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PubMed2001

GABA transporter-1 mRNA in the prefrontal cortex in schizophrenia: decreased expression in a subset of neurons.

OBJECTIVE: Within the prefrontal cortex of schizophrenic subjects, alterations in markers of gamma-aminobutyric acid (GABA) neurotransmission, including decreased immunoreactivity for the GABA membrane transporter GAT-1, may be most prominent in a subset of inhibitory neurons. In the present study, the authors sought to determine whether the alterations in GAT-1 protein could be attributed to a reduction in GAT-1 mRNA expression. METHOD: Tissue sections containing prefrontal cortex area 9 from 10 matched pairs of schizophrenic and comparison subjects were processed for in situ hybridization histochemistry with (35)S-oligonucleotide probes for GAT-1 mRNA. RESULTS: In the schizophrenic subjects, the relative density of labeled neurons was 21%-33% lower in layers 1-5 of the prefrontal cortex but was unchanged in layer 6. In contrast, cellular levels of GAT-1 mRNA expression, as reflected in grain density per labeled neuron, did not differ by more than 11% between subject groups in any layer. These findings indicate that GAT-1 mRNA expression is relatively unaltered in the majority of prefrontal cortex GABA neurons in schizophrenic subjects but is reduced below a detectable level in a subset of GABA neurons. Furthermore, the magnitude and laminar pattern of these results were strikingly similar to those found in a previous study of mRNA expression for the synthesizing enzyme of GABA, glutamic acid decarboxylase(67), in the same subjects. CONCLUSIONS: Both GABA synthesis and reuptake appear to be altered at the level of gene expression in a subset of GABA neurons, and the resulting changes in GABA neurotransmission may contribute to prefrontal cortex dysfunction in schizophrenia.

Adult↗
PubMed1997

Temporal dynamics of glutamate efflux in the prefrontal cortex and in the hippocampus following repeated stress: effects of pretreatment with saline or diazepam.

Acute stress has been associated with activation of glutamate efflux in forebrain structures. The present study sought to characterize the extracellular dynamics of glutamate in response to acute and repeated stress in the prefrontal cortex and hippocampus in rats. One-minute sampling of extracellular glutamate levels was performed during repeated tail-pinch stress. Animals were stressed three times, beginning at approximately 10.30 a.m. and continuing at 2.5-h intervals. In the prefrontal cortex, the initial 10-min tail pinch produced a robust increase in extracellular levels of glutamate. This increase was apparent immediately (i.e. 1 min) after the start of the stress procedure. The second tail pinch produced a smaller increase in glutamate levels while the third tail pinch did not significantly increase these levels. In the hippocampus, the initial stress response was smaller in magnitude than that observed in the prefrontal cortex. Furthermore, responses to subsequent tail pinches were similar to that seen following the first tail pinch. Treatment with diazepam (3 mg/kg/i.p.) 30 min before the first stress session abolished the stress response in the prefrontal cortex and hippocampus. However, in the prefrontal cortex, the second tail pinch (performed approximately 3 h after diazepam administration) produced a robust increase in glutamate efflux. In contrast, in the hippocampus of diazepam-treated rats, the second tail pinch produced a small delayed response. Pretreatment with saline resulted in non-significant responses to all three tail pinches in the prefrontal cortex. The present study suggests that: (i) stress produces a rapid increase in glutamate efflux in the prefrontal cortex and hippocampus, (ii) repeated stress reveals tolerance in the glutamatergic response in the prefrontal cortex, (iii) saline and diazepam pretreatment reduce the stress-induced efflux of glutamate in the prefrontal cortex, and (iv) exposure to diazepam may prevent the prefrontal cortex from adapting its response to the subsequent stressor. These finding are consistent with the role of the prefrontal cortex as a region which may regulate reactions to aversive stimuli.

Animals↗
PubMed1996

Mianserin markedly and selectively increases extracellular dopamine in the prefrontal cortex as compared to the nucleus accumbens of the rat.

