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Results for “Prefrontal Cortex”

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At least 523 records · Page 29Linked to original sources

PubMed2000

Elevation in late-life depression of intercellular adhesion molecule-1 expression in the dorsolateral prefrontal cortex.

OBJECTIVE: Late-life depression may be associated with vascular disease. The authors investigated this association by determining whether intercellular adhesion molecule-1 (ICAM-1), a marker of ischemia-induced inflammation, is elevated in the dorsolateral prefrontal cortex in depression. METHOD: The authors studied postmortem tissue from 20 depressed subjects and a matched comparison group of 20 nondepressed subjects. They used immunocytochemistry to stain ICAM-1 in blood vessels on sections of the dorsolateral prefrontal cortex and occipital cortex and quantitative true color image analysis to measure the proportion of vessels expressing ICAM-1. RESULTS: ICAM-1 was significantly higher in both the gray and white matter of the depressed subjects' dorsolateral prefrontal cortex than the comparison subjects' dorsolateral prefrontal cortex. The difference between these groups was much smaller in the gray and white matter of the occipital cortex. CONCLUSIONS: These findings support the vascular depression hypothesis, which has important implications for the understanding and management of late-life depression.

Age Factors↗

PubMed1999

Effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex in rats.

PURPOSE: To determine the effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex. METHODS: In 14 male Wistar rats, a microdialysis probe with a 2 mm long semipermeable membrane was implanted in the medial prefrontal cortex. The dialysis probe was perfused at a rate of 1 microl x min(-1) with an artificial cerebrospinal fluid solution. The rats were randomly allocated to two groups: ketamine (group K, n=7) and pentobarbital (group P, n=7). Each rat was subsequently given 0 (saline), 1, 10 and 100 mg x kg(-1) ketamine i.p. in group K, and 0 (saline), 0.5, 5 and 50 mg x kg(-1) pentobarbital i.p. in group P. Sixty minutes elapsed between administration. Noradrenaline concentration was measured by HPLC with an electrochemical detector at 20 min intervals. (detection limit: 250 fg x 20 microl(-1), coefficient variation of the assay: 4.9%). The data in the 20-40 min after each dose of ketamine or pentobarbital i.p. were used for the statistical analysis. RESULTS: Noradrenaline release after 100 mg x kg(-1) ketamine increased by 7.7 +/- 2.0 (SEM) pg x collection(-1) compared with 2.7 +/- 0.7, 3.3 +/- 1.0 and 4.2 +/- 0.8 pg x collection(-1) after saline, 1 and 10 mg x kg(-1) ketamine, respectively (P < 0.05). Noradrenaline release did not change after pentobarbital. CONCLUSION: This study suggests the ketamine and pentobarbital have different effects on noradrenergic neurons in the medial prefrontal cortex. The stimulating effect of ketamine on noradrenaline release from the cortex might contribute to unique clinical features of ketamine anesthesia.

Adjuvants, Anesthesia↗

PubMed1990

Behavioral electrophysiology of the prefrontal cortex of the primate.

The prefrontal cortex (PFC) is critical for temporal organization of behavior. It mediates cross-temporal sensorimotor contingencies, integrating motor action (including speech) with recent sensory information. It performs this role through cooperation of 2 cognitive functions represented in its dorsolateral areas: short-term memory (STM) and preparatory set. Supporting data have been obtained from monkeys performing delay tasks, which epitomize the principle of cross-temporal contingency. In a given trial, the animal performs an act contingent on a sensory cue given a few seconds or minutes earlier. During the delay between cue and response, cells in dorsolateral PFC show sustained activation. Two cell categories can be identified in tasks in which cue and response are spatially separate. Cells of the first participate in STM: Their activation tends to diminish as the delay progresses; in some, the activation level depends on the particular cue received. Similar cells are found elsewhere in the cortex. Cells of the second category seem to take part in preparation of motor response: Their activation tends to increase in anticipation of it and may be attuned to the particular movement the cue calls for. This cell type is rare outside of the frontal cortex. The temporally integrative function of the PFC is probably based on local interactions between "memory" and "motor-set" cells, as well as on neural associations between PFC and posterior cortical areas.

Animals↗

PubMed1989

The effects of amphetamine on synaptic plasticity in rat's medial prefrontal cortex.

