durgical.com/en/physiology/)

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: [3.1 The Cell Membrane](https://openstax.org/books/anatomy-and-physiology-2e/pages/3-1-the-cell-membrane) (OpenStax (Rice University), 2022); [3.2 The Cytoplasm and Cellular Organelles](https://openstax.org/books/anatomy-and-physiology-2e/pages/3-2-the-cytoplasm-and-cellular-organelles) (OpenStax (Rice University), 2022); [Familial hypercholesterolemia: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000392.htm) (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 2). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.

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