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PubMed2004

Bilateral volume reduction of the insular cortex in patients with schizophrenia: a volumetric MRI Study.

The morphologic changes of the insular cortex have been described in schizophrenia, but with inconsistencies between reports. We investigated the insular cortex volume by magnetic resonance imaging in 59 schizophrenia patients (31 males, 28 females) and 62 age- and gender-matched healthy controls (31 males, 31 females). The insular cortex volume was measured on consecutive coronal 1-mm slices. Volumes of the left and right insular cortex were significantly reduced in schizophrenia patients compared with control subjects. There were no effects of gender on the insular cortex volume in the patient group or control subjects. Bilateral insular cortex volumes were correlated negatively with illness duration in the patient group. The findings of this study suggest that there is a possible progressive loss of the gray matter volume of the bilateral insular cortices subsequent to the onset of schizophrenia.

Adolescent↗

PubMed1999

Prefrontal cortex regulates inhibition and excitation in distributed neural networks.

Prefrontal cortex provides both inhibitory and excitatory input to distributed neural circuits required to support performance in diverse tasks. Neurological patients with prefrontal damage are impaired in their ability to inhibit task-irrelevant information during behavioral tasks requiring performance over a delay. The observed enhancements of primary auditory and somatosensory cortical responses to task-irrelevant distractors suggest that prefrontal damage disrupts inhibitory modulation of inputs to primary sensory cortex, perhaps through abnormalities in a prefrontal-thalamic sensory gating system. Failure to suppress irrelevant sensory information results in increased neural noise, contributing to the deficits in decision making routinely observed in these patients. In addition to a critical role in inhibitory control of sensory flow to primary cortical regions, and tertiary prefrontal cortex also exerts excitatory input to activity in multiple sub-regions of secondary association cortex. Unilateral prefrontal damage results in multi-modal decreases in neural activity in posterior association cortex in the hemisphere ipsilateral to damage. This excitatory modulation is necessary to sustain neural activity during working memory. Thus, prefrontal cortex is able to sculpt behavior through parallel inhibitory and excitatory regulation of neural activity in distributed neural networks.

Animals↗

PubMed2001

Peripheral homonymous scotomas from a cavernous angioma affecting fibers subserving the intermediate region of the striate cortex.

PURPOSE: To report the case of a pure peripheral homonymous visual field defect and to delineate the representation of the visual field on the striate cortex. METHODS: Observational case report. Neuro-ophthalmologic and neuroimaging assessment of a patient with a cavernous angioma of the right parieto-occipital lobe. RESULTS: The patient had left homonymous scotomas located 40 degrees to 60 degrees from the vertical meridian. Neuroimaging indicated that the lesion was affecting the optic radiations at their termination in the intermediate portion of the striate cortex or the striate cortex itself. CONCLUSION: Homonymous field defects are typically located within 10 degrees of fixation. This patient had a peripheral homonymous field defect from damage to the intermediate striate cortex. Correlation of the neuroimaging findings in this case with the most commonly used maps of the representation of the visual field on the striate cortex suggests that none of the maps correctly predicts the location or extent of lesions that affect the intermediate portion of the cortex.

Adult↗

PubMed2000

Normal cellular levels of synaptophysin mRNA expression in the prefrontal cortex of subjects with schizophrenia.

BACKGROUND: Previous studies have reported that the 38-kd synaptic vesicle-associated protein, synaptophysin, is decreased in the prefrontal cortex of subjects with schizophrenia. METHODS: To determine whether the decreased protein levels reflect diminished expression of the synaptophysin gene by prefrontal cortex neurons, we used in situ hybridization histochemistry to determine the cellular levels of synaptophysin messenger RNA in prefrontal cortex area 9 from 10 matched pairs of schizophrenic and normal control subjects. RESULTS: Neither the density of neurons with detectable levels of synaptophysin messenger RNA nor the mean level of synaptophysin messenger RNA expression per neuron differed between schizophrenic and control subjects in any cortical layer. CONCLUSIONS: These findings indicate that the expression of synaptophysin messenger RNA is not altered in this brain region in schizophrenia. Consequently, reduced levels of synaptophysin protein in the prefrontal cortex of subjects with schizophrenia are more likely to reflect either posttranscriptional abnormalities of synaptophysin in prefrontal cortex neurons or a diminished number of axonal projections to the prefrontal cortex from other brain regions.