Morphometric analysis of medial prefrontal cortex (layer VI) of rats treated daily with amphetamine in a dose of 2.5 mg/kg during 3 weeks was performed on the electron microscopic level. The efficacy of the amphetamine dosage was tested on behavioral observation. Synapses on dendritic shafts and spines were studied. The density of axo-dendritic synapses increase on 74%, while the density of synapses on spine's neck decreased on 53%. Most synaptic parameters measured in axo-dendritic (1) and axo-spinous (2) synapses increased significantly under the influence of 2.5 mg/kg dose of AMPH: area of presynaptic terminal increased on 35% (1) and 21% (2), length of postsynaptic density increased on 13% (1) and 12% (2), area of spine increase on 25%. But the density of synaptic vesicles near the active zone decrease (1-on 16.5%, 2-on 20%).

Amphetamines↗

PubMed1989

The effects of haloperidol on synaptic plasticity in rat's medial prefrontal cortex.

Morphometric analysis of Medial prefrontal cortex (layer VI) of rats treated daily with haloperidol in a dose of 0.1 mg/kg during 3 weeks was performed on the electron microscopic level. The efficacy of the haloperidol dosage was tested on the amphetamine psychosis model. Synapses on dendritic shafts and dendritic spines were studied. The density of synapses on dendritic shafts increased on 51%, while on spine's neck it decreased on 19%. There were significant changes of some synaptic parameters only in axo-dendritic synapses: area of presynaptic terminal decreased on 13% (p less than 0.05), length of postsynaptic density decreased on 15% (p less than 0.05), but the density of synaptic vesicles near the active zone increased on 10% (p less than 0.05).

Animals↗

PubMed2000

Maternal separation followed by early social deprivation affects the development of monoaminergic fiber systems in the medial prefrontal cortex of Octodon degus.

The influence of early postnatal socio-emotional deprivation on the development of tyrosine hydroxylase- and 5-hydroxytryptamine-immunoreactive fiber innervation in the medial prefrontal cortex was quantitatively investigated in the precocial rodent Octodon degus. Forty-five-days-old degus from two groups were compared: (i) degus which were repeatedly separated from their mothers during the first three postnatal weeks and after weaning reared in complete isolation; and (ii) degus which were reared under normal undisturbed social conditions. The two monoaminergic fiber systems in the four subregions of the medial prefrontal cortex responded differentially to the deprivation. While the infralimbic cortex was the only subregion that displayed an increase in 5-hydroxytryptamine-positive fiber densities (129.2%) but no changes in tyrosine hydroxylase-immunoreactive fibers, the precentral medial (82.2%), anterior cingulate (74.6%) and prelimbic cortex (86.9%) showed significantly reduced tyrosine hydroxylase-positive fiber innervation, but no changes in 5-hydroxytryptamine-immunoreactive fiber densities. The number of tyrosine hydroxylase-positive somata in the ventral tegmental area and in the substantia nigra remained unchanged. In cortical areas the number of tyrosine hydroxylase-immunoreactive somata was increased (depending on the medial prefrontal cortex subregion between 241.8% and 398.7%) in deprived animals. This altered balance between the serotonergic and dopaminergic cortical innervation in the different subregions of the medial prefrontal cortex may reflect a counter-regulative anatomical and functional adaptation, which may be triggered by an altered activity of these transmitter systems during the phases of maternal separation and social isolation.

Animals↗

PubMed2003

Category-specific representations of social and nonsocial knowledge in the human prefrontal cortex.

Complex social behavior and the relatively large size of the prefrontal cortex are arguably two of the characteristics that distinguish humans from other animals. Grafman presented a framework concerning how the prefrontal cortex (PFC) controls complex behavior using stored structured event complexes (SECs). We report behavioral and imaging data from a modified go/no-go paradigm in which subjects had to classify words (semantic) and phrases (SEC) according to category. In experimental trials, subjects classified items according to social or nonsocial activity; in control trials, they classified items according to font. Subjects were faster to classify social than nonsocial semantic items, with the reverse pattern evident for the social and nonsocial SEC items. In addition, the conditions were associated with different patterns of PFC activation. These results suggest that there are different psychological and neural substrates for social and nonsocial semantic and SEC representations.

Activities of Daily Living↗

PubMed2000

[Effects of (+/-)-pindolol over increased extracellular 5-HT level induced by fluvoxamine: regional difference in effect among the raphe, dorsal hippocampus and prefrontal cortex as measured by in vivo microdialysis technique].

