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Encoding, learning, and spatial updating of multiple object locations specified by 3-D sound, spatial language, and vision.

Participants standing at an origin learned the distance and azimuth of target objects that were specified by 3-D sound, spatial language, or vision. We tested whether the ensuing target representations functioned equivalently across modalities for purposes of spatial updating. In experiment 1, participants localized targets by pointing to each and verbalizing its distance, both directly from the origin and at an indirect waypoint. In experiment 2, participants localized targets by walking to each directly from the origin and via an indirect waypoint. Spatial updating bias was estimated by the spatial-coordinate difference between indirect and direct localization; noise from updating was estimated by the difference in variability of localization. Learning rate and noise favored vision over the two auditory modalities. For all modalities, bias during updating tended to move targets forward, comparably so for three and five targets and for forward and rightward indirect-walking directions. Spatial language produced additional updating bias and noise from updating. Although spatial representations formed from language afford updating, they do not function entirely equivalently to those from intrinsically spatial modalities.

Adult↗

The effects of serotonin depletion and raphe grafts on hippocampal electrophysiology and behavior.

The involvement of the serotonergic system in spatial learning and a possible correlation between serotonergic modulation of hippocampal electrical activity and spatial learning were studied in rats. Control, partial septal-lesioned (SL), 5,7-dihydroxytryptamine (5,7-DHT)-injected (DHT), double-lesioned (5,7-DHT and SL; DL), and DL rats that were transplanted with embryonic raphe grafts into the hippocampus (RG) were tested in a spatial task in a water maze and in an active avoidance shuttle-box task. The responses of the dentate gyrus (DG) to perforant-path (PP) stimulation were examined in the same rats, under the following conditions: (1) priming stimulation of the PP (testing feedback inhibition), (2) priming stimulation of the commissural pathway (testing feedforward inhibition), (3) during repeated stimulation of the PP at 7 Hz (frequency potentiation), and (4) following tetanic stimulation [long-term potentiation (LTP)]. DL, but not DHT or SL, treatment severely impaired the performance of rats in both reference- and working-memory tasks in the water maze. This effect was not seen in the shuttle box. The ability of the DG to exhibit LTP, which was reduced in the DHT and SL rats, was apparently similar to controls in the DL group, DL, but not DHT or SL alone, resulted in a reduction of inhibition in the DG. Both the behavioral deficits and the reduction in hippocampal inhibition were ameliorated by intrahippocampal raphe grafts. These results indicate that the serotonergic innervation of the hippocampus plays a role in spatial learning when the septohippocampal neurotransmission systems are disrupted. Furthermore, these results suggest that restoration of modulation of hippocampal inhibition, by raphe grafts, underlies the behavioral recovery observed in these rats.

5,7-Dihydroxytryptamine↗

[Long-term effects of early hyperbaric oxygen therapy on neonatal rats with hypoxic-ischemic brain damage].

OBJECTIVE: The application and therapeutic effect of hyperbaric oxygen (HBO) in hypoxic-ischemic brain damage (HIBD) remains controversial. Previous studies have focused on the early pathological and biochemical outcomes and there is a lack of long-term functional evaluation. This study was designed to evaluate the long-term pathological and behavioral changes of early HBO therapy on neonatal rats with HIBD. METHODS: Postnatal 7 days (PD7) rat pups were randomly assigned into Control (n=18), HIBD (n=17) and HBO treatment groups (n=17). HIBD was induced by ligating the left common carotid, followed by 2 hrs hypoxia exposure in the HIBD and HBO treatment groups. The Control group was sham-operated and was not subjected to hypoxia exposure. The HBO therapy with 2 atmosphere absolutes began 0.5-1 hr after HIBD in the HIBD treatment group, once daily for 2 days. The spatial learning and memory ability were evaluated by the Morris water maze test at PD37 to PD41. The morphological and histological changes of the brain, including brain weight, survival neurons, AchE positive unit and NOS positive neurons in hippocampal CA1 region, were detected at PD42. RESULTS: The rats in the HIBD group displayed significant morphological and histological deficits, as well as severe spatial learning and memory disability. In the Morris water maze test, the mean escape latency were longer (56.35 +/- 22.37 s vs 23.07 +/- 16.28 s; P < 0.05) and the probe time and probe length were shorter in the HIBD group (29.29 +/- 6.06 s vs 51.21 +/- 4.59 s and 548 +/- 92 cm vs 989 +/- 101 cm; both P < 0.05) compared with the Control group. The left brain weight in the HIBD group was lighter than that in the Control group (0.601 +/- 0.59 g vs 0.984 +/- 0.18 g; P < 0.05). The survival neurons in the hippocampal CA1 region were less (100 +/- 27/mm vs 183 +/- 8/mm; P < 0.05), as well as the AchE-positive unit and NOS-positive neurons (18.50 +/- 2.24% vs 27.50 +/- 2.18% and 19.25 +/- 4.33 vs 33.75 +/- 5.57 respectively; P < 0.05) after HIBD. Early HBO treatment improved the abilities of spatial learning and alleviated the morphological and histological damage. The mean escape latency (39.17 +/- 21.20 s) was shortened, the probe time (36.84 +/- 4.36 s) and the probe length (686 +/- 76 cm) were longer, and the brain weight (0.768 +/- 0.85 g), the survival neurons (133 +/- 25/mm) and the AchE-positive unit (21.94 +/- 2.73%) increased significantly compared with those of the HIBD group (P < 0.05). CONCLUSIONS: Early HBO treatment resulted in a protective effect against HIBD-induced long-term brain morphological and histological deficits and spatial learning and memory disability.

