SEARCH · PubMed Health

Results for “Prefrontal Cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources

PubMed2006

Neuron number decreases in the rat ventral, but not dorsal, medial prefrontal cortex between adolescence and adulthood.

Neuroimaging studies have established that there are losses in the volume of gray matter in certain cortical regions between adolescence and adulthood, with changes in the prefrontal cortex being particularly dramatic. Previous work from our laboratory has demonstrated that cell death can occur as late as the fourth postnatal week in the rat cerebral cortex. The present study examined the possibility that neuronal loss may occur between adolescence and adulthood in the rat prefrontal cortex. Rats of both sexes were examined during adolescence (at day 35) and young adulthood (at day 90). The volume, neuronal number, and glial number of the medial prefrontal cortex (mPFC) were quantified using unbiased stereological techniques. Neurons were lost from the ventral, but not dorsal, mPFC between adolescence and adulthood, suggesting a late wave of apoptosis that was region-specific. This was accompanied by a decrease in the volume of the female ventral mPFC. In contrast to neuron number, the number of glial cells was stable in the ventral mPFC and increased between adolescence and adulthood in the dorsal mPFC. Sex-specific developmental changes in neuron number, glial number, and volume resulted in sex differences in adults that were not seen during adolescence. The loss of neurons at this time may make the peri-adolescent prefrontal cortex particularly susceptible to the influence of environmental factors.

Aging↗

PubMed2004

Segregation of cognitive and emotional function in the prefrontal cortex: a stereotactic meta-analysis.

Imaging studies of major depressive disorder and schizophrenia strongly implicate the prefrontal cortex. Interpretation of such studies is hindered by the limited knowledge of normal functional segregation. Different anatomical regions may be functionally specialised. Elucidating such specialisation may assist design and interpretation of patient studies. In this meta-analysis, 330 emotion induction and cognitive task studies of normal subjects published over the past decade reporting prefrontal activation have been examined. It was hypothesised that emotion induction would result in inferior medial activation and cognitive tasks dorsolateral activation. A significant difference in the pattern of reported activations was found in keeping with this hypothesis. Estimates of most likely reported activation loci for emotion induction and cognitive task studies have been made. In Montreal Neurological Institute (MNI) stereotactic space, these comprise of +/-5, 46, 18 and +/-5, 28, 31 for the medial prefrontal cortex, and +/-42, 28, -16 and +/-54, 28, 18 for the lateral prefrontal cortex, respectively. Additionally, estimates of the boundaries between emotional and cognitive-processing regions have been made. We restricted the effects of various potential sources of bias on the above estimates by attempting to include all relevant studies and independent selection by both authors of at most two activation loci from each study according to prespecified criteria. Such estimates of most likely reported activation loci may allow improved planning, analysis, and interpretation of imaging studies of psychiatric disorder and of normal function.

Brain Mapping↗

PubMed2006

Modulation of prefrontal cortex activation by emotional words in recognition memory.

We employed event-related functional magnetic resonance imaging to examine emotional valence effects on verbal recognition memory. Using a yes/no recognition task, we focussed on prefrontal cortex responses to positive, negative and neutral words. Behavioral data confirmed enhanced processing of emotional items and functional magnetic resonance imaging revealed different subregions in the prefrontal cortex supporting retrieval of emotional words. Activations in the right mid-ventrolateral prefrontal cortex correlated with the correct retrieval conditions for negative words, whereas the right ventromedial and orbitofrontal prefrontal cortex showed enhanced responses to positive words. Additionally, differences between old and new items mainly affected bilateral orbitofrontal regions when processing positive words. The results are discussed in terms of higher monitoring demands owing to familiarity-based recognition bias for emotional words.

Adult↗

PubMed2006

D1 receptor modulation of memory retrieval performance is associated with changes in pCREB and pDARPP-32 in rat prefrontal cortex.