It is known that the somatodendritic 5-hydroxytryptamine (5-HT)1A autoreceptor works to regulate the action of 5-HT neurons leading to the release of 5-HT. Our present study has addressed the possibility that (+/-)-pindolol, which is a non-selective beta-adrenoceptor antagonist/somatodendritic 5-HT1A autoreceptor antagonist, might have the ability to enhance the level of extracellular 5-HT when used with selective serotonin reuptake inhibitor (SSRI; i.e., fluvoxamine). We have used freely moving rats to measure the extracellular level of 5-HT and dopamine (DA) in the raphe, dorsal hippocampus and prefrontal cortex using an in vivo microdialysis technique. Response power of (+/-)-pindolol (8 mg/kg, i.p.) to the rise in extracellular 5-HT level when used with fluvoxamine (60 mg/kg, i.p.) was significant in the raphe, dorsal hippocampus and prefrontal cortex, while the degree of augmentation was more significant in the prefrontal cortex than in the dorsal hippocampus. The extracellular level of DA when used with (+/-)-pindolol showed a tendency to decrease in the raphe while showing a tendency to increase in the dorsal hippocampus. However, no change occurred in the prefrontal cortex. This indicates that (+/-)-pindolol has the ability to block the somatodendritic 5-HT1A autoreceptors, thereby weakening the fluvoxamine-induced indirect action of the autoreceptors in the raphe. We have obtained positive result for the probability of pindolol augmentation in two regions--dorsal hippocampus and prefrontal cortex. This indicates that augmentation therapy by the combined use of fluvoxamine with 5-HT1A antagonist will be valid and effective.

Animals↗

PubMed2003

Prefrontal cortex transcranial magnetic stimulation does not change local diffusion: a magnetic resonance imaging study in patients with depression.

OBJECTIVE: To determine whether transcranial magnetic stimulation over the left dorsolateral prefrontal cortex produces pathologic changes or leakage of the blood-brain barrier in patients with depression by using apparent diffusion coefficient magnetic resonance imaging. BACKGROUND: Transcranial magnetic stimulation is a new technology for noninvasively stimulating the brain. It appears to be a relatively safe technique, with some important exceptions. Its neurobiologic mechanisms of action are poorly understood. One theory to explain its apparent antidepressant effects involves a potential change in local blood-brain barrier settings, allowing passage of peripheral substances directly into brain parenchyma. Knowing whether transcranial magnetic stimulation changes local brain diffusion is important as well from a safety perspective. To test whether transcranial magnetic stimulation changes local brain diffusion, we used apparent diffusion coefficient magnetic resonance imaging in depressed patients undergoing interleaved transcranial magnetic stimulation/functional magnetic resonance imaging over the left prefrontal cortex. METHODS: Within a 1.5 Tesla magnetic resonance imaging scanner, 14 depressed patients were stimulated with a figure-eight transcranial magnetic stimulation coil over the left prefrontal cortex. Apparent diffusion coefficient magnetic resonance imaging was acquired before, and immediately after, 1 Hertz transcranial magnetic stimulation (147 stimuli) intermittently delivered at a motor threshold of more than 7.35 minutes. Phase maps of the transcranial magnetic stimulation magnetic fields were used to guide region-of-interest placement. RESULTS: No significant qualitative apparent diffusion coefficient differences were observed before and after 1 Hertz transcranial magnetic stimulation underneath the coil. CONCLUSIONS: One Hertz transcranial magnetic stimulation over the left dorsolateral prefrontal cortex as applied in this study did not result in pathologic changes or leakage of the blood-brain barrier in patients with depression. If prefrontal transcranial magnetic stimulation at these usage parameters changes local diffusion, it is not an obvious or large effect.

Adolescent↗

PubMed1991

The anxiogenic beta-carboline FG 7142 selectively increases dopamine release in rat prefrontal cortex as measured by microdialysis.

The effect of the anxiogenic beta-carboline methyl-beta-carboline-3-carboxyamide (FG 7142) on dopamine release in prefrontal cortex and striatum in the awake freely moving rat was determined using the technique of microdialysis. FG 7142 (25 mg/kg, i.p.) caused a time-dependent increase in dopamine release in prefrontal cortex which was statistically significantly greater than the response to vehicle administration. Dopamine release in striatum was unaltered by FG 7142. Pretreatment of animals with the benzodiazepine antagonist Ro 15-1788 (30 mg/kg, i.p., 15 min prior to FG 7142 administration) completely abolished the increase in dopamine release caused by FG 7142 in prefrontal cortex. These data indicate that the anxiogenic benzodiazepine inverse agonist FG 7142 can selectively increase dopamine release in prefrontal cortex, and that this effect appears to be mediated via the gamma-aminobutyric acid/benzodiazepine receptor complex.

Animals↗

PubMed1992

Effects of 6-hydroxydopamine lesions of the prefrontal cortex on tyrosine hydroxylase activity in mesolimbic and nigrostriatal dopamine systems.