Acetylcholinesterase↗

Effects of diazepam or chronic alcohol treatment on spatial reversal learning in mice.

Mice submitted to chronic alcohol consumption (CAC; 11 months) or to systemic diazepam administration were trained in a spatial reversal learning task. Although CAC-treated mice were able to learn the initial acquisition at normal rates, they were impaired during the first reversal of the discrimination and subsequent reversal sessions. In contrast, diazepam administration induced no deficits for any behavioral measure. In conclusion, CAC, but not diazepam administration, induces an exaggerated sensitivity to proactive interference. The two treatments spared, however, the development of the learning set curve. These results are congruent with clinical data showing that nondeclarative or implicit forms of memory processes are spared in diazepam-treated subjects or in chronic alcoholics.

Animals↗

Alterations in the immunoreactivity for muscarinic acetylcholine receptors and colocalized PKC gamma in mouse hippocampus induced by spatial discrimination learning.

This study describes changes in the immunoreactivity for muscarinic acetylcholine receptors (mAChRs) in the hippocampus of mice in relation to spatial discrimination behavior, employing the monoclonal antibody M35 raised against purified bovine mAChR protein. Performance in a hole board in which the animals learned the pattern of 4 baited holes out of 16 holes served as the measure of spatial discrimination learning and memory. Twenty-six adult male house mice were used, divided into four groups. Three groups served as various controls: group N (naive; blank controls); group H (habituated; animals were introduced to the hole board with all holes baited for 5 consecutive days), and group P (pseudo-trained; the animals were admitted to the hole board for 13 consecutive days with all holes baited). The T group (trained) was subjected to the hole board for 5 consecutive habituation days with all holes baited (similar to the H and P groups), followed by 8 successive training days with only four holes baited in a fixed pattern. During the 8 training days, the T group gradually acquired a pattern to visit the baited holes, whereas the P group continued visiting holes in a random fashion. The mice were killed 24 h after the last behavioral session. All principal cells in teh cornu ammonis (CA) and dentate gyrus (DG) of the habituated animals revealed increased levels of mAChR immunoreactivity (mAChR-ir) over the naive mice. A minor increase in mAChR-ir was found in the apical dendrites of the CA1 pyramidal cells. Pseudotraining resulted in a CA1-CA2 region with a low level of mAChR-ir, resembling naive animals, whereas the trained mice showed a further increase in mAChR-ir in the CA1-CA2 pyramidal cell bodies and apical dendrites. Optical density measures of the mAChR-ir in the CA1 region revealed a significant (P < 0.05) increase in the pyramidal cell bodies of the H and T group over the N and P group, and a significant (P < 0.05) increase in the apical dendrites of the T group over all other groups. In contrast to the CA1-CA2 region, both pseudotrained and trained mice revealed high mAChR staining in the CA3-CA4 region and the DG. These results indicate that prolonged exposure to the hole board is sufficient for an enhanced mAChR-ir in the CA3-CA4 and DG, whereas the increase in CA1-CA2 pyramidal cells is a training-specific feature related to spatial orientation. Nonpyramidal neurons within the CA1-CA2 region with enhanced mAChR-ir in the pyramidal cells, however, revealed a decreased level of mAChR-ir. The opposing effect of pyramidal and nonpyramidal cells suggests a shift in the excitability of the hippocampal microcircuitry. Previously we demonstrated an increase and redistribution of hippocampal protein kinase C gamma-immunoreactivity (PKC gamma-ir) induced by hole board learning in mice (Van der Zee et al., 1992, J Neurosci 12:4808-4815). Immunofluorescence double-labeling experiments conducted in the present study in naive and trained animals revealed that the principal cells and DG interneurons co-express mAChRs and PKC gamma, and that the immunoreactivity for both markers increased in relation to spatial orientation within these neurons. The mAChR-positive nonpyramidal cells of the CA1-CA2 region were devoid of PKC gamma and revealed an opposite training-induced effect. These results suggest that the postsynaptic changes in mAChR- and PKC gamma-ir reflect functional alterations of the hippocampal formation induced by spatial learning.