The atypical antidepressant mianserin, administered at doses of 1, 5 and 10 mg/kg SC, dose-dependently increased up to about 6 times extracellular dopamine in the medial prefrontal cortex of the rat, as estimated by vertical concentric microdialysis probes. Mianserin failed to modify extracellular dopamine in the nucleus accumbens. Mianserin also dose-dependently increased extracellular noradrenaline in the prefrontal cortex. Yohimbine, an alpha2 antagonist, increased extracellular dopamine in the prefrontal cortex but the maximal increase was lower than that elicited by mianserin. Yohimbine also increased extracellular noradrenaline in the prefrontal cortex, but to a lesser extent than dopamine. Clonidine, an alpha2 antagonist, decreased extracellular dopamine and noradrenaline in the prefrontal cortex but failed to affect extracellular dopamine in the nucleus accumbens. Ritanserin, a 5HT2 antagonist, at doses of 1.0 mg/kg, failed to increase extracellular dopamine in the prefrontal cortex, but significantly potentiated the increase in extracellular noradrenaline due to yohimbine. Ritanserin failed to potentiate the increase in extracellular noradrenaline elicited by yohimbine in the prefrontal cortex. The results are interpreted to indicate that mianserin increases extracellular DA as a result of the concurrent blockade of alpha2 and 5HT2 receptors. Failure to affect extracellular dopamine in the nucleus accumbens is explained as due to the lack of a significant effect of alpha2 and 5HT2 tone on DA release in the nucleus accumbens as compared to the prefrontal cortex. The results are consistent with the postulated relationship between antidepressant drug action and the ability to increase extracellular dopamine in the prefrontal cortex.

Animals↗
PubMed1999

Picrotoxin in the medial prefrontal cortex impairs sensorimotor gating in rats: reversal by haloperidol.

RATIONALE: Neuropathological data indicate a GABAergic dysfunction in the prefrontal cortex and hippocampus of schizophrenics. On this basis, the construct validity of an animal model of schizophrenia was tested. OBJECTIVE: This study assessed prepulse inhibition (PPI) of startle in rats after injections of the GABA antagonist picrotoxin into the prefrontal cortex and the ventral hippocampus. It was also tested if reductions in PPI are reversed by the dopamine antagonist haloperidol. PPI is a measure of sensorimotor gating and is impaired in schizophrenia patients. The hypothesis underlying this study was that blockade of prefrontocortical and hippocampal GABA receptors disrupts PPI in a dopamine-dependent way. This hypothesis was based on neuropathological data from schizophrenics indicating a loss of GABAergic neurons in the prefrontal cortex and hippocampus and on the observation that PPI is reduced in schizophrenics. METHODS: Picrotoxin (0, 5, 10 ng/0.5 microl) was infused through chronically indwelling cannulae into the medial prefrontal cortex (mPFC), into the lateral prefrontal cortex and into the ventral hippocampus. The effect on PPI was measured directly after picrotoxin infusion. The neuroleptic compound haloperidol (0.1 mg/kg) was administered intraperitoneally 30 min before testing. RESULTS: Picrotoxin in the mPFC dose-dependently reduced PPI and this effect was antagonized by systemic pretreatment with the dopamine antagonist haloperidol. No significant effects on PPI were observed after picrotoxin infusions into the lateral prefrontal cortex or into the ventral hippocampus. CONCLUSIONS: These findings indicate that acute blockade of GABA receptors in the mPFC impairs sensorimotor gating in a dopamine-dependent manner. Since PPI in rats has been shown to possess face, predictive, and construct validity as an animal model for some psychotic symptoms, we discuss the potential relevance of our findings for the pathophysiology of schizophrenia.

Animals↗
PubMed2003

Antipsychotic drug interactions with specific [3H]ketanserin binding sites in membrane fragments derived from human prefrontal cortex and human amygdala.

Two regions of the brain potentially significant for psychopathology in schizophrenia are the prefrontal cortex and the amygdala. Antipsychotic compounds bind at serotonin receptors in human prefrontal cortex. We hypothesized that the serotoninergic antagonist [3H]ketanserin would label similar sets of binding sites in these two brain regions. Further, we hypothesized that all antipsychotic compounds would show appreciable affinity for binding sites labeled by [3H]ketanserin in the prefrontal cortex. Our findings indicate some differences in [3H]ketanserin binding between prefrontal cortex and amygdala. We also observed that several antipsychotic compounds had very high affinity for the [3H]ketanserin binding sites in prefrontal cortex.

Amygdala↗
PubMed1999

Association of storage and processing functions in the dorsolateral prefrontal cortex of the nonhuman primate.

