Progress toward understanding the neurophysiological basis of predator-induced morphology in Daphnia pulex

Previous studies have demonstrated that certain pesticides, including carbaryl and endosulfan, can modulate the expression of predator-induced morphology in Daphnia. These pesticides affect the transmission of nervous impulses in vertebrates and invertebrates. The aim of this study was to determine the role of two neurotransmitter systems, excitatory cholinergic transmission and inhibitory γ-aminobutyric acid (GABA)-mediated transmission, in the regulation of inducible defenses of Daphnia. The effects of chemicals with four different modes of action on the expression of Chaoborus-induced neckteeth in Daphnia pulex were measured. These chemicals included chemicals that could enhance transmission at cholinergic synapses (physostigmine, nicotine), inhibit cholinergic transmission (atropine), stimulate or enhance the effects of GABA (diazepam, muscimol, cis-4-aminocrotonic acid), or antagonise the action of GABA (picrotoxin, bicuculline, SR95531). The development of Chaoborus-induced neckteeth in D. pulex was enhanced by physostigmine and picrotoxin and suppressed by atropine. It was proposed that these chemicals were acting on neurosecretory cells that release the hormones necessary to induce neckteeth development. The results also indicate mechanisms through which anthropogenic pollutants could influence the expression of inducible defenses, leading to inappropriate expression in environments with low predator intensity or to suppression in environments with high risks of predation.