Adult↗

PubMed2000

Reduction of orbital frontal cortex volume in geriatric depression.

BACKGROUND: Postmortem studies have documented abnormalities in the medial orbital frontal cortex in depressed patients. In this study we evaluated whether atrophy of this region can be identified in older depressed patients using magnetic resonance imaging. METHODS: Twenty elderly patients meeting DSM-IV criteria for major depression and 20 matched control subjects were studied. The orbital frontal cortex was measured in both hemispheres using magnetic resonance imaging. RESULTS: Depressive patients had reduced volume in the total orbital frontal cortex, right orbital frontal cortex, and left orbital frontal cortex. CONCLUSIONS: Our finding of a reduction in orbital frontal cortex volume in both sides of the brain suggests that this region of the brain may have a critical role in the development of depression and raises questions about the etiology of the changes.

Aged↗

PubMed2003

Intensity-dependent regional cerebral blood flow during 1-Hz repetitive transcranial magnetic stimulation (rTMS) in healthy volunteers studied with H215O positron emission tomography: I. Effects of primary motor cortex rTMS.

BACKGROUND: Repetitive transcranial magnetic stimulation (rTMS) affects the excitability of the motor cortex and is thought to influence activity in other brain areas as well. We combined the administration of varying intensities of 1-Hz rTMS of the motor cortex with simultaneous positron emission tomography (PET) to delineate local and distant effects on brain activity. METHODS: Ten healthy subjects received 1-Hz rTMS to the optimal position over motor cortex (M1) for producing a twitch in the right hand at 80, 90, 100, 110, and 120% of the twitch threshold, while regional cerebral blood flow (rCBF) was measured using H(2)(15)O and PET. Repetitive transcranial magnetic stimulation (rTMS) was delivered in 75-pulse trains at each intensity every 10 min through a figure-eight coil. The regional relationship of stimulation intensity to normalized rCBF was assessed statistically. RESULTS: Intensity-dependent rCBF increases were produced under the M1 stimulation site in ipsilateral primary auditory cortex, contralateral cerebellum, and bilateral putamen, insula, and red nucleus. Intensity-dependent reductions in rCBF occurred in contralateral frontal and parietal cortices and bilateral anterior cingulate gyrus and occipital cortex. CONCLUSIONS: This study demonstrates that 1-Hz rTMS delivered to the primary motor cortex (M1) produces intensity-dependent increases in brain activity locally and has associated effects in distant sites with known connections to M1.

Adult↗

PubMed2001

Lesion of the insular cortex affects luteinizing hormone and testosterone secretion of rat. Lateralized effect.

The possible involvement of the insular cortex in the neural control of the hypophyseal-testicular axis was studied in male rats. Right- but not left-sided lesion of the insular cortex resulted in a significant decrease in basal testosterone secretion in vitro and serum testosterone concentration. Both right- and left-sided lesions of the insular cortex induced significant increase in serum luteinizing hormone (LH) concentration. Unilateral lesion of the insular cortex on either sides had no effect on serum follicle stimulating hormone (FSH) level. The results indicate that the insular cortex is involved in the control of testosterone and LH secretion. The data further suggest that the right insular cortex plays a predominant role in the control of male endocrine reproductive processes.

Animals↗

PubMed1996

Role of catecholamines in the frontal cortex in the modulation of basal and stress-induced autonomic output in rats.