Animals↗

Spatial memory is related to hippocampal subcellular concentrations of calcium-dependent protein kinase C isoforms in young and aged rats.

Relationships were examined between spatial learning and hippocampal concentrations of the alpha, beta2, and gamma isoforms of protein kinase C (PKC), an enzyme implicated in neuronal plasticity and memory formation. Concentrations of PKC were determined for individual 6-month-old (n = 13) and 24-month-old (n = 27) male Long-Evans rats trained in the water maze on a standard place-learning task and a transfer task designed for rapid acquisition. The results showed significant relationships between spatial learning and the amount of PKC among individual subjects, and those relationships differed according to age, isoform, and subcellular fraction. Among 6-month-old rats, those with the best spatial memory were those with the highest concentrations of PKCgamma in the particulate fraction and of PKCbeta2 in the soluble fraction. Aged rats had increased hippocampal PKCgamma concentrations in both subcellular fractions in comparison with young rats, and memory impairment was correlated with higher PKCgamma concentrations in the soluble fraction. No age difference or correlations with behavior were found for concentrations of PKCgamma in a comparison structure, the neostriatum, or for PKCalpha in the hippocampus. Relationships between spatial learning and hippocampal concentrations of calcium-dependent PKC are isoform-specific. Moreover, age-related spatial memory impairment is associated with altered subcellular concentrations of PKCgamma and may be indicative of deficient signal transduction and neuronal plasticity in the hippocampal formation.

Aging↗

Acquiring new spatial intuitions: learning to reason about rotations.

There are certain simple rotations of objects that most people cannot reason about accurately. Reliable gaps in the understanding of a fundamental physical domain raise the question of how learning to reason in that domain might proceed. Using virtual reality techniques, this project investigated the nature of learning to reason across the domain of simple rotations. Learning consisted of the acquisition of spatial intuitions: there was encoding of useful spatiotemporal information in specific problem types and a gradual accumulation of this understanding across the domain. This pattern of learning through the accumulation of intuitions is especially interesting for rotational motion, in which an elegant domain-wide kinematics is available to support insightful learning. Individual ability to reason about rotations correlated highly with mastery motivation, skill in fluid reasoning, and skill in reasoning about spatial transformations. Thus, general cognitive advantages aided the understanding of individual rotations without guaranteeing immediate generalization across the domain.

Adult↗

Origins of anthropoid intelligence IV. Role of prefrontal system in delayed alternation and spatial reversal learning in a conservative eutherian (Paraechinus hypomelas).

A conservative eutherian mammal (the hedgehog, Paraechinus hypomelas) was tested on delayed alternation performance and spatial reversal learning before and after ablations of the prefrontal cortex. The anatomical results show that the cortical focus of the projections of the medial dorsal nucleus, the prefrontal cortex, does not include the neocortex on the dorsal convexity of the hedgehog's frontal lobe but, instead, the perirhinal and pregenual neocortex immediately surrounding the frontal convexity. The behavioral results show that normal performance of hedgehogs on these two behavioral tests depends upon the integrity of their prefrontal cortex, but not on the integrity of their frontal convexity or olfactory bulbs. The similarity in the results obtained from prefrontal hedgehogs and a divergent variety of other species with prefrontal ablations indicates that the role of the prefrontal system in the abilities measured by these two tests is at least as old as Eutheria and, thus, probably imposed persistent constraints on subsequent evolutionary modifications of the prefrontal system.

