Succinylcholine is a direct nicotinic receptor agonist but is used clinically as an indirect anticholinergic. 

Succinylcholine (suxamethonium) is a highly potent agonist at the neuromuscular junction (NMJ) nicotinic acetylcholine receptors.  It is a direct cholinergic agonist in that it binds to the same binding site as the endogenous transmitter acetylcholine and activates the receptor in the same manner as acetylcholine. In contrast, non-depolarising neuromuscular blocking agents (NMBAs), such as pancuronium, are direct antagonists at NMJ nicotinic acetylcholine receptors. NMBAs are direct anticholinergics and can be used to produce paralysis when required under surgical anaesthesia.

In the context of autonomic pharmacology, indirect agonist effects are any effects mimicking the effect of the endogenous transmitter and other direct agonists not caused by direct agonism at the receptor. Conversely, indirect antagonist effects are any effects mimicking the effect of direct antagonists not caused by direct antagonism at the receptor.

Although it is a direct agonist of nicotinic acetylcholine receptors, clinically succinylcholine is used as an indirect anticholinergic to block the action of nicotinic acetylcholine receptors at the NMJ causing paralysis when required under surgical anaesthesia. The paralysis is caused because succinylcholine activates the nicotinic acetylcholine receptors so intensely that depolarising block occurs (Phase I) followed by desensitising block (Phase II).  The clinically desired paralysis mimics the direct anticholinergic effect of the NMBAs but is produced indirectly via the depolarising block and desensitising block secondary to direct agonism at the receptor. Therefore, succinylcholine is an indirect anticholinergic.