Exposure of animals to noxious or stressful stimuli increases heart rate (HR) and blood pressure through activation of the autonomic nervous system (ANS) and elicits the release of the catecholamines noradrenaline (NA) and dopamine (DA) in the frontal cortex. Subregions of the frontal cortex, such as the medial frontal cortex (MFC) and agranular insular cortex (AIC) project directly to brainstem nuclei involved in autonomic control. It may be hypothesized that catecholamines in the frontal cortex could influence autonomic output through actions on these descending pathways. To evaluate this hypothesis, the effects of intracortical microinjections of drugs acting at NAergic and DAergic receptors were assessed on an autonomically mediated response, the increase in HR induced by tail pinch, in rats anesthetized with urethane. Intra-MFC or AIC injections of an antagonist of beta-adrenoceptors reduced the magnitude of the HR response to pinch. Injections of an agonist of beta-adrenoceptors into these regions increased basal HR but did not affect the pinch response. Injections of drugs acting at alpha-adrenoceptors were without effect. When injected alone, drugs acting at DAergic receptors did not effect basal HR or the response to pinch, but intra-AIC injections of a combination of a D2 antagonist and an agonist of beta-adrenoceptors increased the magnitude of the pinch response. These results suggest that catecholamines, especially NA, released in the frontal cortex are important modulators of the basal and stress-induced output of the ANS.

Anesthesia, General↗

PubMed1997

Modulation of anxiety-related behaviours following lesions of the prelimbic or infralimbic cortex in the rat.

A series of experiments examined behavioural and autonomic aspects of stress and anxiety in rats subjected to either: (1) electrolytic lesions of the infralimbic cortex subregion of the medial prefrontal cortex; (2) electrolytic lesions of the prelimbic cortex subregion of the medial prefrontal cortex; (3) sham lesions of infralimbic or prelimbic cortex (sham control); or (4) no lesions (control). In exploration-based models of anxiety, infralimbic- or prelimbic-lesioned rats spent less time in the centre of an open field and less time on the exposed arms of an elevated plus maze, indicating increased anxiety. Locomotor activity was normal in the lesioned rats when tested in a non-stressful enclosed environment. In a step-down passive avoidance task, infralimbic-lesioned rats stepped down more quickly than controls onto a grid floor where they had been shocked 24 h previously. Prelimbic-lesioned rats were no different to controls on this test, although they showed greater latencies to step down onto the grid floor during conditioning. In a final experiment, indirect calorimetry was used to show that both infralimbic- and prelimbic-lesioned rats have essentially normal alterations in oxygen consumption and energy substrate utilisation when exposed to brief footshock. Thus, the impaired passive avoidance in infralimbic-lesioned rats cannot be attributed to decreased nociception. It is concluded that both the prelimbic and infralimbic regions play a role in anxiety, and that this role may be subtly differentiated. In particular, the infralimbic cortex may have a specific role in mediating the inhibition of behaviours associated with aversive outcomes.

Acute Disease↗

PubMed1999

Regional expressions of Fos-like immunoreactivity in rat cerebral cortex after stress; restraint and intraperitoneal lipopolysaccharide.

To demonstrate regional activation in the rat cerebral cortex related to stress-evoked neuroendocrine response, Fos expression in both the cerebral cortex and hypothalamic paraventricular nucleus (PVN) was immunohistochemically examined in two experimental groups; a lipopolysaccharide (LPS) intraperitoneally injected group for inflammatory stress and a restraint group for emotional stress. The LPS injection (100 microg/100 g b.w.) and restraint (for 30 min) had similar effect on Fos-like immunoreactivity (Fos-LI) in PVN with regard to the number of immunoreactive nuclei and their distribution pattern, while the times to maximize Fos-LI were different. Numerical analysis of cortical Fos-LI in untreated rats showed a distinct region-specific pattern. Statistical analysis revealed no significant increase in Fos-LI density in any cortical regions in the LPS group, but restraint resulted in a dramatic and region-specific increase. A significant increase was detected in the prefrontal cortex (the cingulate, orbital and agranular insular cortex), the frontal area 2, the agranular retrosplenial cortex, the parietal cortex, and the medial and lateral occipital area 2. These results indicate that cortical activation relevant to specific functions may be involved in stress-specific neural circuitry.

