Anaerobic bacterium Clostridium botulinum produces seven different serotypes of botulinum neurotoxins (A-G), which specifically act at the peripheral cholinergic nerve terminals blocking the release of acethylcholine. Primary site of action of botulinum toxin type A (BT-A) is neuromuscular end plate where it specifically cleaves SNAP-25, one of the proteins necessary for neuroegzocytosis. The consequence is long-lasting muscle paralysis. Although BT-A is one of the most potent toxins in nature, over the last 20 years, intramuscular injections of nanogram quantities of BT-A have been used to treat various conditions characterized by increased muscle contraction, like dystonias, spasticity related to cerebral palsy etc but also for autonomic nervous system disorders, like hyperhydrosis. Long duration of action (several months) after peripheral application is the most prominent feature of the toxin's action. Although the acute mechanism of action on neuromuscular junction is largely investigated, there are still some unknowns related to: the passage of BT-A through epithelial barriers, specific recognition of peripheral cholinergic neurons. The mechanism of long duration of action, which is the base of therapeutic use of BT-A, is poorly understood.