The prominent role of the prefrontal cortex (PFC) in working memory (WM) is widely acknowledged both in nonhuman primates and in humans. However, less agreement exists on the issue of functional segregation within different subregions of the PFC with regard to the domains of spatial and nonspatial processing or involvement in simpler versus more complex aspects of WM, e.g., maintenance versus processing function. To address these issues, six monkeys were trained to perform four WM tasks that differed with respect to domain (spatial vs nonspatial) and level of WM demand (recall of one vs three items). The delayed response format was used to assess simple one-item memory, whereas self-ordering tasks were used to require the monkey to maintain and organize three items of information within WM. After training, the monkeys received bilateral PFC lesions in one of two different areas, Walker's areas 9 and 8B (dorsomedial convexity; n = 3) or areas 46 and 8A (dorsolateral cortex, n = 3) and then tested postoperatively on all tasks. Monkeys with lesions of the dorsomedial convexity were not impaired either on spatial or nonspatial WM tasks, whether the task required simple storage or sequential processing. By contrast, lesions of the dorsolateral cortex produced a significant and persistent impairment in both simple and complex spatial WM but no impairment in the two nonspatial WM tasks. These results support a functional segregation within the dorsolateral prefrontal cortex for WM: the dorsolateral prefrontal cortex (area 46/8A) is selectively involved in spatial WM, whereas the dorsomedial convexity (area 9/8B) is not critically engaged in either spatial or nonspatial working memory. Furthermore, the specific involvement of area 46/8A in spatial sequencing as well as in single-item storage WM tasks supports, in the nonhuman primate, an areal dissociation based on domain rather than on processing demand.

Animals↗
PubMed2001

The noradrenaline-dopamine interaction in the rat medial prefrontal cortex studied by multi-probe microdialysis.

Multi-probe microdialysis was used to investigate the interaction between the release of noradrenaline and dopamine in the medial prefrontal cortex. Retrograde microdialysis was used to stimulate or inhibit the activity of the locus coeruleus for a restricted period of time, and the response of extracellular noradrenaline and dopamine in the ipsilateral and contralateral medial prefrontal cortex was recorded with microdialysis probes. Infusion of clonidine into the locus coeruleus (100 microM for 45 min) suppressed noradrenaline release and slightly inhibited dopamine release in the ipsilateral medial prefrontal cortex. Application of carbachol to the locus coeruleus (100 microM for 45 min) stimulated both the noradrenaline and dopamine release in the ipsilateral medial prefrontal cortex. No changes were seen in the contralateral medial prefrontal cortex. In the ipsilateral nucleus accumbens, extracellular noradrenaline levels increased, but dopamine levels remained unchanged. Application to the locus coeruleus (during 10 min) of the glutamate receptor agonists N-methyl-D-aspartate (NMDA) (300 microM) or kainate (100 microM) strongly increased extracellular noradrenaline and dopamine levels in the ipsilateral medial prefrontal cortex. However, in the contralateral probe the release of dopamine (but not of noradrenaline) was also stimulated. Application of carbachol to the locus coeruleus was used as a model to further investigate the presumed noradrenaline-dopamine interaction. In a series of dual-probe experiments, alpha(1)-, alpha(2)-, and beta-adrenoceptor antagonists (prazosin, idazoxan, propranolol) or a reuptake-inhibitor (nomifensine) was administered during carbachol stimulation of the locus coeruleus. Prazosin and propranolol were administered systemically in a dose of 3 mg/kg, whereas idazoxan (10 microM) and nomifensine (100 microM) were infused into the medial prefrontal cortex. However, none of these pretreatments modified the effects of the control carbachol-infusions. The results did not identify a receptor-interaction or a common reuptake site that explained the presumed interaction between dopamine and noradrenaline in the medial prefrontal cortex. Therefore, the noradrenaline-dopamine interaction hypothesis could not be confirmed or refuted.

Adrenergic beta-Antagonists↗
PubMed1992

The catecholaminergic innervation of primate prefrontal cortex.

This paper reviews recent studies indicating that the marked expansion and differentiation of the prefrontal cortex in primates is associated with an increase in the complexity of both the regional density and laminar distribution of catecholaminergic afferents. The innervation patterns of these systems in monkey prefrontal cortex appear to accurately predict those in human prefrontal cortex, suggesting that studies in non-human primates may be reasonably used to generate hypotheses about the nature of involvement of these systems in disorders such as schizophrenia. In addition, the distinctive developmental pattern of the dopaminergic innervation of primate prefrontal cortex and the possibility of an intrinsic catecholaminergic innervation of primate prefrontal cortex may reveal new avenues of investigation into the roles of prefrontal catecholamines in both normal and pathological states.