Animals↗

PubMed1998

Synaptic density of the prefrontal cortex regulated by dopamine instead of serotonin in rats.

Recent findings indicate that monoamine contributes to synaptic plasticity. We examined the synaptic density of the prefrontal cortex and parietal cortex of rats using dopamine (DA) antagonists and agonists, as well as serotonin (5-HT) depleters and found a reduction in synaptic density in the prefrontal cortex lamina V-VI at a maximum of 20% with administration of a D1 antagonist (SCH23390) and at a maximum of 30% with a D2 antagonist (YM09151). Further, with the administration of D1+D2 antagonists there was a 27% decrease in synaptic density, which was a larger reduction than the total of the single dosages of each DA antagonist at equal levels. Increase in synaptic density was seen at a maximum of 8.5% with dosage of a D1 agonist (SKF38390) and 14.5% with dosage of a D2 agonist (PPHT). The dosage of D1+D2 agonists showed a 27.1% increase in synaptic density. There was no change in synaptic density of the parietal cortex with either DA antagonist or agonist administration. Administration of 5-HT depleter pCPA resulted in a 13.8% reduction of synaptic density in the parietal cortex, though there was no change identified in the synaptic density in the prefrontal cortex. Based on these results, it was suggested that the area of the brain with affected synaptic plasticity could differ, depending on the type of monoamine.

Animals↗

PubMed1999

The expression of mRNAs for hepatocyte growth factor/scatter factor, its receptor c-met, and one of its activators tissue-type plasminogen activator show a systematic relationship in the developing and adult cerebral cortex and hippocampus.

The temporal and spatial expression in brain of the mRNAs for the pleiotropic cytokine hepatocyte growth factor/scatter factor (HGF/SF) and its receptor c-met were compared to those of a known HGF/SF activator, tissue-type plasminogen activator (tPA). In addition to the previously described expression in the developing and adult olfactory system [D.P. Thewke, N.W. Seeds, Expression of hepatocyte growth factor/scatter factor, its receptor, c-met, and tissue-type plasminogen activator during development of the murine olfactory system, J. Neurosci. 16 (1996) 6933-6944] two other regions of the mouse brain were found where the expression of tPA mRNA appeared to co-localized with HGF/SF and/or c-met mRNA. In the developing hippocampus, tPA mRNA was expressed coincident with HGF/SF and c-met mRNAs in the CA1 field. tPA mRNA was expressed in all areas of the adult hippocampus, while HGF/SF expression was restricted to the CA2 and CA3 fields, and c-met mRNA was seen primarily in the CA1 field. In the developing cerebral cortex, the expression of tPA mRNA was observed in the subplate and inner cortical plate between two layers of c-met expression, whereas HGF/SF mRNA was localized to the proliferative zone lining the lateral ventricle. Layer specific expression of both HGF/SF and c-met mRNA were observed in the adult cortex, where HGF/SF was expressed in layers IV and V and c-met in layers II-III, IV and V. The expression of tPA mRNA in the adult cortex was low and not layer specific, although homogenates of adult cortex did have detectable levels of tPA activity when subjected to zymography. Immunohistochemical analysis using HGF/SF and c-met antibodies on adult brain sections showed a distribution similar to the in situ hybridization results. C-met antibodies appeared to stain large neurons in the cortex and hippocampus. These results are consistent with the hypothesis that HGF/SF plays a role in the development and maintenance of both the cerebral cortex and hippocampus, and that tPA may act as a regulator of HGF/SF activity in these structures.

Age Factors↗

PubMed1999

Changes in occipital cortex activity in early blind humans using a sensory substitution device.