Animals↗

Flupirtine reduces functional deficits and neuronal damage after global ischemia in rats.

Global cerebral ischemia leads to selective neuronal damage in the CA1 sector of the hippocampus and in the dorsolateral striatum. In addition, it results in deficits in spatial learning and memory as shown by an increase in escape latency and swim distance during the escape trials and a reduction of time spent in the quadrant of the former platform position during the probe trial of the water maze. Flupirtine is a non-opioid, centrally acting analgesic which has been shown to be neuroprotective against N-methyl-D-aspartate (NMDA)-mediated toxicity in vitro. The purpose of the present study was to investigate the potential protective effect of flupirtine in vivo with both behavioural and histological measures of global cerebral ischemia. Global ischemia was induced by four-vessel-occlusion (4VO) for 20 min in rats. Flupirtine was administered at a dose of 5 mg/kg i.p. either 20 min before and 50 min after occlusion (pre-treatment) or directly and 70 min after occlusion (post-treatment). 1 week after surgery, spatial learning and memory was tested in the Morris water maze. Pre-treatment with flupirtine reduced the increase in escape latency and in swim distance induced by 4VO. It also diminished the deficit in spatial memory as revealed by an increase in time spent in the quadrant of the former platform position during the probe trial which was reduced by 4VO. Post-treatment with flupirtine had no effect on the deficits in spatial learning and memory induced by 4VO. Neuronal damage in the CA1 sector of the hippocampus and in the striatum produced by 4VO was significantly attenuated with pre-treatment of flupirtine whereas post-treatment did not affect this neuronal damage. The present data demonstrate that pre-treatment with flupirtine exerts a protective effect on hippocampal and striatal neuronal damage and on deficits in spatial learning induced by 4VO.

Aminopyridines↗

Faster is not surer--a comparison of C57BL/6J and 129S2/Sv mouse strains in the watermaze.

In recent years the use of genetic manipulations to investigate the molecular mechanisms underlying learning and memory has become a common approach. In a great many cases, the spatial learning ability of mutant mice has been assessed using the Morris watermaze task. The performance of these mice may, however, be strongly influenced by their genetic background and, therefore, the interpretation of their phenotype requires a preliminary characterization of the parental strains. The present study compared 129S2/Sv and C57/BL/6J inbred mouse strains, which have been widely used in deriving lines of genetically modified mice, on the hidden platform version of the watermaze task. During acquisition, the C57 mice displayed shorter escape latencies to find the platform than the 129S2s. Further analysis revealed, however, that the C57 mice also swam faster than the 129S2s. The analysis of path lengths was thus a more reliable measure of spatial learning, and revealed an equal level of performance in the two strains. This conclusion was confirmed during the two probe trials with both strains showing a similar spatial preference for the training site. These results suggest that the 129S2 substrain is no less proficient than the C57 substrain in terms of spatial learning in the watermaze, and also demonstrates the importance of not relying solely on escape latency as a measure of watermaze performance.

Animals↗

Electrophysiological evidence for right frontal lobe dominance in spatial visuomotor learning.

Slow negative potential shifts were recorded together with the error made in motor performance when two different groups of 14 students tracked visual stimuli with their right hand. Various visuomotor tasks were compared. A tracking task (T) in which subjects had to track the stimulus directly, showed no decrease of error in motor performance during the experiment. In a distorted tracking task (DT) a continuous horizontal distortion of the visual feedback had to be compensated. The additional demands of this task required visuomotor learning. Another learning condition was a mirrored-tracking task (horizontally inverted tracking, hIT), i.e. an elementary function, such as the concept of changing left and right was interposed between perception and action. In addition, subjects performed a no-tracking control task (NT) in which they started the visual stimulus without tracking it. A slow negative potential shift was associated with the visuomotor performance (TP: tracking potential). In the learning tasks (DT and hIT) this negativity was significantly enhanced over the anterior midline and in hIT frontally and precentrally over both hemispheres. Comparing hIT and T for every subject, the enhancement of the tracking potential in hIT was correlated with the success in motor learning in frontomedial and bilaterally in frontolateral recordings (r = 0.81-0.88). However, comparing DT and T, such a correlation was only found in frontomedial and right frontolateral electrodes (r = 0.5-0.61), but not at the left frontolateral electrode. These experiments are consistent with previous findings and give further neurophysiological evidence for frontal lobe activity in visuomotor learning. The hemispherical asymmetry is discussed in respect to hemispherical specialization (right frontal lobe dominance in spatial visuomotor learning).

