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 1,675 records · Page 93Linked to original sources

PubMed2004

The right dorsolateral prefrontal cortex is essential in time reproduction: an investigation with repetitive transcranial magnetic stimulation.

This study used repetitive transcranial magnetic stimulation (rTMS) to investigate the roles of the right dorsolateral prefrontal cortex (DLPFC) and supplementary motor area (SMA) in short (500 ms) and long (2 s) interval timing. The results were compared with rTMS over the leg area of motor cortex, an area not thought to be involved with time estimation. rTMS was delivered during one of two phases of a time reproduction task: at the onset of the Estimation Phase (presentation of the interval to be timed) and at the onset of the Reproduction Phase (subjects' reproduction of the timed interval). There was a significant main effect of Site (SMA vs. right DLPFC vs. leg motor area) due to the fact that rTMS over the right DLPFC caused subjects to underestimate time intervals compared with rTMS over the leg motor area. There was also a significant three-way interaction between Site, Duration and Phase (Estimation Phase vs. Reproduction Phase) that post hoc analyses showed was due to underestimation of long intervals when rTMS was given over the right DLPFC at the start of the Reproduction Phase. There was no effect of rTMS over the right DLPFC or SMA in the short interval task. This is consistent with previous studies showing that the right DLPFC is important in estimating time intervals in the seconds-range. In addition, we suggest that the selectivity of the rTMS effect for the Reproduction Phase indicates that the right DLPFC plays a particular role in memory processes.

Adult↗

PubMed1997

The anatomical relationships of the prefrontal cortex with limbic structures and the basal ganglia.

This paper briefly discusses the anatomical criteria that have been used to delineate the prefrontal cortex (PFC) from the (pre)motor cortical areas in the frontal lobe. Single anatomical criteria, such as cytoarchitecture, connectivity with the mediodorsal thalamic nucleus or a dopaminergic innervation, are insufficient to unequivocally define the PFC. It is argued that, with respect to a number of structural aspects, the prefrontal and the (pre)motor cortical areas must be viewed as a continuum, whereas a (functional) differentiation is based on the type of information that is being processed in different parts of the frontal lobe. The involvement of the PFC, like the premotor cortex, in a number of basal ganglia-thalamocortical circuits may be interpreted in the same way. The paper also summarizes the organization of the inputs from midline/intralaminar thalamic nuclei, the basal amygdaloid complex and the hippocampus into the PFC-ventral striatal system. The results of tracing studies in rats indicate that these thalamic and limbic inputs both at the level of the PFC and the ventral striatum show various patterns of convergence and segregation. This leads to the conclusion that the PFC-ventral striatal system consists of a number of smaller modules.

Amygdala↗

PubMed2004

Biphasic effects of ethanol on acetylcholine release in the rat prefrontal cortex.

Low doses of ethanol (0.5 g/kg i.p.) increased, while higher doses (1 g/kg i.p.) reduced acetylcholine (ACh) release in the rat prefrontal cortex (PFC). Ethanol (50-300 mM) applied in the nucleus basalis through a second dialysis probe caused concentration-dependent biphasic changes in prefrontocortical ACh release. Ethanol apparently acts on cholinergic fibers to modulate ACh transmission in the PFC. These results could be of relevance for the bidirectional modulation of working memory by ethanol.

Acetylcholine↗

PubMed2004

5-HT6 receptor antagonist SB-271046 enhances extracellular levels of monoamines in the rat medial prefrontal cortex.

The present study investigated the neurochemical effects of the selective 5-HT(6) receptor antagonist SB-271046 in the rat medial prefrontal cortex (mPFC). The effect of SB-271046 on extracellular levels of dopamine (DA), norepinephrine (NE), and serotonin (5-HT) in the mPFC was examined using in vivo microdialysis in the freely moving rat. SB-271046 (10 mg/kg, p.o.) produced a significant increase in extracellular levels of both DA and NE without altering 5-HT neurotransmission. These results further support the rationale for the use of 5-HT(6) receptor antagonists in the treatment of cognitive dysfunction associated with psychiatric diseases.

