Brief embryonic strychnine exposure in zebrafish causes long-term adult behavioral impairment with indications of embryonic synaptic changes.

Zebrafish provide a powerful model of the impacts of embryonic toxicant exposure on neural development that may result in long-term behavioral dysfunction. In this study, zebrafish embryos were treated with 1.5mM strychnine for short embryonic time windows to induce transient changes in inhibitory neural signaling, and were subsequently raised in untreated water until adulthood.

Zebrafish provide a sensitive model of persisting neurobehavioral effects of developmental chlorpyrifos exposure: comparison with nicotine and pilocarpine effects and relationship to dopamine deficits.

Chlorpyrifos (CPF) an organophosphate pesticide causes persisting behavioral dysfunction in rat models when exposure is during early development. In earlier work zebrafish were used as a complementary model to study mechanisms of CPF-induced neurotoxicity induced during early development. We found that developmental (first five days after fertilization) chlorpyrifos exposure significantly impaired learning in zebrafish.

Nicotine effects on learning in zebrafish: the role of dopaminergic systems.

Rationale: Nicotine improves cognitive function in a number of animal models including rats, mice, monkeys, and recently, zebrafish. The zebrafish model allows higher throughput and ease in discovering mechanisms of cognitive improvement.

Materials And Methods: To further characterize the neural bases of nicotine effects on learning in zebrafish, we determined changes in dopaminergic systems that accompany nicotine-enhanced learning.

Anxiolytic effects of nicotine in zebrafish.

Anxiolytic effects of nicotine have been documented in studies with rodents and humans. Understanding the neural basis of nicotine-induced anxiolysis can help both with developing better aids for smoking cessation as well as with the potential development of novel nicotinic ligands for treating anxiety. Complementary non-mammalian models may be useful for determining the molecular bases of nicotine effects on neurobehavioral function.

Time-sharing in pigeons: Independent effects of gap duration, position and discriminability from the timed signal.

Previous data suggest that in a peak-interval procedure with gaps, memory for the pre-gap interval varies with the discriminability of the gap from the to-be-timed signal. Here we extend this finding by manipulating the pre-gap and gap intervals as well as the visual contrast between the gap and the to-be-timed signal. The delay in response function after the gap was found to vary with the duration and position of the gap.

Timing in choice experiments.

In Experiment 1, pigeons chose between variable- and fixed-interval schedules. The timer for 1 schedule was reset by a reinforcement on that schedule or on either schedule. In both cases, the pigeons timed reinforcement on each schedule from trial onset.