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Results for “Prefrontal Cortex”

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PubMed1999

Effects of antipsychotic drugs on extracellular dopamine levels in rat medial prefrontal cortex and nucleus accumbens.

The present study was designed to compare the effects of typical and atypical antipsychotic drugs on extracellular dopamine (DA) levels in the medial prefrontal cortex (mPFC) and the nucleus accumbens (NAC), using in vivo microdialysis with dual probe implantation in awake, freely moving rats. Amperozide (2 and 10 mg/kg), clozapine (5 and 20 mg/kg), and olanzapine (10 mg/kg), all of which are atypical antipsychotics, produced greater increases in extracellular DA levels in the mPFC than in the NAC. Olanzapine (1 mg/kg), risperidone (0.1 and 1 mg/kg), also an atypical antipsychotic, and S-(-)-sulpiride (25 mg/kg), a typical antipsychotic, produced comparable increases in extracellular DA levels in the mPFC and the NAC. S-(-)-sulpiride (10 mg/kg) and haloperidol (0.1 and 1 mg/kg), another typical antipsychotic, significantly increased extracellular DA levels in the NAC but not in the mPFC. The effects of the six antipsychotic drugs to increase extracellular DA levels in the mPFC relative to those in the NAC was positively correlated with the difference between their pKi values for serotonin (5-hydroxytryptamine, 5-HT2A) and DA-D2 receptors and was inversely correlated to their pKi values for D2 or D3 receptors, but was not for 5-HT2A receptors alone. These results are consistent with the hypothesis that the ability of antipsychotic drugs to produce a greater increase in prefrontal compared with NAC extracellular DA levels may be related, in part, to weak D2 and D3 receptor affinity relative to 5-HT2A receptor antagonism.

Animals↗

PubMed2004

Nucleus accumbens and medial prefrontal cortex dopaminergic response to self-administered cocaine in naive rats.

Cocaine reinforcement is strongly associated with increased nucleus accumbens dopamine (NAcc DA). The involvement of medial prefrontal cortex (mPFC) DA in cocaine reward is less defined, but substantial evidence indicates that increased mPFC DA may suppress NAcc DA levels. Using in vivo microdialysis, NAcc or mPFC DA was determined in cocaine-naive rats after a self-administered cocaine injection (3.0 mg/kg). Extracellular levels of NAcc DA were dramatically enhanced 10 min post-cocaine injection, but dropped significantly at each subsequent assessment. mPFC DA also increased significantly, but to a lesser extent than observed in the NAcc. Findings of prominent DA increases in both the NAcc and mPFC terminals during the test session indicate that NAcc DA responses do not appear to be inhibited by increased mPFC DA during cocaine self-administration.

Analysis of Variance↗

PubMed2006

Ventral hippocampal neurons project axons simultaneously to the medial prefrontal cortex and amygdala in the rat.

The ventral hippocampus (VH) may have an important role in spatial memory processes and emotional behaviors through connections with the medial prefrontal cortex (mPFC) and amygdala. Although the mPFC and amygdala receive afferent projections from the VH, it has not been determined whether the individual VH neurons project to both the mPFC and the amygdala. In this study, antidromic responses to the mPFC and amygdala stimulation were evoked in single VH neurons. In addition, VH neurons were retrogradely double-labeled with fluorescent tracers injected in the mPFC and amygdala. VH neurons projecting to both the mPFC and amygdala were predominantly located in the subiculum and CA1 and bifurcated near or at the soma. Our anatomical and electrophysiological evidence for the presence of VH neurons projecting to both the mPFC and amygdala provides a previously unrecognized pathway from the hippocampus that simultaneously activates the mPFC and amygdala.

Amygdala↗

PubMed1993

In vivo release of dopamine from rat striatum, substantia nigra and prefrontal cortex: differential modulation by baclofen.