Contingent Negative Variation↗

Disconnection analysis of CA3 and DG in mediating encoding but not retrieval in a spatial maze learning task.

The dentate gyrus (DG) subregion of the hippocampus has been shown to be involved in encoding but not retrieval in a spatial maze task (modified Hebb-Williams maze). The first experiment in this study examined whether a lesion to the CA3 would contribute to a similar encoding deficit. A DG group was included in order to replicate previous results. Relative to controls, animals receiving CA3 lesions were impaired in encoding, not retrieval, on the modified Hebb-Williams maze--similar to a group that received DG lesions. This suggests the possibility that CA3 and DG are working together to mediate encoding processes. The second experiment in this study was designed to test the interaction between CA3 and DG using a disconnection paradigm. Animals with contralateral lesions (CA3 lesioned in one hemisphere, DG lesioned in the other hemisphere) showed a significant disruption effect on encoding, but not retrieval, when compared with animals with ipsilateral lesions (CA3 and DG lesioned in the same hemisphere, leaving the other hemisphere intact). This suggests an interaction between CA3 and DG in supporting encoding but not retrieval processes in a spatial maze learning task.

Animals↗

Effects of ketamine and 1-glutamic acid diethyl ester on concept learning in rats.

The effects of ketamine, an NMDA receptor antagonist, and 1-glutamic acid diethyl ester (LGDE), a non-NMDA glutamate antagonist, were evaluated in the acquisition of concept learning in a water maze. In concept learning, the rats must locate an invisible platform whose location changes from day to day. In spatial learning (Morris task), the rats must locate an invisible (or visible) platform whose location does not change. Ketamine increased quadrant entries at 5, 10 and 20 mg/kg, and latencies at 10 and 20 mg/kg on the final two days of training on the concept task. At 5 mg/kg ketamine disrupted concept learning but not spatial learning or visuo-motor coordination as assessed by invisible and visible platform conditions of the Morris maze. Progressively higher doses of ketamine affected first the invisible condition and then the visible platform condition. On the other hand, LGDE did not affect the Morris task at any dose. However, there was no decrease in latencies over days in concept learning at the two highest doses (240 and 360 mg/kg) of LGDE. Thus LGDE appeared to slow down decision time in the concept task but not the spatial task in the absence of an effect on quadrant entries in any version. These results indicate that NMDA receptors are involved in spatial and concept learning. Non-NMDA receptors appear to be involved only in concept learning.

Animals↗

A behavioural analysis of rats with damage to the medial prefrontal cortex using the Morris water maze: evidence for behavioural flexibility, but not for impaired spatial navigation.

In this study, the functional properties of the medial prefrontal cortex (mPFC) of the rat were examined in a task for spatial navigation. The dorsomedial (dmPFC) and ventromedial (vmPFC) parts of the PFC differ in their connectivity with the hippocampus, vmPFC being the main recipient of hippocampal input. Therefore, it is hypothesized that in a spatial task known to be particularly sensitive to hippocampal, but also to prefrontal cortical damage, especially vmPFC is committed to proper spatial learning and memory. Using the Morris water maze task, with an invisible platform, male rats with either partial (dmPFC or vmPFC) or whole (mPFC) bilateral lesions were subjected to various procedures reflecting spatial learning and memory, including a spatial reversal. Animals with dmPFC, vmPFC and mPFC lesions learned and remembered the spatial task equally well as their controls, regardless of the size or site of the bilateral lesion. However, when presented with a spatial reversal, animals with whole mPFC lesions were initially slower in locating the invisible platform than controls and animals with partial mPFC damage, but this effect was only short-lasting. When subsequently presented with a visible platform, all animals with partial (dmPFC or vmPFC) or whole mPFC damage needed significantly more time to locate the platform than the controls. This effect was transient and lasted longer in the animals with whole mPFC damage than in animals with partial damage. On the basis of these findings we conclude that an intact mPFC is not necessary for proper spatial learning and memory. The impairments in the reversal task and especially in the visually-cued task can best be explained as a diminished behavioural flexibility when a shift in task demands occurs. Since the degree of this impairment was related to the size of these lesions, but not to their sites, these differences are ascribed to a 'mass action' of medial prefrontal cortex lesions.