Afferent Pathways↗
PubMed2001

Antipsychotic drugs classified by their effects on the release of dopamine and noradrenaline in the prefrontal cortex and striatum.

Dose-effect curves were established for the effects of the antipsychotic drugs haloperidol, clozapine, olanzapine, risperidone and ziprasidone on extracellular levels of dopamine and noradrenaline in the medial prefrontal cortex, and of dopamine in the striatum. Haloperidol was more effective in stimulating the release of dopamine in the striatum, whereas clozapine was much more effective in the medial prefrontal cortex. The efficacy of risperidone, olanzapine and ziprasidone did not differ for the two brain areas. The benzamides sulpiride and raclopride increased dopamine release in the striatum but did not affect the release of dopamine and noradrenaline in the medial prefrontal cortex. In the presence of dopamine/noradrenaline reuptake inhibitors, the benzamides strongly increased the release of dopamine-but not of noradrenaline-in the medial prefrontal cortex. The 5-HT(2) receptor antagonist R-(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl]-4-piperidinemethanol (MDL100,907) (800 nmol/kg) and the dopamine D(2) receptor antagonist raclopride (2 micromol/kg) displayed a clear synergism in increasing the release of dopamine in the medial prefrontal cortex. No such synergism was seen in the case of noradrenaline. Co-administration of the 5-HT(2) receptor agonist (+/-)-2,5-dimethoxy-4-iodoamphetamine HCl (DOI) (850 nmol/kg) with clozapine (10 micromol/kg) or haloperidol (800 nmol/kg) blocked the increase in dopamine as well as noradrenaline in the medial prefrontal cortex. It is concluded that typical and non-benzamide atypical antipsychotics increase extracellular dopamine in the medial prefrontal cortex via a synergistic interaction by blocking 5-HT(2) as well as dopamine D(2) receptors. The increase in extracellular noradrenaline in the medial prefrontal cortex that was observed after administration of antipsychotics is explained by inhibition of 5-HT(2) receptors and not dopamine D(2) receptors. Finally, the significance of the classification of antipsychotic drugs based on their selective action on the release of dopamine and noradrenaline in the medial prefrontal cortex is discussed. In particular, the position of the benzamides is discussed.

Animals↗
PubMed2004

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors.

To address the role of D1 receptors in the medial prefrontal cortex, we combined pharmacological and genetic manipulations to examine long-term synaptic potentiation (LTP)/long-term synaptic depression (LTD) in brain slices of rats and mice. We found that the D1 antagonist SCH23390 selectively blocked the maintenance but not the induction of LTP in the prefrontal cortex. Conversely, activation of D1 receptors facilitated the maintenance of LTP, and this effect is impaired in heterozygous D1 receptor knockout mice. Low-frequency stimulation induced a transient depression in the medial prefrontal cortex. This depression could be transformed into LTD by coapplication of dopamine. Coapplication of dopamine, however, shows no facilitating effect on LTD in heterozygous D1 receptor knockout mice. These results provide pharmacological and genetic evidence for a role of D1 receptors in the bidirectional modulation of synaptic plasticity in the medial prefrontal cortex. The absence of this modulation in heterozygous knockout mice shows that a dysregulation of dopamine receptor expression levels can have dramatic effects on synaptic plasticity in the prefrontal cortex.

Animals↗
PubMed1986

Contribution of noradrenergic neurons to the regulation of dopaminergic (D1) receptor denervation supersensitivity in rat prefrontal cortex.