The purpose of this study was to investigate the neural networks involved when using an ultrasonic echolocation device, which is a substitution prosthesis for blindness through audition. Using positron emission tomography with fluorodeoxyglucose, regional brain glucose metabolism was measured in the occipital cortex of early blind subjects and blindfolded controls who were trained to use this prosthesis. All subjects were studied under two different activation conditions: (i) during an auditory control task, (ii) using the ultrasonic echolocation device in a spatial distance and direction evaluation task. Results showed that the abnormally high metabolism already observed in early blind occipital cortex at rest [C. Veraart, A.G. De Volder, M.C. Wanet-Defalque, A. Bol, C. Michel, A.M. Goffinet, Glucose utilization in human visual cortex is, respectively elevated and decreased in early versus late blindness, Brain Res. 510 (1990) 115-121.] was also present during the control task and showed a trend to further increase during the use of the ultrasonic echolocation device. This specific difference in occipital cortex activity between the two tasks was not observed in control subjects. The metabolic recruitment of the occipital cortex in early blind subjects using a substitution prosthesis could reflect a concurrent stimulation of functional cross-modal sensory connections. Given the unfamiliarity of the task, it could be interpreted as a prolonged plasticity in the occipital cortex early deprived of visual afferences.

Acoustic Stimulation↗

PubMed2002

The medial prefrontal cortex mediates 3-methoxytyramine-induced behavioural changes in rat.

L-3,4-Dihydroxyphenylalanine (L-DOPA) remains a common treatment for Parkinson's disease; however, side effects (i.e., dyskinesia and hallucinations) also remain problematic. We recently reported that the dopamine metabolite 3-methoxytyramine causes stereotypy in rats via dopamine receptors, raising the possibility that 3-methoxytyramine is involved in the adverse side effects of chronic L-DOPA treatment. Thus, the present study examined the sites of 3-methoxytyramine action in the rat brain. After intracerebroventricular administration of 3-methoxytyramine, significantly more neurones expressed c-Fos in mesocortico-limbic dopamine areas including frontal cortex, medial prefrontal cortex, parietal cortex, piriform cortex, the nucleus accumbens shell, and ventral tegmental area. 3-Methoxytyramine injection into the medial prefrontal cortex specifically resulted in behavioural changes characteristic of those elicited by the more general intracerebroventricular injection of 3-methoxytyramine. This suggests that the medial prefrontal cortex mediates the 3-methoxytyramine-induced behavioural changes and that a reduction of its action there may alleviate the adverse effects of chronic L-DOPA treatment.

Animals↗

PubMed1997

Identification of multiple neuropeptide Y receptor subtypes in the human frontal cortex.

Recently, we found abundant mRNA and binding sites for neuropeptide Y Y1-like receptors in the human cerebral cortex. However, an earlier study using indirect labeling methods failed to detect substantial neuropeptide Y1-like receptor binding in numerous areas of the human brain, including the cerebral cortex. To resolve the disparity in these findings, we characterized the neuropeptide Y receptor subtypes labeled with [125I]peptide YY in homogenates of human frontal cortex. Competition experiments using 100 pM [125I]peptide YY binding to human frontal cortex homogenates indicated predominantly neuropeptide Y Y2 receptors are labeled with this concentration of ligand. However, saturation analysis of [125I]peptide YY binding to frontal cortex membranes resulted in isotherms best characterized by a two-site fit. Binding of [125I]peptide YY to the high affinity (Kd = 40 pM) binding site was prevented using a 100 nM concentration of the neuropeptide Y Y2 receptor agonist peptide YY-(3-36). By masking the higher affinity site, we found a low affinity [125I]peptide YY binding site (Kd = 1.4 nM) exhibiting a pharmacology consistent with a neuropeptide Y Y1-like receptor. It appears that neuropeptide Y Y2 receptors are the predominant subtype labeled with low concentrations of[125I]peptide YY and that the neuropeptide Y Y1 receptor is a low affinity [125I]peptide YY binding site in the human frontal cortex.

