Cell-to-cell and cell-environment interactions are known to play a rol
e during the first events of sea urchin development. Larval metamorpho
sis in benthic invertebrates is induced by environmental signals (cues
), received by membrane receptors. The activity of such cues may be di
sturbed by the presence of toxic agents from pollution. We consider th
e possibility that neurotransmitter receptor-like molecules may have a
role in the regulation of larval development and metamorphosis. To in
vestigate the effects exerted on these processes by neuroactive pollut
ants, such as neurotoxic insecticides, we tested the function of acety
lcholine receptors (muscarinic acetylcholine receptors mAChR and nicot
inic acetylcholine receptors nAChR) in larvae of Paracentrotus lividus
in the presence of four neuroactive drugs: carbamylcholine, an agonis
t of mAChR; atropine, an antagonist of the same; nicotine, an agonist
of nAChR; and eserine (physostigmine), which mimics an excess of ACh i
n the receptorial sites. Under the conditions of our experiments, the
effect of these neuroactive drugs on larval development was mainly a g
rowth delay in comparison with the development of controls. At metamor
phosis, the neurotransmission system, which is predominantly cholinerg
ic in larvae, shifts to a biogenic-amine system in the rudiment. At th
is stage, the weaker effects of the tested drugs show that their actio
n was not exerted on transcription but rather on the regulation of mot
ility in the ciliary bands.