We have recently shown a significant role of dopamine D(1) receptors in recognition and temporal order memory retrieval for objects in rodents [Hotte M, Naudon L, Jay TM. Modulation of recognition and temporal order memory retrieval by dopamine D(1) receptor in rats. Neurobiol Learn Mem 2005;84:85-92]. The present study investigates the signal transduction pathways underlying dopamine D(1) receptor modulation of retrieval performance in these memory tasks at different delays. We analyzed the level of phosphorylation of both CREB (cAMP response element binding protein) and DARPP-32 (dopamine and cAMP-regulated phosphoprotein, 32 kDa) in (1) the prefrontal cortex of rats that had performed the object recognition task, (2) the prefrontal and perirhinal cortices of rats that had performed the temporal order memory task for objects. For comparison, we explored the phosphorylation state of CREB and DARPP-32 in the prefrontal cortex, nucleus accumbens and hippocampus of rats having performed badly on the delayed spatial win-shift task after D(1) blockade. The improvement in recognition and temporal order memory performance at a 4h-delay was associated with an increased phosphorylation of both CREB and DARPP-32 in the prefrontal cortex of rats treated with the D(1) agonist SKF 81297. By contrast, the significant impairment of delayed spatial memory retrieval after administration of the selective D(1) antagonist SCH 23390 was associated with decreased phosphorylation of CREB and DARPP-32 in the prefrontal cortex. These results provide insight into molecular mechanisms involved in D(1) receptor-dependent modulation of short- versus long-term memory in prefrontal cortex where DARPP-32 in synergy with CREB may represent a pivotal role.

Animals↗

PubMed2001

Lamina-specific deficits in parvalbumin-immunoreactive varicosities in the prefrontal cortex of subjects with schizophrenia: evidence for fewer projections from the thalamus.

OBJECTIVE: Neuronal number in the mediodorsal thalamic nucleus, the principal source of thalamic projections to the prefrontal cortex, has been reported to be lower in subjects with schizophrenia. The authors tested the hypothesis that schizophrenia is associated with a selective deficit in a marker of thalamic axon terminals in the middle layers of the prefrontal cortex, the primary zone of termination of thalamic axons. METHOD: The densities of parvalbumin-immunoreactive varicosities (putative axon terminals) were determined in the superficial and middle layers of prefrontal cortex area 9 from 20 matched pairs of subjects with schizophrenia and normal comparison subjects. In order to determine the specificity of these observations, similar studies were conducted in subjects with major depressive disorder and in monkeys after 9-12 months of haloperidol treatment. RESULTS: The relative densities of parvalbumin-immunoreactive varicosities did not differ between schizophrenic and comparison subjects in the superficial layers. However, in the middle layers, mean varicosity density was significantly lower (24% difference) in the subjects with schizophrenia. In contrast, neither subjects with major depressive disorder nor haloperidol-treated monkeys exhibited a middle-layer density of parvalbumin-immunoreactive varicosities that was lower than that of their matched comparison groups. CONCLUSIONS: Although not definitive, these findings are consistent with the hypothesis of fewer projections from the mediodorsal thalamic nucleus to the prefrontal cortex in schizophrenic subjects and thus converge with other lines of evidence demonstrating an abnormality in thalamo-prefrontal cortical circuitry in persons with schizophrenia.

Adult↗

PubMed2006

The role of medial prefrontal cortex in context-specific inhibition during reversal learning of a visual discrimination.

Rats with medial prefrontal cortex or sham lesions were trained on a visual discrimination task designed for the eight-arm radial maze. After reaching asymptotic performance on this task, both groups were divided into sub-groups that would experience reversal learning in the same or different context from original training. The results showed that both groups reversed in the different context had accelerated learning compared to the groups reversed in the same context. Reversal learning in rats with medial prefrontal cortex damage was faster than sham animals in the same context. These and other results from a transfer test suggest that the medial prefrontal cortex participates in the behavioral effects of a context-specific inhibitory association acquired during visual discrimination learning.

Animals↗

PubMed1998

Quantitation of regional cerebral blood flow increases in prefrontal cortex during a working memory task: a steady-state arterial spin-tagging study.

Steady-state arterial spin-tagging MRI approaches were used to quantitate regional cerebral blood flow increases in prefrontal cortex during a working memory ("two-back") task in six normal subjects. Statistically significant increases in cerebral blood flow in prefrontal cortex were observed in all six subjects: the average increase in cerebral blood flow in activated prefrontal cortex regions was 22 +/- 5 cc/100 g/min (23 +/- 7%). The results demonstrate that spin-tagging approaches can be used to follow focal activation in prefrontal cortex during cognitive tasks.

Adult↗

PubMed2001

M2 muscarinic autoreceptors modulate acetylcholine release in prefrontal cortex of C57BL/6J mouse.