3,4-Dihydroxyphenylethylamine (DA, dopamine) levels in the rat prefrontal cortex were selectively decreased by 52%, leaving noradrenaline (NA) levels unaffected, 4 weeks following restricted bilateral electrolytic lesions of the ventral mesencephalic tegmentum (VMT). These lesions also induced a significant increase in DA-sensitive, but not isoproterenol-sensitive, adenylate cyclase activity in tissue homogenates (+38%). We had shown previously that chemical (6-hydroxydopamine, 6-OHDA) lesions of the VMT destroy both ascending DA and NA fibers but do not alter the D1-receptor density in the prefrontal cortex. In this study, electrolytic lesions of the VMT were combined with bilateral injections of 6-OHDA made laterally in the pedunculus cerebellaris superior to assess the role of NA fibers in the development of D1-receptor supersensitivity. This combined treatment produces a large decrease of cortical NA levels (-95%), an increase in beta-adrenergic-sensitive adenylate cyclase activity (+110%), and a decrease in DA levels (-60%), but does not alter D1-receptor density in the prefrontal cortex. These results indicate that the development of D1-receptor supersensitivity in the prefrontal cortex following electrolytic lesion of the VMT depends on the presence of an intact NA innervation.

Adenylyl Cyclases↗
PubMed1997

Morphometric methods for studying the prefrontal cortex in suicide victims and psychiatric patients.

Neurochemical studies demonstrate altered numbers of monoaminergic receptors in the prefrontal cortex in suicide and depression victims, implicating dysfunction of the prefrontal cortex in the neuropathology of suicide and psychiatric disorders. Neuroimaging studies in vivo have revealed an altered pattern of cortical metabolism and reductions in frontal lobe volume in patients with schizophrenia (SCZ) or depression. However, the precise morphopathology underlying these abnormalities and their relevance to suicide are unknown. Our recent three-dimensional cell counting of dorsolateral prefrontal cortex from 16 postmortem SCZ brains (10 suicide completers) revealed cellular changes (increased neuronal density, and reduced laminar width and neuronal size) that may be associated with neuroimaging observations. Evaluation of the same morphometric parameters in the prefrontal cortex in seven bipolar brains (three committed suicide) revealed similarities (decreased cortical and laminar thickness) and differences (unchanged overall neuronal density and laminar densities) between morphopathology of SCZ and bipolar disorder. In another population of suicide victims with major depression (nonpsychotic), further morphopathological differences from SCZ and similarities to bipolar disorder were observed in the prefrontal cortex. From these data we can conclude that the morphopathology observed in brain tissue from suicide victims appears to vary based on psychiatric symptomatology. In order to confirm this hypothesis and to establish the specificity of morphometric findings in relation to psychiatric disorders and suicide, additional studies are warranted in nonsuicide subjects with SCZ, major depression, or bipolar disorder.

Humans↗
PubMed1993

Behavioural changes after ablation of subdivisions of the rat prefrontal cortex.

Sham operated controls and four groups of rats subjected to ablation of various parts of their frontal cortex were compared in food and water intake and four behavioural tasks. The ablations were aimed at removing (1) the ventral prefrontal cortex, (2) the dorsal part of the medial prefrontal cortex, (3) the total medial prefrontal cortex, and (4) the anterior dorsolateral (non-prefrontal) cortex. Only two groups had a significantly impaired food and water intake: the ventral prefrontal and the non-prefrontal anterolateral. The latter group was not adipsic. Two variants of spontaneous alternation were administered in a T-maze: a non-cued version in which both arms were grey and a cued version in which one arm was white and the other black. While all ablated groups behaved like the control group on the non-cued test, the number of perseverative responses of the total anteromedial group was significantly increased in the cued version of the test. Significant group differences could be seen neither in a test of conditioned taste aversion nor in extinction of operantly conditioned bar presses. Finally, in a vertical hole-board exploration test the only significant group difference was a prolongation of the mean visit duration of the ventrally lesioned animals in comparison with all other groups. The results of the present study further indicate functional differentiation within the prefrontal cortex of the rat.

Animals↗
PubMed1998

Task-dependent selectivity of movement-related neuronal activity in the primate prefrontal cortex.

Task-dependent selectivity of movement-related neuronal activity in the primate prefrontal cortex. J. Neurophysiol. 80: 3392-3397, 1998. We studied movement-related neuronal activity in the dorsolateral prefrontal cortex from the perspective of a general role for the prefrontal cortex in controlling motor behavior to achieve a specific goal according to the requirements of a given task. Monkeys were trained to perform two delayed motor tasks. The first task involved reaching for a target that matched the shape of a cue. The second task involved reaching for a target that matched the location of the cue. A majority (54%) of 175 movement-related prefrontal neurons exhibited preference for either the target shape or the type of task requirements. Sixty-four neurons (36%) were selectively active while reaching for a circle or a triangle. On the other hand, the activity of 59 neurons (34%) depended on whether the task required matching the shape or the location. These properties, characterizing the movement-related neuronal activity in the prefrontal cortex, rarely were found in the arm area of the primary motor cortex. Only 1 of 130 movement-related neurons (0.8%) showed task selectivity, and none showed target-shape selectivity.