Animals↗

Adult neurological function following neonatal hypoxia-ischemia in a mouse model of the term neonate: water maze performance is dependent on separable cognitive and motor components.

BACKGROUND AND PURPOSE: Hypoxic-ischemic injury in term neonates remains a significant cause of long-term neurological morbidity. The post-natal day 10 (P10) mouse is accepted as a model for the term human. This study was designed to assess the relationships between the duration of hypoxia-ischemia (HI) on P10 and the structural and functional neurological deficits that appear in the adult mouse as a consequence. METHODS: Post-natal day 10 129T2xC57Bl/6 F1 hybrid mice were subjected to 0, 45, 60 or 75 min of hypoxia-ischemia using the Rice-Vannucci model. Beginning on P50 these mice were tested over the next 8 weeks using zero maze, locomotor activity, novel object recognition, cued, hidden and reduced Morris water mazes, delayed probe trials and response to apomorphine injection. Brain weights and histology were obtained at the end of testing. RESULTS: The degree of structural and behavioral abnormalities in adult mice correlated with the duration of hypoxia-ischemia on P10. Useful behavioral tests for separating adult mice according to duration of hypoxia-ischemia on P10 include locomotor activity, the Morris water mazes and response to apomorphine. We found cued "learning" persisted, although latencies increased, with increasing HI time while spatial learning decayed as a function of HI time. Severe HI injury involving the ventral hippocampus resulted in excessive locomotor activity. CONCLUSIONS: After correcting for motor deficits, there is evidence for persistence of "cued" learning but not spatial learning with increasing hypoxia-ischemia time on P10 in this model system.

Aging↗

Nitric oxide as a retrograde messenger during long-term potentiation in hippocampus.

Nitric oxide (NO) is widespread in the nervous system and is thought to play a role in a variety of different neuronal functions, including learning and memory (see other chapters, this volume). A number of behavioral studies have indicated that NO is involved in several types of learning such as motor learning (Yanagihara and Kondo, 1996), avoidance learning (Barati and Kopf, 1996; Myslivecek et al., 1996), olfactory learning (Okere et. al., 1996; Kendrick et al., 1997), and spatial learning (Holscher et al., 1995; Yamada et al., 1996) (for review of earlier papers see Hawkins, 1996). Moreover, NO is thought to be involved in neuronal plasticity contributing to these different types of learning in different brain areas including the cerebellum (chapter by R. Tsien, this volume) and hippocampus. In this chapter we review evidence on the role of NO in long-term potentiation (LTP), a type of synaptic plasticity in hippocampus that is believed to contribute to declarative forms of learning such as spatial learning.

Animals↗

Spatial localization in the Morris water maze in rats: acquisition is affected by intra-accumbens injections of the dopaminergic antagonist haloperidol.

Previous studies (G. E. Ploeger, B. M. Spruijt, & A. R. Cools, 1992) showed that low doses of systemically injected haloperidol affected spatial learning in the Morris water maze. This study investigated effects of intra-accumbens injections of haloperidol on spatial learning. To control for motivation and sensorimotor coordination, the researchers trained the rats to escape onto a visible platform. Low doses (50-100 ng) of haloperidol impaired spatial learning, whereas escaping on a visible platform was undisturbed. The 500-ng dose of haloperidol completely blocked acquisition because of combined learning and motor impairments. Retrieval of an acquired escape response was unaffected by 500 ng haloperidol. The data show that mesolimbic dopaminergic activity is involved in the acquisition of spatial localization. The results are related to studies demonstrating the involvement of the nucleus accumbens in cue-directed behaviors.

Animals↗

Spatial pattern learning in rats: control by an iterative pattern.

Rats searched in a matrix of vertical poles for food hidden on top of the poles. The only information available about the location of the food was the consistent spatial pattern of the baited poles, which was a checkerboard. This spatial pattern of hidden-food locations came to control the choices of poles made by the rats. The experiments ruled out the possibility that this control can be explained by the acquisition of simple response tendencies to move from pole to pole. Instead, this behavioral control of choices was attributed to the development of a representation of the checkerboard pattern of baited locations. Spatial pattern learning may have mechanisms in common with other forms of pattern learning.

Animals↗