Muscarinic autoreceptors modulate cholinergic neurotransmission in animals ranging from insects to humans. No previous studies have characterized autoreceptor modulation of acetylcholine (ACh) release in prefrontal cortex of intact mouse. Data obtained from experiments in 45 mice considered ACh as a phenotype and tested the hypothesis that pharmacologically defined M2 receptors modulate ACh release in prefrontal cortex of C57BL/6J mouse. In vivo microdialysis quantified ACh release during delivery of Ringer's (control) or Ringer's containing muscarinic receptor antagonists. The lowest concentration of each antagonist [scopolamine, pirenzepine, or 11-2[(-[(diethylamino)methyl]-1-piperidinyl)-acetyl]-5,11-dihydro-6H-pyrido(2,3-b)(1,4)-benzodiazepine-one (AF-DX116)] that significantly increased ACh release was determined and defined as the minimum ACh-releasing concentration. Dialysis delivery of scopolamine caused a concentration-dependent increase in ACh release, consistent with the existence of muscarinic autoreceptors. The order of potency for causing increased ACh release was scopolamine = AF-DX116 > pirenzepine. Administration of pertussis toxin into prefrontal cortex blocked the AF-DX116-induced increase in ACh release. These findings support the conclusion that M2 receptors modulate ACh release in C57BL/6J mouse prefrontal cortex. Nearly every human gene has a mouse homolog and the appeal of mouse models is reinforced by the identification of mouse genes causing phenotypic deviants. The present data encourage comparative phenotyping of cortical ACh release in additional mouse strains.

Acetylcholine↗

PubMed2002

Implications for altered glutamate and GABA metabolism in the dorsolateral prefrontal cortex of aged schizophrenic patients.

OBJECTIVE: Pharmacological, clinical, and postmortem studies suggest altered gamma-aminobutyric acid (GABA)-ergic and glutamatergic function in patients with schizophrenia. The dorsolateral prefrontal cortex is one key locus of abnormality. The precise neurochemical mechanisms underlying neurotransmitter alterations, such as hypoglutamatergia or GABA dysfunction, are not well understood. This study investigated key biochemical elements of GABA and glutamate metabolism in brain specimens from schizophrenic patients. The activities of nine principal GABA and glutamate-associated metabolic enzymes were measured concurrently in the dorsolateral prefrontal cortex of antemortem-assessed and neuropathologically characterized schizophrenic and comparison subjects. METHOD: Postmortem dorsolateral prefrontal cortex specimens from schizophrenia, Alzheimer's disease, and normal nonpsychiatric comparison subjects were assayed to determine activities of the principal glutamate and GABA-metabolizing enzymes glutamine synthetase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, phosphate-activated glutaminase, alanine aminotransferase, aspartate aminotransferase, glutamic acid decarboxylase, GABA-transaminase, and succinic semialdehyde dehydrogenase. RESULTS: Glutamic acid decarboxylase activities were twofold greater and phosphate-activated glutaminase activities were fourfold greater in the schizophrenic group than in the comparison group. Differences in postmortem interval, tissue pH, inhibition of phosphate-activated glutaminase, and medication effects could not account for the differences. Differences in phosphate-activated glutaminase and glutamic acid decarboxylase activities in equivalent specimens from Alzheimer's patients were not observed. The activities of the remaining enzymes were unchanged. CONCLUSIONS: Greater phosphate-activated glutaminase and glutamic acid decarboxylase activities, specific to schizophrenia patients, provide additional biochemical evidence that dorsolateral prefrontal cortex glutamate and GABA metabolism is altered in schizophrenic subjects. These greater activities are consistent with models of a dysregulated glutamatergic/GABA-ergic state in schizophrenia.

Age Factors↗

PubMed2006

Potential contributions of efferents from medial prefrontal cortex to neural activation following sexual behavior in the male rat.