1. The effect of baclofen, a GABAB receptor agonist, on the release of dopamine from the striatum (ST), substantia nigra (SN) and prefrontal cortex (PFC) of the rat was examined by intracerebral microdialysis. 2. Perfusion of baclofen 50 microM did not affect the striatal release of dopamine. However, dopamine release was markedly reduced in the SN and PFC. 3. 3,4-Dihydroxyphenylacetic acid and homovanillic acid output increased in the ST and decreased in the SN and PFC when baclofen was perfused through the microdialysis probe. 5-Hydroxyindoleacetic acid levels were not affected in any experimental condition by baclofen perfusion. 4. The results suggest that GABAB receptors modulate the release of dopamine in the SN and PFC, but do not affect the striatal release of dopamine, which indicates that the role of GABA receptor activation is different in the dopaminergic terminals of the ST and PFC.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1999

Blockade of NMDA receptors located at the dorsomedial prefrontal cortex impairs spatial working memory in rats.

We investigated the effects of NMDA and muscarinic acetylcholine receptor blockade in the rostral part of dorsomedial (dmPFC) and dorsolateral prefrontal cortex (dlPFC) on spatial working memory (SWM) (delayed non-matching to position task (DNMTP)). The NMDA antagonist, CPP (0.01, 0.03, 0.1 and 0.3 microg/hemisphere) and the muscarinic antagonist, scopolamine (10 microg/hemisphere) were locally infused into the brain of male Wistar rats. In the mPFC CPP 0.1 microg disrupted SWM delay-dependently and CPP 0.3 microg caused a delay-independent performance deficit. Scopolamine disrupted non-cognitive performance, but did not affect SWM accuracy. In the dlPFC, scopolamine or lower doses of CPP did not affect SWM accuracy, but CPP 0.3 microg disrupted non-cognitive performance. We concluded that the NMDA receptors in the dmPFC regulate SWM processes, whereas the muscarinic receptors in the dmPFC mediate non-cognitive performance in the DNMTP task.

Animals↗

PubMed2003

Synaptic basis of persistent activity in prefrontal cortex in vivo and in organotypic cultures.

Persistent activity is observed in many cortical and subcortical brain regions, and may subserve a variety of functions. Within the prefrontal cortex (PFC), neurons transiently maintain information in working memory via persistent activity patterns; however, the mechanisms involved are largely unknown. The present study used intracellular recordings from deep layer PFC neurons in vivo and patch-clamp recordings from PFC neurons in organotypic brain slice cultures to examine the ionic mechanisms underlying persistent activity states evoked by various inputs. Persistent activity had consistent features regardless of the initiating stimulus; it was driven by non-NMDA glutamate receptors yet consisted of an initial GABA mediated component, followed by a prolonged synaptically mediated inward current that maintained the sustained depolarization on which rode many asynchronous GABA-mediated events. The stereotyped nature of the multiple-component persistent activity pattern reported here might be a common feature of interconnected cortical networks but within PFC could be related to the persistent activity required for working memory.

Action Potentials↗

PubMed2003

Effects of acute repetitive transcranial magnetic stimulation on extracellular serotonin concentration in the rat prefrontal cortex.

Repetitive transcranial magnetic stimulation (rTMS) changes the function of the cortex. This study clarified the effects of acute rTMS treatment on extracellular serotonin (5-HT) concentrations in the rat prefrontal cortex (PFC) by using in vivo microdialysis methods. Each rat received acute rTMS treatment of the frontal brain at 500 stimuli from twenty trains applied at 25 Hz for 1 s at 1-min intervals between trains. Sham-treated rats received the same handling procedure and sound of the stimulator. Sham treatment increased the extracellular 5-HT levels compared with the non-treated group. However, rTMS treatment using the stimulation intensity of 110% motor threshold eliminated the increase in 5-HT levels induced by the sham treatment. Acute rTMS treatment of the frontal brain is related to the serotonergic neuronal system in the rat PFC, and it may have therapeutic implications for emotional disorders.

Animals↗

PubMed2005

Forming impressions of people versus inanimate objects: social-cognitive processing in the medial prefrontal cortex.