Animals↗
PubMed2001

Neuronal mechanisms of executive control by the prefrontal cortex.

Executive function is considered to be a product of the coordinated operation of various processes to accomplish a particular goal in a flexible manner. The mechanism or system responsible for the coordinated operation of various processes is called executive control. Impairments caused by damage to the prefrontal cortex are often called dysexecutive syndromes. Therefore, the prefrontal cortex is considered to play a significant role in executive control. Prefrontal participation to executive control can be partly explained by working memory that includes mechanisms for temporary active storage of information and processing stored information. For the prefrontal cortex to exert executive control, neuronal mechanisms for temporary storage of information and dynamic and flexible interactions among them are necessary. In this article, we present the presence of dynamic and flexible changes in the strength of functional interaction and extensive functional interactions among temporal information-storage processes in the prefrontal cortex. In addition, recent imaging studies show dynamic changes in functional connectivity between the prefrontal cortex and other cortical and subcortical structures depending upon the characteristics or the temporal context of the task. These observations indicate that the examination of dynamic and flexible modulation in neuronal interaction among prefrontal neurons as well as between the prefrontal cortex and other cortical and subcortical areas is important for explaining how the prefrontal cortex exerts executive control.

Animals↗
PubMed1981

Thalamic afferents to the prefrontal cortex in the cat traced with horseradish peroxidase.

Thalamic afferents to the prefrontal cortex in the cat were traced with horseradish peroxidase (HRP). Following injections of HPR into the medial prefrontal cortex and the ventral portion of the lateral prefrontal cortex, a large number of labeled cells were found in the dorsomedial nucleus of the ipsilateral thalamus, particularly its medial and dorsal parts. Labeled cells were also detected in the submedial and ventral medial nuclei, more in the former. Very few cells were labeled in the medial part of the medial pulvinar nucleus and in the paratenial and medial central nuclei. Occasional labeled cells were seen in the paracentral, rhomboid and reuniens nuclei. Injections of HRP into the dorsal part of the lateral prefrontal cortex, including the medial bank of the presylvian sulcus, resulted in heavy labeling of cells particularly in the lateral and ventral parts of the ipsilateral dorsomedial nucleus. Some labeled cells were found in the ventral medial nucleus, and a lesser number in the submedial nucleus. Very few cells were labeled in the paratenial nucleus and in the medial part of the medial pulvinar nucleus. Occasional labeled cells were detected in the paracentral, lateral central and reuniens nuclei. The above results reveal that with regard to the thalamic afferents, appreciable differences between the dorsolateral and ventromedial prefrontal cortices were noted.

Afferent Pathways↗
PubMed2006

Categorization of behavioural sequences in the prefrontal cortex.

Although it has long been thought that the prefrontal cortex of primates is involved in the integrative regulation of behaviours, the neural architecture underlying specific aspects of cognitive behavioural planning has yet to be clarified. If subjects are required to remember a large number of complex motor sequences and plan to execute each of them individually, categorization of the sequences according to the specific temporal structure inherent in each subset of sequences serves to facilitate higher-order planning based on memory. Here we show, using these requirements, that cells in the lateral prefrontal cortex selectively exhibit activity for a specific category of behavioural sequences, and that categories of behaviours, embodied by different types of movement sequences, are represented in prefrontal cells during the process of planning. This cellular activity implies the generation of neural representations capable of storing structured event complexes at an abstract level, exemplifying the development of macro-structured action knowledge in the lateral prefrontal cortex.

Action Potentials↗
PubMed2005

Spatial maps in frontal and prefrontal cortex.

Though the function of prefrontal cortex has been extensively investigated, little is known about the internal organization of individual prefrontal areas. Functional magnetic resonance imaging was used to show that some frontal and prefrontal cortical areas represent visual space in orderly, reproducible, topographic maps. The map-containing areas partly overlap dorsolateral prefrontal areas engaged by working memory tasks. These maps may be useful for attending to task-relevant objects at various spatial locations, an aspect of the executive control of attention.

Adult↗