The effects of prefrontal cortical dopamine depletion on subcortical dopamine function in the rat were examined. 6-Hydroxydopamine lesions of the dopaminergic innervation of the prefrontal cortex did not alter concentrations of dopamine or its metabolite 3,4-dihydroxyphenylacetic acid in either the striatum or nucleus accumbens. Similarly, the activity of the catecholamine biosynthetic enzyme tyrosine hydroxylase in the striatal complex was not changed in animals with prefrontal cortical lesions. Animals sustaining neurotoxic lesions of the prefrontal cortex were challenged with haloperidol in order to activate submaximally tyrosine hydroxylase activity. The magnitude of the haloperidol-induced increase in enzyme activity in the nucleus accumbens was significantly greater in lesioned subjects than in control animals. These data suggest that lesions of the prefrontal cortical dopamine innervation do not result in significant alterations in basal dopaminergic function in the striatal complex. However, lesions of the dopaminergic innervation of the prefrontal cortex significantly increase the responsiveness of mesolimbic dopamine afferents to pharmacological challenge.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2004

Reciprocal modulation and attenuation in the prefrontal cortex: an fMRI study on emotional-cognitive interaction.

Everyday and clinical experience demonstrate strong interactions between emotions and cognitions. Nevertheless the neural correlates underlying emotional-cognitive interaction remain unclear. Using event-related fMRI, we investigated BOLD-signal increases and decreases in medial and lateral prefrontal cortical regions during emotional and non-emotional judgment of photographs taken from the International Affective Picture System (IAPS). Emotional and non-emotional judgment conditions were compared to each other as well as with baseline allowing for distinction between relative signal changes (comparison between conditions) and true signal changes (referring to baseline). We have found that: (1) both emotional and non-emotional judgment of IAPS pictures were characterized by signal increases in ventrally and dorsally located lateral prefrontal cortical areas and concurrent signal decreases in ventro- and dorsomedial prefrontal cortex; (2) direct comparison between emotional and non-emotional judgment showed relative signal increases in ventro- and dorsomedial prefrontal cortex, and in contrast, relative signal increases were detected in ventrally and dorsally located lateral prefrontal cortical areas when comparing non-emotional to emotional judgment; and (3) as shown in separate comparisons with baseline, these relative signal changes were due to smaller signal decreases in ventro- and dorsomedial prefrontal cortex and smaller signal increases in ventrally and dorsally located lateral prefrontal cortical areas during emotional judgment. Therefore, the emotional load of a cognitive task lead to both less deactivation of medial prefrontal regions and, at the same time, less activation of lateral prefrontal regions. Analogous patterns of reciprocal modulation and attenuation have previously been described for other cortical regions such as visual and auditory areas. Reciprocal modulation and attenuation in medial and lateral prefrontal cortex might constitute the neurophysiologic basis for emotional-cognitive interaction as observed in both healthy and psychiatric subjects.

Adult↗

PubMed2004

Transient dopamine synthesis modulation in prefrontal cortex: in vitro studies.

The present study provides further evidence for transient D1 autoreceptor-like synthesis modulation in prefrontal cortex, but not striatum, of developing rats. DOPA accumulation was attenuated in a concentration-dependent manner in slices from the prefrontal cortex and striatum at 15 days of age by the partial D1 agonist SKF 38393 (0.01-10 microM) and the full D1 agonist SKF-81297 (0.01-10 microM) following NSD-1015; the response was no longer apparent by 40 days. Both agonists had greater potency in prefrontal cortex than striatum, and SKF-81297 exerted greater maximal inhibitory effects than SKF-38393. The inhibitory effects of both agonists were antagonized by pre-incubation with the D1 antagonist SCH-23390 in cortex, but not in striatum.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1996

Mediation by neurotensin-receptors of effects of neurotensin on self-stimulation of the medial prefrontal cortex.

1 Intracortical microinjections of neurotensin (NT) selectively decreased intracranial self-stimulation (ICSS) of the medial prefrontal cortex in the rat. 2 To elucidate whether this effect is mediated by NT receptors or by the formation of NT-dopamine complexes, we investigated the effects on ICSS of intracortical microinjections of neurotensin (1-11), an NT fragment that forms extracellular complexes with dopamine but does not bind to NT receptors. 3 We also studied the effects of the peripheral administration of SR 48692, a selective antagonist of NT receptors, on the inhibition of ICSS produced by the intracortical administration of NT. 4 Unilateral microinjections of neurotensin (1-11) at doses of 10, 20 and 40 nmol into the medial prefrontal cortex did not change the basal ICSS rate of this area. 5 The intraperitoneal administration of SR 48692 at doses of 0.08 and 0.16 mg kg-1 30 min before microinjection of 10 nmol of NT into the medial prefrontal cortex, antagonized the inhibition of ICSS produced by the neuropeptide. 6 These results demonstrate that the inhibitory effect of NT on ICSS is mediated by NT receptors.