Analysis of Variance↗

PubMed2000

Medial prefrontal cortex acetylcholine injection-induced hypotension: the role of hindlimb vasodilation.

The injection of acetylcholine (ACh) into the cingulate region of the medial prefrontal cortex (MPFC) causes a marked fall in arterial blood pressure which is not accompanied by changes in heart rate. The purpose of the present study was to investigate the hemodynamic basis for this stimulus-induced hypotension in Sprague-Dawley rats. The study was designed to determine whether a change in the vascular resistance of hindlimb, renal or mesenteric vascular beds contributes to the fall in arterial pressure in response to ACh injection into the cingulate cortex. Miniature pulsed-Doppler flow probes were used to measure changes in regional blood flow and vascular resistance. The results indicated that the hypotensive response was largely due to a consistent and marked vasodilation in the hindlimb vascular bed. On this basis, an additional experiment was then undertaken to determine the mechanisms that contribute to hindlimb vasodilation. The effect of interrupting the autonomic innervation of one leg on the hindlimb vasodilator response was tested. Unilateral transection of the lumbar sympathetic chain attenuated the cingulate ACh-induced vasodilation in the ipsilateral, but not in the contralateral hindlimb. These results suggest that the hypotensive response to cingulate cortex-ACh injection is caused by skeletal muscle vasodilation mediated by a sympathetic chain-related vasodilator system.

Acetylcholine↗

PubMed2006

Glial fibrillary acidic protein and glutamine synthetase in subregions of prefrontal cortex in schizophrenia and mood disorder.

Several theories of schizophrenia suggest dysfunction in glutamate neurotransmission in higher brain regions such as the prefrontal cortex (PFC). Previous studies have investigated whether astroglial abnormalities could give rise to glutamate dysfunction using glial fibrillary acidic protein (GFAP) immunocytochemistry. We have used quantitative immunoautoradiography to measure glutamine synthetase (GS), the glial enzyme which recycles synaptic glutamate, as a more direct test of glial mechanisms of abnormal glutamate function in schizophrenia. We compared GS with GFAP immunoautoradiography in dorsolateral (area 9) and orbitofrontal (area 11/47) cortex. Optical density measures from film autoradiographs revealed an increase in GFAP immunoreactivity in area 9 in schizophrenia and a decrease in area 11/47 in both schizophrenia and bipolar disorder. The increase in GFAP in area 9 significantly correlated with lifetime antipsychotic drug treatment, whereas the reduction in area 11/47 occurred despite this effect. There were no changes in GS immunoreactivity in any psychiatric disorder. Regional and antigen-specific down-regulation of GFAP protein in OFC in schizophrenia and bipolar disorder may relate to disease mechanisms of psychosis.

Adult↗

PubMed1997

Prefrontal cortex fMRI signal changes are correlated with working memory load.

We investigated whether a nonspatial working memory (WM) task would activate dorsolateral prefrontal cortex (DLPFC) and whether activation would be correlated with WM load. Using functional magnetic resonance imaging we measured regional brain signal changes in 12 normal subjects performing a continuous performance, choice reaction time task that requires WM. A high WM load condition was compared with a non-WM choice reaction time control condition (WM effect) and a low WM load condition (load effect). Significant changes in signal intensity occurred in the DLPFC, frontal motor regions and the intraparietal sulcus (IPS) in both comparisons. These findings support the role of DLPFC and IPS in WM and suggest that signal changes in DLPFC correlate with WM load.

Adult↗

PubMed2003

Effects of acetylcholine antagonist injection into the prefrontal cortex on the progress of lever-press extinction in rats.

To determine the relationship between cholinergic modulation within the rat medial prefrontal cortex (mPFC) and the progress of lever-press extinction, we conducted an experiment in which muscarinic and nicotinic acetylcholine (ACh) receptor antagonists were microinjected into the mPFC. The muscarinic antagonist injected immediately before the initial extinction training did not affect the progress of extinction during the training (no within-session effect), but disrupted a second re-training session the next day (across-session effect). By contrast, the nicotinic antagonist disrupted the progress of extinction both within and across training sessions. These results confirm that ACh in the mPFC modulates lever-press extinction and suggest that nicotinic and muscarinic receptors are involved in short- and long-term memory processes.

