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J Bachevalier

Publications and source records attributed to J Bachevalier.

At least 19 recordsLinked to original sources
PubMed1997

Neonatal ablations of the amygdala and inferior temporal cortex alter the vocal response to social separation in rhesus macaques.

Rhesus macaques that had received bilateral ablations to either the amygdala or area TE in inferior temporal cortex in the 1st week of life were briefly separated from familiar conspecifics at 10-14.5 months of age in order to assess the vocal response to this mild challenge. Sound spectrograms were subjected to quantitative analysis and compared with calls from normal, age-matched controls subjected to the same testing conditions. Animals with TE damage called at a higher rate than animals in the other two groups. TE subjects also produced more coos than controls. Males with TE lesions produced noisy calls at a higher rate than males of the other two groups. Females did not differ between groups in this measure. Analysis of the detailed acoustic structure of the 'coo' indicated significant differences in a measure of slope of the fundamental frequency (rate of frequency change over time) between amygdalectomized animals and those of the other 2 groups. The amygdalectomized monkeys produced calls with lower slope values, giving the calls a less inflected quality both in sonagrams and to the listener. These findings suggest an important role for the amygdala and inferior temporal cortex in regulating the vocal response to social separation during development.

Amygdala↗
PubMed1997

Thalamic and temporal cortex input to medial prefrontal cortex in rhesus monkeys.

To determine the source of thalamic input to the medial aspect of the prefrontal cortex, we injected retrograde tracers (wheat germ agglutinin conjugated to horseradish peroxidase, nuclear yellow, and/or bisbenzimide) into seven medial prefrontal sites and anterograde tracers (tritiated amino acids) into six thalamic sites, in a total of nine rhesus monkeys. The results indicated that ventral precallosal and subcallosal areas 14 and 25, and the ventral, subcallosal part of area 32, all receive projections from the mediodorsal portion of the magnocellular division of the medial dorsal nucleus (MDmc). The dorsal, precallosal part of area 32 receives projections mainly from the dorsal portion of the parvocellular division of the medial dorsal nucleus (MDpc), which also provides some input to area 14. Polar area 10 receives input from both MDpc and the densocellular division of the medial dorsal nucleus (MDdc), as does supracallosal area 24. Area 24 receives additional input from the anterior medial nucleus and midline nuclei. All medial prefrontal cortical areas were also found to receive projections from a number of cortical regions within the temporal lobe, such as the temporal pole, superior temporal gyrus, and parahippocampal gyrus. Areas 24, 25, and 32 receive, in addition, input from the entorhinal cortex. Combining these results with prior anatomical and behavioral data, we conclude that medial temporal areas that are important for object recognition memory send information directly both to dorsal medial prefrontal areas 24 and 32 and to ventral medial prefrontal areas 14 and 25. Only the latter two areas have additional access to this information via projections from the mediodorsal part of MDmc.

Animals↗
PubMed1997

Effects of orbital frontal and anterior cingulate lesions on object and spatial memory in rhesus monkeys.

Object memory processes, evaluated in rhesus monkeys by delayed nonmatching-to-sample with trial-unique stimuli and object reversal learning, were more severely impaired by orbital frontal than by anterior cingulate lesions. Spatial memory processes, assessed by spatial delayed response and spatial reversal learning, showed a weak trend in the opposite direction, though on these tasks neither lesion produced a serious loss. Comparison of the present results with those of earlier studies on the effects of various limbic system lesions suggests that object memory processes, including object recognition and object-reward association, are served by a circuit consisting mainly of the rhinal cortex, orbitofrontal cortex, and the magnocellular division of the medial dorsal thalamic nucleus. Although both the rhinal and orbitofrontal components of this circuit appear to participate in both functions, evidence from the present and earlier studies suggests that the orbitofrontal component is the more important one for associative memory, i.e. the formation across trials of associations between particular objects or classes of objects and reward, whereas the rhinal component is the more critical one for recognition memory, i.e. the storage and retrieval within trials of the representations of particular objects.

Animals↗
PubMed1997

Altered development of prefrontal neurons in rhesus monkeys with neonatal mesial temporo-limbic lesions: a proton magnetic resonance spectroscopic imaging study.

