Cell-to-cell and cell-environment interactions are known to play a role during the first events of sea urchin development. Larval metamorphosis in benthic invertebrates is induced by environmental signals (cues), received by membrane receptors. The activity of such cues may be disturbed by the presence of toxic agents from pollution. We consider the possibility that neurotransmitter receptor-like molecules may have a role in the regulation of larval development and metamorphosis. To investigate the effects exerted on these processes by neuroactive pollutants, such as neurotoxic insecticides, we tested the function of acetylcholine receptors (muscarinic acetylcholine receptors mAChR and nicotinic acetylcholine receptors nAChR) in larvae of Paracentrotus lividus in the presence of four neuroactive drugs: carbamylcholine, an agonist of mAChR; atropine, an antagonist of the same; nicotine, an agonist of nAChR; and eserine (physostigmine), which mimics an excess of ACh in the receptorial sites. Under the conditions of our experiments, the effect of these neuroactive drugs on larval development was mainly a growth delay in comparison with the development of controls. At metamorphosis, the neurotransmission system, which is predominantly cholinergic in larvae, shifts to a biogenic-amine system in the rudiment. At this stage, the weaker effects of the tested drugs show that their action was not exerted on transcription but rather on the regulation of motility in the ciliary bands.