Binding Sites↗

PubMed2003

T2-low signal intensity in the cortex in multiple system atrophy.

To determine the clinical significance of T2-low signal intensity in the cortex of patients presenting parkinsonism, T2-weighted magnetic resonance (MR) images of the cortex of patients with multiple system atrophy (MSA), Parkinson's disease (PD) and progressive supranuclear palsy (PSP), and compared with those of patients with amyotrophic lateral sclerosis (ALS) and age-matched normal controls. The MR images were gathered and presented randomly to three neurologists who were blind to information on the patients. There was a significant increase in the frequency of T2-low signal intensity in the cortex of patients with ALS and MSA. Particularly in those with MSA, the T2-low signal intensity was observed not only in the motor cortex but also in the frontal association cortex. The cortical T2-low signal intensity in MSA might reflect the spread of degenerative processes in the cortex.

Aged↗

PubMed2001

Repeated but not acute clomipramine decreases the effect of N-methyl-D-aspartate receptor activation on serotonergic transmission between the raphe nuclei and frontal cortex.

The effect of acute or repeated treatment with the antidepressant clomipramine (CIM) on N-methyl-D-aspartate (NMDA) evoked changes in extracellular 5-hydroxytryptamine (5-HT) in the raphe nuclei and frontal cortex of the same rat has been studied using microdialysis. Acute injection of CIM (10 or 20 mg/kg) caused an increase in raphe extracellular 5-HT but did not significantly alter extracellular 5-HT in the frontal cortex. Infusion of 25 microM NMDA into the raphe decreased extracellular 5-HT in this region and increased terminal extracellular 5-HT in the frontal cortex. In contrast, infusion of 100 microM NMDA into the raphe was followed by an increase in local dialysate 5-HT and a decrease in 5-HT release in the cortex. When NMDA infusion, at either 25 or 100 microM was preceded by one acute injection of CIM the effects of NMDA on 5-HT release in both brain structures were generally more marked than in vehicle injected controls. Repeated (15 day) treatment with CIM (10 or 20 mg/kg) caused a dose-dependent increase in basal extracellular 5-HT in both raphe and frontal cortex. In these animals, however, the effects of infusion of both 25 and 100 microM NMDA on 5-HT release in raphe and frontal cortex were greatly attenuated or abolished. This suggests that adaptive functional changes occur in NMDA receptor function during treatment with an antidepressant. The possible significance of this in the aetiology and treatment of depression is discussed.

Animals↗

PubMed2001

Effect of transgenic overexpression of NR2B on NMDA receptor function and synaptic plasticity in visual cortex.

The NMDA receptor (NMDAR) is a heteromer comprised of NR1 and NR2 subunits. Mice that overexpress the NR2B subunit exhibit enhanced hippocampal LTP, prolonged NMDAR currents, and improved memory ( Tang et al., 1999). In the current study, we explored visual cortex plasticity and NMDAR function in NR2B overexpressing transgenic mice. Unlike the hippocampus, in vitro synaptic plasticity of the visual cortex was unaltered by NR2B overexpression. Consistent with the plasticity findings, NMDAR excitatory postsynaptic current (EPSC) durations from layer 2/3 pyramidal cells were similar in wild-type (wt) and transgenic (tg) mice. Furthermore, temporal summation of NMDAR EPSCs to 10, 20, and 40 Hz stimulation did not differ between cells from wt and tg mice. Finally, although in situ studies clearly demonstrate overexpression of NR2B mRNA in visual cortex, we failed to observe a significant elevation in the synaptic expression of NR2B protein. We conclude that the synaptic ratio of NR2B over NR2A in the NMDA receptor complex in the visual cortex is not significantly influenced by the transgene overexpression. These data suggest that mRNA availability is not a limiting factor for the synthesis of NR2B protein in the visual cortex, and support the hypothesis that levels of NR2A, rather than NR2B, normally determine the subunit composition of NMDARs in visual cortex.

Animals↗