Focal brain damage occurring early in development can have widespread repercussions throughout the developing brain. In living adult rhesus monkeys, we studied the long-term effects of early mesial temporo-limbic (MTL) lesions on prefrontal cortex (PFC) neurons using proton magnetic resonance spectroscopic imaging (1H-MRSI), an in vivo neurochemical assay technique for measuring signals from metabolites such as N-acetyl-aspartate (NAA, a neuronal marker), choline-containing compounds (CHO) and creatine + phosphocreatine (CRE). Six monkeys (NL) had undergone surgical ablation of MTL structures within 3 weeks of birth, six monkeys received the same lesion at approximately 5 years of age and six monkeys were normal controls. We found significant bilateral reductions of NAA relative signals exclusively in the PFC of the NL group in comparison with either of the other groups. Our results indicate that neonatal MTL damage specifically affects PFC neurons of adult monkeys as indicated by a reduction of NAA. The basis of this effect involves developmental processes as implicated by two arguments: analogous damage during adulthood does not have the same effect; NAA in the healthy brain increases during development. This finding may have implications for understanding developmental aspects of prefrontal-temporolimbic connectivity, and the reduction of NAA levels observed in prefrontal cortex of patients with schizophrenia.

Aging↗
PubMed1996

Cerebral ischemia: are the memory deficits associated with hippocampal cell loss?

The long-standing notion that damage restricted to the hippocampal formation is sufficient to produce a significant global memory deficit derives from clinical data. Specifically, it is based on the observation that transient global ischemia, which leads to partial cell loss within the hippocampal formation but not in other brain areas important for memory, can produce global amnesia in humans. This view is, however, challenged by a number of experimental findings. First, in both monkeys and rats, there is evidence that ischemia disrupts delayed object recognition, a memory process found to be largely intact following selective hippocampal lesions. These findings indicate that damage confined to the hippocampal formation cannot account for all aspects of the ischemia-induced memory impairments. Second, although some groups of hippocampal neurons are the most prone to degeneration following ischemia, a wide array of extra-hippocampal damage has been observed in all species, for which the precise extent and distribution may well be underestimated by conventional histological evaluations of ischemic brains. Partial neuronal degeneration reported in regions such as the rhinal areas, medial dorsal thalamic nucleus, or cingulate cortex may contribute to varying degrees to ischemia-induced memory deficits. Third, experimental studies have failed to generate a general consensus on the correlation between extent of hippocampal cell loss and memory performance. In sum, the experimental studies do not, as yet, support the view that hippocampal damage is solely responsible for ischemia-induced memory deficits. Rather, they suggest that both the intra- and extra-hippocampal damage contribute to the pattern of memory impairments observed following ischemia. Consequently, although animals with global and focal ischemia represent valuable models for neuropathological and therapeutic studies, they may not be so useful in assessing the role of the hippocampal formation and its sub-components in memory processes.

Animals↗
PubMed1996

Children's performance on "animal tests" of oddity: implications for cognitive processes required for tests of oddity and delayed nonmatch to sample.

To investigate the ontogenesis of oddity learning, children (16 to 102 months of age) and adults were tested on two versions of the oddity task using non-verbal procedures originally developed for monkeys. On the standard, "one-part" or "simultaneous" oddity task (Experiment 1), young children (16 to 74 months of age) performed more poorly than older children (81-102 months of age) who were as proficient as adults. The delayed mastery of one-part oddity contrasts to mastery, at much younger ages (3 to 4 years of age) of a similar, but two-part task, delayed non-match to sample (DNMS) (Overman, 1990). In Experiment 2, those children from the first experiment who had difficulty in learning the one-part oddity task were tested on a two-part oddity task, and a subset of the subjects was retested on the one-part oddity task, and, finally, given verbal instructions for the one-part oddity task. The two-part oddity task was mastered significantly more rapidly than the previous one-part task; however, children's performance dropped significantly when tested on the one-part oddity task, and finally, children rapidly mastered the one-part oddity task when given verbal instructions. The data suggested that (a) children used different strategies to solve the different versions of the oddity task, (b) the solution for the two-part-task appeared earlier in life than the solution for the one-part task and did not involve the use of the concept of "oddity relations", and (c) in tasks in which stimuli are shown twice, behavior may come under control of the absolute properties of the exemplar stimulus via a simple "win-shift" pattern of behavior. In contrast, in tasks in which all stimuli are presented simultaneously, behavior may be controlled by stimulus relations, the analysis of which has a protracted ontogenetic development.

