A stereotaxic atlas of the rat brain

Although the mammalian basal ganglia have long been implicated in motor behavior, it is generally recognized that the behavioral functions of this subcortical group of structures are not exclusively motoric in nature. Extensive evidence now indicates a role for the basal ganglia, in particular the dorsal striatum, in learning and memory. One prominent hypothesis is that this brain region mediates a form of learning in which stimulus-response (S-R) associations or habits are incrementally acquired. Support for this hypothesis is provided by numerous neurobehavioral studies in different mammalian species, including rats, monkeys, and humans. In rats and monkeys, localized brain lesion and pharmacological approaches have been used to examine the role of the basal ganglia in S-R learning. In humans, study of patients with neurodegenerative diseases that compromise the basal ganglia, as well as research using brain neuroimaging techniques, also provide evidence of a role for the basal ganglia in habit learning. Several of these studies have dissociated the role of the basal ganglia in S-R learning from those of a cognitive or declarative medial temporal lobe memory system that includes the hippocampus as a primary component. Evidence suggests that during learning, basal ganglia and medial temporal lobe memory systems are activated simultaneously and that in some learning situations competitive interference exists between these two systems.

Learning and memory functions of the Basal Ganglia.

There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias. In this essay, I discuss the implications of these problems for the conduct and interpretation of research.

Why most published research findings are false

This study investigated the respective roles of the hippocampus, the amygdala, and the dorsal striatum in learning and memory. A standard set of experimental conditions for studying the effects of lesions to the three brain areas using an 8-arm radial maze was used: a win-shift version, a conditioned cue preference (CCP) version, and a win-stay version. Damage to the hippocampal system impaired acquisition of the win-shift task but not the CCP or win-stay tasks. Damage to the lateral amygdala impaired acquisition of the CCP task but not the win-shift or win-stay tasks. Damage to the dorsal striatum impaired acquisition of the win-stay task but not the win-shift or CCP tasks. These results are consistent with the hypothesis that the mammalian brain may be capable of acquiring different kinds of information with different, more-or-less independent neural systems. A neural system that includes the hippocampus may acquire information about the relationships among stimuli and events. A neural system that includes the amygdala may mediate the rapid acquisition of behaviors based on biologically significant events with affective properties. A neural system that includes the dorsal striatum may mediate the formation of reinforced stimulus-response associations.

A triple dissociation of memory systems: hippocampus, amygdala, and dorsal striatum

A compendium of neuropsychological tests: administration, norms, and commentary

A critical review of some relevant literature concerning the effects of prenatal administration of drugs and several other substances on postnatal behavior. Significant variables and problems in the adequate design of experiments to assess these effects are discussed. Although the evidence concerning prenatal drug effects on behavior is equivocal, sufficient data exist to indicate that this will continue to be a viable and important area of research in the future. Present results demonstrate the complexity of drug interactions with other variables.

Behavioral teratogenesis: a critical evaluation.

Offspring of rats given oral doses of Saline or Imipramine (5 mg/kg) from 14–21 days prior to mating till parturition were reared, after weaning, in deprived or enriched environments. At 25–27 days and at 80–83 days the home cage behaviour of the Ss reared in the enriched environment was observed. Histological measures of brain development in both the deprived and enriched Ss were taken at the conclusion of behavioural observations. The Imipramine exposed offspring failed to show the characteristic histological changes associated with enriched rearing conditions. In addition they were behaviourally unresponsive and spent significantly less time than the Saline offspring interacting with other animals and the environment. It was argued that the physiological and behavioural unresponsiveness of the Imipramine offspring was due to a subtle teratogenic effect which prevented the Ss from interacting with the environment.

The interactive effects of prenatal imipramine exposure and postnatal rearing conditions on behaviour and histology.

Female rats were given oral doses of Imipramine (5mg/kg) from 14–21 days prior to mating to conception or Day 19 of gestation and the physical maturation and behavioral development of their offspring was compared with that of controls. There were significant differences between the weights of the Impramine and control animals at 21 days and the appearance of some reflexes was delayed. Behavior in an open field was observed when the rats were 9, 13, 17 and 21 days of age and it was found that exploratory responses were less frequent in the drug exposed offspring. In contrast there were no obvious physical anomalies and the adult behavior of the Imipramine animals on a spontaneous alternation task and a swimming maze did not differ from that of controls.

Changes in developing behavior following prenatal administration of imipramine.

Offspring of rats given oral doses of imipramine (5 mg/kg) from 14–21 days prior to mating till parturition or vitamin-A (100000 i.u./kg) between days 8 and 10 of gestation were reared, after weaning, in deprived or enriched environments. When tested in both a Henderson-type maze and a swimming maze no behavioural effects due to prenatal drug exposure were observed when the Ss were reared in a deprived environment. When the Ss were reared in an enriched environment the maze performance of those animals which had been exposed to imipramine or vitamin-A was significantly inferior to that of the control animals. The implications of these findings are discussed with respect to environmental interaction with prenatal drug effects on behaviour.

The interaction of post-weaning housing conditions and prenatal drug effects on behaviour.

Learning to run down a straight alley for a food reward was investigated in rats with lesions of the telencephalon. Over 84 trials the running latencies of rats with lesions of the caudate nucleus were significantly greater than those of subjects with lesions of the frontal cortex or sham-lesioned rats. The running latencies of the cortical- and the sham-lesioned groups were not significantly different. It was suggested that the performance of the caudotomized rats reflected a learning deficit.

Caudate nucleus lesions impair the ability of rats to learn a simple straight-alley task.

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