Acetylcholine↗

PubMed1995

Concentration-dependent dual action of locally applied N-methyl-D-aspartate on extracellular dopamine in the rat prefrontal cortex in vivo.

Using microdialysis, the glutamate agonist N-methyl-D-aspartate (NMDA) was perfused for 20 min through the medial prefrontal cortex of freely moving rats, and its effects on extracellular concentrations of dopamine (DA) were determined. NMDA (1 mM) increased DA to 170-1500%, depending on the intensity and duration of the clonic forelimb jerks and convulsions that were induced. NMDA (0.1 mM), however, decreased DA to 61%. Metabolites of DA were decreased after both concentrations of NMDA. The effects of both 0.1 mM and 1 mM NMDA were blocked by 0.5 mM of the competitive NMDA-antagonist D-AP-5. The NMDA-induced decrease in release and metabolism possibly results from an indirect action via an inhibitory local interneuron or polysynaptic circuit.

2-Amino-5-phosphonovalerate↗

PubMed2001

Posttraining lesions of the medial prefrontal cortex impair performance of Pavlovian eyeblink conditioning but have no effect on concomitant heart rate changes in rabbits (Oryctolagus cuniculus).

The medial prefrontal cortex (mPFC) plays a critical role in conditioned autonomic adjustments but is not involved in classically conditioned somatomotor responses unless the training conditions include reversal or trace conditioning. The studies showing these effects have all used pretraining lesions. The present study assessed the effects of posttraining lesions on eyeblink (EB) and heart rate (HR) conditioned responses (CRs) in both delay and trace conditioning paradigms in the rabbit (Oryctolagus cuniculus). Posttraining lesions lowered the percentage of EB CRs during retesting compared with pretesting levels for both delay and trace conditioning. Control lesions and pretraining lesions produced no significant effects during retesting. Posttraining lesions had no effect on the HR CR. These findings suggest that a critical mechanism in the mPFC is involved in retrieval of information during EB conditioning but that the mPFC integration of autonomic and somatomotor processes is not critical to this retrieval process.

Animals↗

PubMed2002

Integration of emotion and cognition in the lateral prefrontal cortex.

We used functional MRI to test the hypothesis that emotional states can selectively influence cognition-related neural activity in lateral prefrontal cortex (PFC), as evidence for an integration of emotion and cognition. Participants (n = 14) watched short videos intended to induce emotional states (pleasant/approach related, unpleasant/withdrawal related, or neutral). After each video, the participants were scanned while performing a 3-back working memory task having either words or faces as stimuli. Task-related neural activity in bilateral PFC showed a predicted pattern: an Emotion x Stimulus crossover interaction, with no main effects, with activity predicting task performance. This highly specific result indicates that emotion and higher cognition can be truly integrated, i.e., at some point of processing, functional specialization is lost, and emotion and cognition conjointly and equally contribute to the control of thought and behavior. Other regions in lateral PFC showed hemispheric specialization for emotion and for stimuli separately, consistent with a hierarchical and hemisphere-based mechanism of integration.

Adult↗

PubMed2004

Resistance to extinction is associated with impaired immediate early gene induction in medial prefrontal cortex and amygdala.

Extinction of classical fear conditioning is thought to involve activity-dependent potentiation of synaptic transmission in the medial prefrontal cortex (mPFC), resulting in the inhibition of amygdala-dependent fear responses. While many studies have addressed the mechanisms underlying extinction learning, it is unclear what determines whether extinction memory is consolidated or whether spontaneous recovery of the fear response occurs. Here we show, using a combined electrophysiological and immunocytochemical approach, that spontaneous recovery of conditioned fear in mice is associated with a prolonged expression of long-term depression of synaptic transmission in the mPFC and the failure of induction of the immediate-early genesc-Fos and zif268 in the mPFC and the basolateral nucleus of the amygdala. This suggests that coordinated activity-dependent changes in gene expression in the mPFC and the amygdala may underlie the formation of long-term fear extinction memory.

Amygdala↗

PubMed2004

Medial prefrontal cortex and precision of temporal discrimination: a lesion, microinjection, and microdialysis study.