Adult↗
PubMed1996

Cognitive gender differences in very young children parallel biologically based cognitive gender differences in monkeys.

Infant humans were trained on 2 cognitive tests that have previously revealed, in infant monkeys, a double dissociation that was reversible by perinatal manipulations of androgens and ablations of specific brain sites. Children showed the same sex-linked behavior found with infant monkeys: young boys were superior on the object reversal task and young girls were superior on the concurrent discrimination task. As happened previously with infant monkeys, the gender difference was not apparent in older human subjects. Thus, early in ontogeny, cognitive gender differences have now been discovered in both humans and monkeys, probably a result of gender differences in androgens that influence the maturation rate of specific brain systems.

Adolescent↗
PubMed1996

Effects of rhinal cortex lesions combined with hippocampectomy on visual recognition memory in rhesus monkeys.

1. We assessed the visual recognition abilities, as measured by delayed nonmatching-to-sample with trial-unique objects, of rhesus monkeys with hippocampectomy (i.e., removal of the hippocampal formation plus parahippocampal gyrus) combined with ablations of the rhinal cortex (i.e., entorhinal cortex plus perirhinal cortex). 2. Relative to unoperated controls, monkeys with combined hippocampectomy and rhinal cortex ablation (H+Rh) were significantly impaired in visual recognition. 3. Comparison of the scores of the monkeys in the present H+Rh group, which sustained near-complete rhinal cortex damage, with the scores of monkeys in an earlier H+Rh group in which the rostral part of the rhinal cortex had been spared indicates that the magnitude of the impairment is greater in the group with the more complete rhinal cortex damage. This finding is consistent with the idea that the rhinal cortex is critical for visual recognition. 4. Comparison of the present results with those from an earlier study on visual recognition that employed lesions limited to the rhinal cortex (Rh group) shows, paradoxically, that adding removal of the hippocampal formation and parahippocampal gyrus to a rhinal cortex lesion significantly reduces the recognition impairment produced by rhinal cortex lesions alone. 5. Our findings do not fit the view that the hippocampal formation, parahippocampal gyrus, and rhinal cortex constitute parts of a single functional system, such that the greater the damage to the entire system, the more severe the impairment. Instead, the results are consistent with the view that there are multiple functional subdivisions within the medial temporal lobe.

Animals↗
PubMed1996

Neonatal insult to the hippocampal region and schizophrenia: a review and a putative animal model.

OBJECTIVE: To review the mounting evidence implicating early hippocampal dysfunction in the pathogenesis and the pathophysiology of schizophrenia. An account is made of recent neurodevelopmental hypotheses indicating how an early dysfunction of the hippocampal region disrupts maturational events in brain systems connected to that structure, thus inducing dysfunctional connectional development. Finally, an animal model is presented. METHOD: Socioemotional behaviour of monkeys (Macaca mulatta) with selective neonatal hippocampal lesions was assessed by analyzing their interactions with their age-matched controls at 2 months, 6 months, and 5 to 8 years of age and by comparing the social interactions at each age with those of normal controls paired together. RESULTS: At 2 months of age, monkeys with neonatal hippocampal lesions presented minor disturbances in initiation of social interactions. These subtle changes of behaviour were less evident at 6 months, although by that age, the operated monkeys displayed more withdrawals in response to an increase in aggressive responses from their unoperated peers. In adulthood, the amount of time spent by the hippocampectomized monkeys in social contacts with their normal peers decreased markedly. In addition, operated monkeys exhibited more locomotor stereotypies than normal controls. CONCLUSION: These experimental findings indicate that the time-course and nature of the behavioural disturbances resulting from early trauma to the hippocampal region have some similarities with the clinical symptoms of schizophrenic patients and the typical time-course of the disease.

Animals↗
PubMed1995

Stereotypies and loss of social affiliation after early hippocampectomy in primates.