The limbic system plays an important role in the regulation of sexual motivation and reward. At the core of this system is an interconnected mesocorticolimbic circuit, comprised of the ventral tegmental area, nucleus accumbens and medial prefrontal cortex. Previously, our laboratory showed that sexual behavior causes neural activation in the ventral tegmental area of male rats. The main goal of this study is to identify afferent inputs to ventral tegmental area neurons that may contribute to their activation during sexual behavior. Hence, the anterograde tracer biotinylated dextran amine was injected into subregions of the rat medial prefrontal cortex, which is known to project to the ventral tegmental area. Visualization of biotinylated dextran amine-labeled axons was combined with immunostaining for sex-induced Fos expression. Quantitative analysis showed that the majority of sex-activated ventral tegmental area neurons receive putative contacts from the infralimbic and prelimbic--but not the anterior cingulate--subregions of the medial prefrontal cortex. Thus, inputs from infralimbic area and prelimbic are in an anatomical position to provide a major source of input during sexual behavior. A second goal of this study was to determine if the medial prefrontal cortex projects to sex-activated neurons in other brain regions important for sexual behavior and motivation. Infralimbic area and prelimbic area sent projections to nucleus accumbens, medial preoptic area, principal nucleus of the bed nucleus of the stria terminalis, basolateral amygdala, and parvocellular subparafasicular thalamic nucleus. Thus, the infralimbic and prelimbic subregions of the medial prefrontal cortex may also influence sexual behavior and motivation via brain regions other than the ventral tegmental area.

Animals↗

PubMed1998

Activation of neurotensin receptors in the prefrontal cortex stimulates midbrain dopamine cell firing.

The effects of medial prefrontal cortex microinjections of 3 nmol/0.5 microl of neurotensin-(1-13), the inactive fragment neurotensin-(1-8), or vehicle on the firing rate of midbrain dopamine neurons were studied in anesthetized rats. Twelve of 19 cells tested with neurotensin-(1-13) showed an average 20-25% increase in firing rate between 10 and 20 min after the injection. This effect was not mimicked by neurotensin-(1-8) (9 cells), nor by a control injection (10 cells) suggesting that it is mediated by high-affinity neurotensin receptors. These results suggest that activation of neurotensin receptors in the medial prefrontal cortex can modulate neural activity of a subpopulation of midbrain dopamine neurons.

Animals↗

PubMed1989

Prefrontal cortex lesions differentially disrupt cocaine-reinforced conditioned place preference but not conditioned taste aversion.

The reinforcing efficacy of cocaine is thought to involve, at least in part, mesocortical dopaminergic (DA) neurons. Rats will self-administer cocaine applied directly into the medial prefrontal cortex but not into nucleus accumbens or the ventral tegmental area (Goeders & Smith, 1983). The present experiments were conducted to assess whether lesions of prefrontal cortex (mesocortical DA target regions) attenuate the reinforcing properties of systemically administered cocaine. Male Sprague-Dawley rats were anesthetized, and one of three subfields (medial, orbital, or precentral) of the prefrontal cortex was removed by aspiration or no brain injury was done (sham operates). In four experiments the rats were tested on conditioned place preference (CPP), conditioned taste aversion (saccharin conditioned stimulus, cocaine unconditioned stimulus), general activity in the running wheel and open field, and food-reinforced spatial alternation in the T-maze. Sham operates demonstrated a cocaine-induced place preference, rats with medial frontal lesions showed a cocaine-induced place aversion, and other operates showed neither a conditioned place preference nor an aversion. The results of this experiment suggest that lesions of the DA projection fields of the prefrontal cortex in the rat reduce the positive reinforcing properties of systemically injected cocaine. In the second experiment, all subjects showed a conditioned taste aversion of equal magnitude. This suggests that whereas the positive reinforcing properties were affected differentially by prefrontal cortex lesions, the aversive properties were not affected. In Experiment 3 there were no lesion-induced differences in activity in either the running wheel or the open field. Therefore, changes in motor activity cannot account for the CPP data. In the final experiment, the medial frontal operates were impaired relative to the precentral and sham operates on learning to alternate choices in the T-maze, but the orbital frontal operates' performance was not different from that of any other group. This suggests that a general disruption of all reinforcement mechanisms did not occur following these lesions. Instead, these results indicate that mesocortical DA projection regions are involved with mediating the reinforcing properties of cocaine and that there is a separate system mediating the aversive properties of cocaine.

Animals↗

PubMedDate not supplied

Bilateral prefrontal cortex oxygenation responses to a verbal fluency task: a multichannel time-resolved near-infrared topography study.