Animals↗

PubMed2000

Neuromodulation of the prefrontal cortex during sleep: a microdialysis study in rats.

To test the hypothesis that biogenic amines of the prefrontal cortex are involved in state-dependent cortical and behavioural activation, changes in extracellular levels of serotonin (5-HT), dopamine (DA), and noradrenaline (NA) were determined during the sleep-wake cycle in freely moving rats using microdialysis probes with parallel EEG recording. Serotonin gradually increased up to 450% during wakefulness (W) as compared to slow wave sleep (SWS), before decreasing toward stable levels during the next episode of SWS. Dopamine and its metabolite homovanillic acid (HVA) were reduced during W as compared to SWS. Although contradictory with the generally admitted enhancement of DA activity related to vigilance, this may be due to the particular role of DA neurons in the prefrontal cortex. However, DA and HVA showed dramatic changes announcing the transition between SWS and W. During paradoxical sleep (PS), DA and 5-HT showed complex changes, the direction of which depended on whether PS was followed by SWS or W. Biogenic amines of the prefrontal cortex are probably involved in cortical and behavioural activation.

Animals↗

PubMed1997

Impact of corticotropin-releasing hormone on extracellular norepinephrine in prefrontal cortex after chronic cold stress.

We have previously demonstrated that exposing rats to cold (5 degrees C) for 3-4 weeks potentiates the increase in extracellular norepinephrine (NE) in the medial prefrontal cortex produced by acute tail shock. In the present study, we used microdialysis to determine the duration of cold exposure required to produce this sensitization and explored the mechanism of the phenomenon. Tail shock elicited a twofold greater increase in extracellular NE in the medial prefrontal cortex of rats exposed to cold for 2 weeks than in naive control rats or in rats exposed to cold for 1 week and tested either immediately or after a 2-week delay. Local infusion of 10 microM D-amphetamine or 30 mM K+ increased extracellular NE in the medial prefrontal cortex (approximately 350 and 190%, respectively) comparably in control rats and rats exposed to cold for 3 weeks. In contrast, intraventricular administration of 3.0 microg of corticotropin-releasing hormone increased extracellular NE in the medial prefrontal cortex by 65% in rats exposed to cold for 2 weeks, but only 35% in control rats. These results indicate that an enhanced responsiveness of noradrenergic neurons to acute tail shock (1) requires approximately 2 weeks of cold exposure to develop and (2) may be mediated by a change at the level of the noradrenergic cell bodies rather than the nerve terminals.

Adrenergic Agents↗

PubMed2002

Differential activation of the human orbital, mid-ventrolateral, and mid-dorsolateral prefrontal cortex during the processing of visual stimuli.

There is considerable uncertainty about the precise functional contribution of the different parts of the prefrontal cortex to mnemonic processing. Changes in regional cerebral blood flow were measured with positron emission tomography in normal human subjects exposed to abstract visual designs under various conditions. It was demonstrated that the processing of stimuli that deviate from expectations involves selectively the orbitofrontal cortex, namely the part of the frontal cortex that is preferentially linked with the limbic system. By contrast, when the subject is making an explicit decision on the contents of memory (e.g., judgments of relative stimulus familiarity), the mid-ventrolateral prefrontal cortex is involved. The mid-dorsolateral prefrontal cortex is engaged when monitoring of information within working memory is required.

Adult↗

PubMed2001

The relative involvement of anterior cingulate and prefrontal cortex in attentional control depends on nature of conflict.

While numerous studies have implicated both anterior cingulate and prefrontal cortex in attentional control, the nature of their involvement remains a source of debate. Here we determine the extent to which their relative involvement in attentional control depends upon the levels of processing at which the conflict occurs (e.g., response, non-response). Using a combination of blocked and rapid presentation event-related functional magnetic resonance imaging techniques, we compared neural activity during incongruent Stroop trial types that produce conflict at different levels of processing. Our data suggest that the involvement of anterior cingulate and right prefrontal cortex in attentional control is primarily limited to situations of response conflict, while the involvement of left prefrontal cortex extends to the occurrence of conflict at non-response levels.

Adolescent↗