The present study was aimed at determining whether early hippocampal damage alters the development of normal social interactions. Results showed that, at 2 months of age, animals with neonatal hippocampal lesions presented minor disturbances in initiation of social interactions. These subtle changes in behavior were less evident at 6 months, although at this age, the operated animals displayed more withdrawals in response to an increase in aggressive responses from their unoperated peers. Finally, in adulthood, the amount of time spent by the operated monkeys in social contacts with their normal peers was markedly less than that in normal dyads. Only in adulthood did the operated animals exhibit more locomotor stereotypies than normal controls. This finding suggest that the hippocampal formation may directly or indirectly affect the maintenance of social bounds in primates.

Animals↗
PubMed1995

Transient subcortical connections of inferior temporal areas TE and TEO in infant macaque monkeys.

As part of a long-term study designed to examine the ontogeny of visual memory in monkeys and its underlying neural circuitry, we have examined the subcortical connections of the inferior temporal cortex in infant monkeys and compared them to those previously described in adult monkeys (Webster et al. [1993] J. Comp. Neurol. 335:73-91). Inferior temporal areas TEO and TE were injected with wheat germ agglutinin conjugated to horseradish peroxidase and tritiated amino acids, respectively, or vice versa, in 1-week-old (N = 6) and 3-4-year-old (N = 6) Macaca mulatta, and the distributions of labeled cells and terminals were examined in subcortical structures. Although the connections of inferior temporal cortex with subcortical structures were found to be similar in infant and adult monkeys, several projections appear to undergo refinement during development. Quantitative analysis showed that 1) whereas the projection from TE to the superior colliculus is consistent (5 of 5 cases) and widespread in infants, it is less reliable (2 of 7 cases) and limited in areal extent in adults; 2) although the projections from TE to nucleus medialis dorsalis and the tail of the caudate are present in infants and adults, they are reduced in adults; and 3) TEO receives input from the dorsal lateral geniculate nucleus in both infants and adults, but the number of cells giving rise to this projection is lower in adults. There was also a suggestion that TE projects to nucleus paracentralis in infants (2 of 5 cases) but not in adults (0 of 7 cases). No differences between infants and adults were apparent in other subcortical connections, including those with the pulvinar, reticular nucleus, claustrum, and putamen.

Animals↗
PubMed1995

Long-term effects of selective neonatal temporal lobe lesions on learning and memory in monkeys.

Rhesus monkeys with neonatal damage to either the medial temporal lobe or the inferior temporal cortical area TE, and their normal controls, were reassessed in visual habit formation (24-hour intertrial interval task) and visual recognition (delayed nonmatching to sample; DNMS) at 4-5 years of age and then tested on tactile and spatial DNMS. Results on the two visual tasks were the same as those obtained when the monkeys were under 1 year of age. Specifically, early medial temporal lesions, like late lesions, left habit formation intact but severely impaired recognition memory. Furthermore, the memory deficit extended to the tactile and spatial modalities. By contrast, early damage to TE, unlike late damage to it, yielded only mild deficits on both visual tasks and had no effect on tactile or spatial DNMS. Compensatory mechanisms that promote substantial and permanent recovery thus appear to be available after neonatal TE lesions but not after neonatal medial temporal lesions.

Animals↗
PubMed1995

Development and plasticity of the neural circuitry underlying visual recognition memory.

In adult monkeys, visual recognition memory, as measured by the delayed nonmatching to sample (DNMS) task, requires the interaction between inferior temporal cortical area TE and medial temporal lobe structures (mainly the entorhinal and perirhinal cortical areas). Ontogenetically, monkeys do not perform at adult levels of proficiency on the DNMS task until 2 years of age. Recent studies have demonstrated that this protracted development of visual recognition memory is due to an immaturity of the association areas of the neocortex rather than the medial temporal lobe. For example, lesions of the medial temporal lobe structures in infancy or in adulthood yield profound and permanent visual recognition loss, indicating that the medial temporal lobe structures operate early in life to sustain visual memory. In contrast, early lesions of area TE, unlike late lesions, result in a significant and long-lasting sparing of visual memory ability. Further evidence for neocortical immaturity is provided by studies of the development of opiatergic and cholinergic receptors, of the maturation of metabolic activity, and of the connectivity between inferior temporal areas TE and TEO and cortical and subcortical structures. Together these results indicate greater compensatory potential after neonatal cortical than after neonatal medial temporal removals. In support of this view, early damage to area TE leads to the maintenance of normally transient projections as well as to reorganization in cortical areas outside the temporal lobe. In addition, lesion studies indicate that, during infancy, visual recognition functions are widely distributed throughout many visual association areas but, with maturation, these functions become localized to area TE. Thus, the maintenance of exuberant projections together with reorganization in other cortical areas of the brain could account for the preservation of visual memories in monkeys that have had area TE removed in infancy.