The letter-fluency task-induced response over the prefrontal cortex is investigated bilaterally on eight subjects using a recently developed compact, eight-channel, time-resolved, near-IR system. The cross-subject mean values of prefrontal cortex oxygen saturation (SO2) were 68.8+/-3.2% (right) and 71.0+/-3.6% (left), and of total hemoglobin concentration (tHb) were 69.6+/-9.6 microM (right) and 69.5+/-9.9 microM (left). The typical cortical activation response to the cognitive task [characterized by an increase in oxyhemoglobin (O2Hb) with a concurrent decrease in deoxyhemoglobin (HHb)] at each measurement point is observed in only four subjects. In this subset, the amplitude of the O2Hb increase and HHb decrease is uniform over each prefrontal cortex area and comparable between the two hemispheres. These findings agree with previous studies using continuous wave functional near-IR spectroscopy and functional magnetic resonance imaging, therefore demonstrating the potential of a time-resolved spectroscopy approach. In addition, a significant increase in SO2 levels was observed in the right (1.1+/-0.5%) compared to left side of the prefrontal cortex (0.9+/-0.5%) (P=0.005). A different pattern of cortical activation (characterized by the lack of HHb decrease or even increased HHb) was observed in the remaining subjects.

Adult↗

PubMed2006

Fear-related activity in the prefrontal cortex increases with age during adolescence: a preliminary fMRI study.

An emerging theory of adolescent development suggests that brain maturation involves a progressive "frontalization" of function whereby the prefrontal cortex gradually assumes primary responsibility for many of the cognitive processes initially performed by more primitive subcortical and limbic structures. To test the hypothesis of developmental frontalization in emotional processing, we analyzed the correlation between age and prefrontal cortex activity in a sample of 16 healthy adolescents (nine boys; seven girls), ranging in age from 8 to 15 years, as they viewed images of fearful and happy faces while undergoing functional magnetic resonance imaging (fMRI). During fear perception, age was significantly positively correlated with greater functional activity within the prefrontal cortex, whereas no significant relationship was evident between age and activity in the amygdala. Consistent with previous gender-related findings, age was significantly correlated with bilateral prefrontal activity for the sample of females, but was only significantly related to right prefrontal activity for the males. In contrast, similar age-related correlations were not evident during the perception of happy faces. These results suggest that the maturation of threat-related emotional processing during adolescence is related to the progressive acquisition of greater functional activity within the prefrontal cortex. The hypothesis of age related decreases in amygdala activity was not supported, but may have been due to low signal-to-noise and inadequate power in the present sample to resolve subtle changes in this small structure.

Adolescent↗

PubMed1998

Layer V neurons bear the majority of mRNAs encoding the five distinct dopamine receptor subtypes in the primate prefrontal cortex.

In situ hybridization histochemistry was used to determine the laminar distribution of D1, D2, D3, D4, and D5 dopamine receptor mRNAs in the primate prefrontal cortex and to compare striatal and cortical levels of these messages within the same tissue sections. All five subtypes of dopamine receptor mRNA are present in both the monkey striatum and the cerebral cortex but in different proportions within each structure. Thus, levels of D1 and D2 mRNAs are noticeably stronger in the striatum than in the cortex, whereas D4 and D5 expression is clearly higher in the cortex. The D3 transcripts appear nearly equivalent in the striatum and the cortex. A major finding is that, within the prefrontal cortex, mRNAs encoding all dopamine receptor subtypes are expressed most strongly in layer V. This laminar pattern of mRNA distribution does not hold in all cortical regions. The relatively high levels of mRNAs encoding known dopamine receptor subtypes in the primate cerebral cortex, including the D4 receptor, underscore the importance of this structure as a target for therapeutic actions of antipsychotic drugs. Further, their prominence in layer V of the prefrontal cortex, which contains the corticostriatal and corticotectal projection neurons, provides a neural basis for dopaminergic regulation of the descending control systems.

Animals↗

PubMed2001

Corticosterone exerts site-specific and state-dependent effects in prefrontal cortex and amygdala on regulation of adrenocorticotropic hormone, insulin and fat depots.