In this paper, we examined the role of the medial prefrontal cortex in temporal discrimination in three experiments using rats. Experiment 1 attempted to dissociate the roles of the medial precentral (PrCm) area from the prelimbic and infralimbic (PL-IL) area in temporal discrimination using fixed-interval (FI) schedule. The gradient of response rate distribution became more moderate by a lesion of the PrCm, but not by a lesion of the PL-IL. In experiment 2, the efflux of acetylcholine (ACh) in the PrCm area during temporal discrimination tasks was compared to that during non-temporal discrimination tasks. ACh efflux was not different between these two tasks. In experiment 3, microinjection of the anticholinergic drug scopolamine (10 microg) into the PrCm area made the gradient of response rate distribution moderate. These findings suggest that reduced activity of the ACh system within the PrCm area impairs the precision of temporal discrimination, even though enhancement of this system is not indispensable for performing temporal discrimination.

Acetylcholine↗

PubMed2004

Role of catecholaminergic inputs to the medial prefrontal cortex in local and subcortical expression of Fos after psychological stress.

A wide variety of stressors elicit Fos expression in the medial prefrontal cortex (mPFC). No direct attempts, however, have been made to determine the role of the inputs that drive this response. We examined the effects of lesions of mPFC catecholamine terminals on local expression of Fos after exposure to air puff, a stimulus that in the rat acts as an acute psychological stressor. We also examined the effects of these lesions on Fos expression in a variety of subcortical neuronal populations implicated in the control of adrenocortical activation, one classic hallmark of the stress response. Lesions of the mPFC that were restricted to dopaminergic terminals significantly reduced numbers of Fos-immunoreactive (Fos-IR) cells seen in the mPFC after air puff, but had no significant effect on stress-induced Fos expression in the subcortical structures examined. Lesions of the mPFC that affected both dopaminergic and noradrenergic terminals also reduced numbers of Fos-IR cells observed in the mPFC after air puff. Additionally, these lesions resulted in a significant reduction in stress-induced Fos-IR in the ventral bed nucleus of the stria terminalis. These results demonstrate a role for catecholaminergic inputs to the mPFC, in the generation of both local and subcortical responses to psychological stress.

Animals↗

PubMed2000

GABA(A) and GABA(B) receptors modulating basal and footshock-induced nitric oxide releases in rat prefrontal cortex.

Using an in vivo brain microdialysis technique, we measured extracellular levels of nitric oxide (NO) metabolites (NO(x)(-)) in the medial prefrontal cortex (mPFC) upon perfusion of gamma-aminobutyric acid (GABA) receptor antagonists as well as agonists, and also examined the effects of GABA receptor agonists on mild intermittent footshock-induced NO releases in the mPFC in conscious rats. Perfusion of either bicuculline methiodide, a GABA(A) receptor antagonist, or saclofen, a GABA(B) receptor antagonist, through a microdialysis probe resulted in dose-dependent increases in NO(x)(-) levels. Higher-dose perfusion of either muscimol (50 microM), a GABA(A) receptor agonist, or baclofen (250 microM), a GABA(B) receptor agonist resulted in a significant decrease in NO(x)(-) levels. The elevated levels of NO(x)(-) after mild intermittent footshock were attenuated by perfusion of either muscimol (10 microM) or baclofen (50 microM), either of which alone did not affect basal NO(x)(-) levels. These findings are likely to provide helpful clues to our understanding of the inhibitory modulation of basal and footshock-induced NO metabolites releases by GABA(A) and GABA(B) receptors in the mPFC.

Animals↗

PubMed2006

Somal size of immunolabeled pyramidal cells in the prefrontal cortex of subjects with schizophrenia.