Animals↗
PubMed1994

Medial temporal lobe structures and autism: a review of clinical and experimental findings.

Although substantive understanding of brain dysfunction in autism remains meager, clinical evidence as well as animal brain research on the effects of early damage to selective brain system have now yielded enough knowledge that some provisional hypotheses concerning the etiology of autism can be generated. Basically, the underlying premise of this review is that a major dysfunction of the autistic brain resides in neural mechanisms of the structures in the medial temporal lobe, and, perhaps, more specifically the amygdaloid complex. This review begins with a summary of clinical evidence of the involvement of the medial temporal lobe structures in autism. The major behavioral disturbances seen in monkeys that had received neonatal lesions of the medial temporal lobe structures are then described. From this survey it can be seen that distinct patterns of memory losses and socioemotional abnormalities emerge as a result of extent of damage to the medial temporal lobe structures. The potential value of the experimental findings for an understanding of neural dysfunction in autism as well as directions of future research are discussed in the final section of the review.

Animals↗
PubMed1994

Effects of selective neonatal temporal lobe lesions on visual recognition memory in rhesus monkeys.

Ten-month-old infant monkeys that had received neonatal ablations of either inferior temporal cortex (area TE) or the medial temporal region were compared with age-matched normal infant monkeys in visual delayed nonmatching-to-sample with trial-unique objects. Both types of early damage caused impairment in visual recognition, but the degree of deficit after early area TE lesions differed sharply from that after early medial temporal removals. Thus, whereas early medial temporal damage yielded a marked decline in visual recognition when the delays and lists were gradually increased, early area TE damage yielded normal recognition up to a delay of 60 sec and only mild impairment at longer delays and lists. The data indicate that, unlike adult monkeys, which suffer severe and nearly equivalent losses in visual object recognition after both types of ablation, the infant monkeys' recognition ability is largely spared after early damage to area TE but not after early damage to the medial temporal lobe. Together with recent clinical reports of profound memory loss in children with early dysfunction of the medial temporal region, the present findings demonstrate that medial temporal lobe structures operate early to sustain visual recognition memory, and recovery from early damage is limited at best. Early damage to higher-order visual cortex, however, can be largely compensated, presumably by one or more of the visual cortical areas that were left intact.

Animals↗
PubMed1993

Subcortical connections of inferior temporal areas TE and TEO in macaque monkeys.

To investigate the subcortical connections of inferior temporal cortex, we injected its anterior and posterior portions (Bonin and Bailey's cytoarchitectonic areas TE and TEO, respectively) in 6 rhesus monkeys with retrograde and anterograde tracers. The results indicate that both areas TE and TEO receive nonreciprocal inputs from several thalamic nuclei, including paracentralis, ventralis anterior, centralis, and limitans, and that TE also receives input from reuniens. Additional nonreciprocal inputs to both areas arise from the hypothalamus, basal nucleus of Meynert, dorsal and median raphe, locus coeruleus, and reticular formation. TE and TEO are reciprocally connected with the lateral, medial, and inferior nuclei of the pulvinar and with the ventral portion of the claustrum. The main subcortical nonreciprocal output from TE and TEO is to the striatum and from TEO to the superior colliculus. TE also sends a very limited projection to nucleus medialis dorsalis magnocellularis of the thalamus. Although the connections of areas TE and TEO are overlapping in most subcortical structures, they are partially segregated in the pulvinar, the reticular nucleus of the thalamus, and the striatum. Specifically, relative to those of TE, the projections of TEO are located more laterally in the medial, lateral, and inferior nuclei of the pulvinar, more ventrally in the reticular nucleus, and more caudally in both the ventral putamen and tail and head of the caudate nucleus.

Animals↗