Chronic stress stimulates corticosterone secretion and recruits brain pathways that regulate energy balance (caloric acquisition and deposition) and facilitate hypothalamic-pituitary-adrenal responsiveness to new stressors. We implanted corticosterone or cholesterol bilaterally either near the central nucleus of the amygdala (CeA) or in the prefrontal cortex to determine whether high concentrations of the steroid act at either site, with or without chronic stress. Rats were adrenalectomized and treated systemically with low doses of corticosterone. Half were maintained at room temperature and the other half were exposed to 5 degrees C cold for 5 days before all rats were restrained. There was limited diffusion of corticosterone from brain implants. Corticosterone in prefrontal cortex, but not CeA, decreased plasma insulin and adrenocorticotropic hormone (ACTH) responses to acute restraint in both control and chronically cold stressed rats. Corticosterone implants near CeA decreased the weight of fat depots only in cold; corticosterone implants in prefrontal cortex were ineffective. We conclude that (i) corticosterone inhibits insulin and ACTH secretion by an action in prefrontal cortex but not CeA; (ii) high concentrations of corticosterone secreted during chronic stress alter metabolism through (autonomic) outputs of the CeA and prefrontal cortex in site- and variable-specific fashion; and (iii) the amygdala is a component of a stress-recruited, state-dependent pathway.

Adipose Tissue↗

PubMed1999

Induction of stable long-term depression in vivo in the hippocampal-prefrontal cortex pathway.

We studied excitatory field potentials in the medial prefrontal cortex (mPFC, prelimbic area) to electrostimulation of the ventral hippocampus (CA1/subicular region) in the anaesthetized rat. Nine hundred stimulus trains (5 pulses at 250 Hz) applied at 1 Hz to the ventral hippocampus significantly and persistently depressed the amplitude and maximal slope ( approximately 55% for each index) of the prelimbic field potentials, but did not change the latency of the maximal slope or peak negativity. Twelve stimulus trains (50 pulses at 250 Hz) applied subsequently at 0.1 Hz restored the depression back to control level, and this reversible depression was maintained for at least 13 h. Cumulative depressive effects on the prelimbic field potential amplitude and maximal slope were observed upon addition of stimulus trains in the hippocampus. An important implication of the results is that the direct pathway from the hippocampus to the mPFC in the rat retains long-term depression (LTD) as a neuroplastic form in vivo. This form could cooperate with long-term potentiation (LTP) and such a bi-directional synaptic plasticity in the prefrontal cortex contributes to how cortical neural networks store information.

Animals↗

PubMed2002

Specific abnormalities in serotonin release in the prefrontal cortex of isolation-reared rats measured during behavioural performance of a task assessing visuospatial attention and impulsivity.

RATIONALE: Rats reared in social isolation exhibit hyperactivity and specific attentional disturbances in later adult life. These behavioural abnormalities may be relevant to impulsivity and other neuropsychiatric syndromes such as attention-deficit hyperactivity disorder and schizophrenia where disturbances in circuitry involving the prefrontal cortex have been identified. OBJECTIVE: To establish whether isolation-reared rats show a differential susceptibility to cognitive processes that depend on the prefrontal cortex and its monoaminergic innervation. METHODS: Rats were reared in isolation from postnatal day 28 or in social groups of four and trained on the five-choice serial reaction time task, which assesses spatially divided visual attention. Following a range of manipulations designed to tax visual attention and response control, in vivo microdialysis was used in conjunction with behavioural testing to assess dopamine (DA) and serotonin (5-HT) release in the prefrontal cortex, either under baseline conditions prior to task initiation, or during task performance. Subjects were challenged with amphetamine (0.125 mg/kg intravenously) every 15 min, commencing 15 min after the start of the task. RESULTS: Apart from being consistently slower to collect food rewards and showing more perseverative responses to an auditory distractor, isolates were unimpaired on accuracy, impulsivity and correct latency measures on the five-choice task. Basal levels of DA and 5-HT in the prefrontal cortex were also unaffected by isolation rearing. Amphetamine increased the speed of responding in control and isolation-reared animals and increased premature (impulsive) responding, but only in socially-reared animals. Cortical DA release increased to a similar extent in both groups following amphetamine challenge. By contrast, 5-HT release was attenuated in isolates under these conditions. CONCLUSIONS: These findings highlight a rather specific deficit in 5-HT release in the prefrontal cortex of isolation-reared rats, although this appears not to affect visual attentional function. Rather, these data may be relevant to reduced impulsiveness of isolation-reared rats on the five-choice task. These findings are important in the context of animal models of attentional disturbances in schizophrenia.

Amphetamine↗