NBTS 2010 Abstracts

NBTS1Delay discounting by humans and other animals: Does thespecies matter?

Leonard GreenWashington University, Saint Louis, MO, United States

When rats, pigeons, and people choose between immediate anddelayed rewards, the subjective value of the delayed reward decreasesas time to its receipt increases. In all three species, this decrease, whichrepresents the discounting of thedelayed reward, iswell describedbyahyperboloid function. Interestingly, we have observed a magnitudeeffect (in which larger delayed rewards are discounted less steeplythan smaller delayed rewards) with humans but not with rats orpigeons. Humans consistently discounted larger delayed rewards lesssteeply than smaller delayed rewards. In contrast, the nonhumananimals showed equivalent discounting of both large and smallrewards, as well as of both more- and less-preferred rewards. Inaddition, we have observed that in humans, if an additional waitingperiod is added prior to both rewards, thus creating a delay common toboth alternatives, rate of discounting decreases as the common delayincreases. We recently have examined the effect of adding a commondelay on discounting in pigeons. When the sooner and lateralternatives were differentially signaled throughout, the pigeons (incontrast to humans) showed substantial increases in discounting ratewith increases in the common delay. When the common delay to bothrewards had the same signal but the additional time to the later rewardwas differentially signaled, however, rate of discounting decreased asthe common delay increased, a result consistent with that obtainedwith humans. Taken together, these results illustrate the difficultiesinvolved in determining whether delay discounting relies on similarprocesses in different species.

doi:10.1016/j.ntt.2010.04.002

NBTS2Ontogeny of Hippocampal-Dependent Memory Processes:Developmental Amnesia in Monkeys and Humans

Maria C. Alvarado, Jocelyne BachevalierYerkes National Primate Research Center, Emory University, Atlanta, GA

Substantial progress has been made in the understanding of theneural substrates of memory processes in human and nonhumanprimates. How these processes emerge during development and how

the brain systems that mediate them mature during ontogeny areimportant questions that give us insight into adult memory and thecognitive consequences of perinatal perturbations to those neuralsubstrates. Using a variety of cognitive paradigms we have begun tomap out normal developmental changes in memory and haveexplored the consequences of neonatal damage to medial temporallobe structures to normal memory development. In particular, threeclasses of cognitive task: delay-dependent recognition, spatialrecognition/navigation, and non-spatial relational memory, showsimilar protracted development and sensitivity to early hippocampaldamage in monkeys. We will demonstrate that: A) cognitiveprocesses that are sensitive to hippocampal dysfunction are late-developing in monkeys; B) within those tasks that depend upon thehippocampus, the degree to which the behavior requires thetrisynaptic pathway may develop later than those which engage thedirect pathway; and C) in comparison with reports in the literature,developmentally amnesic children or adults with hippocampaldamage, performance on the same or similar cognitive tasks producesstriking similarities to the results we find in monkeys.

doi:10.1016/j.ntt.2010.04.003

NBTS3Modeling the cognitive deficits of Parkinson's disease

Jay SchneiderThomas Jefferson University, Philadelphia, PA, United States

Cognitive dysfunction is an important aspect of Parkinson'sdisease (PD). PD patients often display a variety of cognitive deficits,many of which resemble those found in patients with frontal lobedysfunction and appear to involve primarily fronto-striatal circuits.Cognitive improvement has not been consistently reported, or at leasthas not been significant after treatment with dopaminergic agents.Remediation of cognitive deficits of PD is a major unmet medicalneed. There is significant need for therapies that can be administeredadjunctively with levodopa to improve cognition or counteractdetrimental effects of levodopa on cognition and not diminish thetherapeutic effects of levodopa on motor functioning. Unfortunately,such development efforts have been hampered in part due to lack ofan appropriate animal model in which to carryout critical preclinicalstudies. To overcome this problem, we have developed a model basedon chronic administration of low doses of the neurotoxin MPTP tonon-human primates. These animals develop early appearing at-tention and executive function deficits with minimal or no motor

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Neurotoxicology and Teratologyj ourna l homepage: www.e lsev ie r.com/ locate /neutera

Neurotoxicology and Teratology 32 (2010) 496–510

pii:S0892-0362(10)00054-1