BACKGROUND: Although the somal volume of Nissl-stained deep layer 3 pyramidal cells is reduced in prefrontal cortex area 9 of subjects with schizophrenia, the subset of large pyramidal cells immunoreactive (IR) for nonphosphorylated neurofilament protein (NNFP) is not. Consequently, we hypothesized that the somal volume of another subset of pyramidal cells immunoreactive for neuronal calcium binding protein-1 (Necab-1) is significantly reduced in schizophrenia. METHODS: We labeled Necab-1-IR pyramidal neurons using immunoperoxidase techniques and estimated the mean somal volume in deep layer 3 of area 9 in 13 matched pairs of control and schizophrenic subjects. Identical studies were conducted for pyramidal neurons immunoreactive for neuronal nuclear protein (Neu-N), which is present in all neurons. RESULTS: In subjects with schizophrenia, neither the mean somal volume of Necab-1-IR pyramidal neurons nor of Neu-N-IR pyramidal neurons was significantly different from control subjects. In addition, the mean somal volume of Neu-N-IR cells was larger than that of Nissl-stained cells in both subject groups, and the magnitude of this difference was greater for the subjects with schizophrenia. CONCLUSIONS: These findings suggest that immunoperoxidase techniques are associated with an overestimation of the volume of labeled neurons. This confound appears to interact with disease state, and thus obscures differences between diagnostic groups.

Adult↗

PubMed1996

Characterization of excitatory amino acid modulation of dopamine release in the prefrontal cortex of conscious rats.

The effect of various classes of excitatory amino acid agonists on the release of dopamine in the medial prefrontal cortex (PFC) of awake rats was examined using intracerebral microdialysis. Local infusion of 20 muM alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), through the microdialysis probe, produced a significant increase of more than twofold in extra-cellular levels of dopamine. Application of 100 microM AMPA increased these levels nearly 15 fold. The AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (50microM) blocked the increase in dopamine release produced by 20 microM AMPA. Local infusion of kainate at concentrations of 5 and 20 microM increased dopamine release by nearly 150 and 500%, respectively. Local application of CMQX (50 microM) before 20 microM kainate significantly attenuated the stimulatory effect of kainate on dopamine levels. In contrast to AMPA and kainate, infusion of N-methyl-D-aspartate (NMDA) at 20 or 100 microM did not increase dopamine release. In fact, a trend toward a decrease in dopamine release was evident after 100 microM NMDA. The present study indicates that the in vivo release of dopamine in the PFC is facilitated by AMPA and kainate receptors. This modulation is more profound than that previously reported in basal ganglia. The lack of an excitatory effect of NMDA is in agreement with recent reports that the NMDA receptor may inhibit indirectly dopaminergic neurotransmission in the PFC.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1994

Electrophysiological evidence for a functional interaction between 5-HT1A and 5-HT2A receptors in the rat medial prefrontal cortex: an iontophoretic study.

In this study, we examined the interaction of 5-HT1A and 5-HT2A receptors in the rat medial prefrontal cortex (mPFc) using the techniques of extracellular single unit recording and microiontophoresis. The iontophoresis of the selective 5-HT1A receptor agonist (+-)-8-hydroxy-2-(di-n-propylamino) tetralin (8-OHDPAT) produced a current-dependent suppression (2.5-20 nA) of the basal firing rate of spontaneously active mPFc cells. The iontophoretic (5-10 nA) and systemic administration (0.1-0.5 mg/kg, i.v.) of the 5-HT2A/5-HT2C receptor antagonist ritanserin and the selective 5-HT2A receptor antagonist MDL 28727 significantly potentiated and prolonged 8-OHDPAT's suppressant action. In addition, the systemic administration of another selective 5-HT2A antagonist MDL 100907, but not its less active enantiomer MDL 100009, also potentiated and prolonged 8-OHDPAT's action. The potentiating effect of the 5-HT2A receptor antagonists on the action of 8-OHDPAT is specific in that neither the iontophoresis of ritanserin nor MDL 28727 altered the suppressant action produced by the iontophoresis of the 5-HT3 receptor agonist 2-methylserotonin onto mPFc cells. Moreover, the suppressant action of 8-OHDPAT was not altered by the systemic administration of the selective 5-HT3 receptor antagonist granisetron (0.1-0.5 mg/kg, i.v.). On the other hand, the iontophoresis of a low current (0.5 nA) of the 5-HT2A,2C receptor agonist (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) potentiated the excitation induced by the iontophoresis of l-glutamate on quiescent mPFc cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamines↗