Recent neuroimaging research has linked the task of forming a "person impression" to a distinct pattern of neural activation that includes dorsal regions of the medial prefrontal cortex (mPFC). Although this result suggests the distinctiveness of social cognition - the processes that support inferences about the psychological aspects of other people - it remains unclear whether mPFC contributions to this impression formation task were person specific or if they would extend to other stimulus targets. To address this unresolved issue, participants in the current study underwent fMRI scanning while performing impression formation or a control task for two types of target: other people and inanimate objects. Specifically, participants were asked to use experimentally-provided information either to form an impression of a person or an object or to intentionally encode the sequence in which the information was presented. Results demonstrated that activation in an extensive region of dorsal mPFC was greater for impression formation of other people than for all other trial types, suggesting that this region specifically indexes the social-cognitive aspects of impression formation (i.e., understanding the psychological characteristics of another mental agent). These findings underscore the extent to which social cognition relies on distinct neural mechanisms.

Adolescent↗

PubMed2003

Norepinephrine in the prefrontal cortex is critical for amphetamine-induced reward and mesoaccumbens dopamine release.

Increasing evidence points to a major involvement of cortical areas in addictive mechanisms. Noradrenergic transmission in the medial prefrontal cortex (mpFC) has been shown to affect the motor effects of amphetamine, although there is no evidence of its involvement in the rewarding effects of this psychostimulant. The present experiments were aimed at investigating the possibility of a selective involvement of prefrontal cortical norepinephrine (NE) in the rewarding-reinforcing effects of amphetamine. To do so, we evaluated the effects of mpFC NE selective depletion in mice of C57BL/6J inbred strain, a background commonly used in molecular approaches that is known to be highly susceptible to the rewarding effects of the psychostimulant. In a first set of experiments, we demonstrated the absence of amphetamine-induced conditioned place preference in mice bearing prefrontal NE depletion. In a second series of experiments, we demonstrated that the same lesion dramatically reduced amphetamine-induced mesoaccumbens dopamine release as measured by intracerebral microdialysis. These results indicate that noradrenergic prefrontal transmission, by allowing increased dopamine release in the nucleus accumbens induced by amphetamine, is a critical factor for the rewarding-reinforcing effects of this drug.

Amphetamine↗

PubMedDate not supplied

Hippocampal train stimulation modulates recall of fear extinction independently of prefrontal cortex synaptic plasticity and lesions.

It has been shown that long-term potentiation (LTP) develops in the connection between the mediodorsal thalamus (MD) and the medial prefrontal cortex (mPFC) and between the hippocampus (HPC) and the mPFC following fear extinction, and correlates with extinction retention. However, recent lesion studies have shown that combined lesions of the MD and mPFC do not interfere with extinction learning and retention, while inactivation of the dorsal HPC disrupts fear extinction memory. Here we found in rats that immediate post-training HPC low-frequency stimulation (LFS) suppressed extinction-related LTP in the HPC-mPFC pathway and induced difficulties in extinction recall. HPC tetanus, applied several hours later, failed to re-establish mPFC LTP but facilitated recall of extinction. Delayed post-training HPC LFS also provoked mPFC depotentiation and difficulties with extinction recall. HPC tetanus abolished these two effects. We also found that damage to the mPFC induced fear return only in rats that received HPC LFS following extinction training. HPC tetanus also reversed this behavioral effect of HPC LFS in lesioned rats. These data suggest that the HPC interacts with the mPFC during fear extinction, but can modulate fear extinction independently of this interaction.

Animals↗

PubMedDate not supplied

Effect of acute and chronic administration of citalopram on glutamate and aspartate release in the rat prefrontal cortex.

The present study was designed to determine whether peripheral administration of the selective serotonin reuptake inhibitor (SSRI) citalopram influenced glutamate and aspartate release in the rat prefrontal cortex using in vivo microdialysis. Citalopram was given acutely at doses of 10 and 20 mg/kg or chronically at a dose of 10 mg/kg daily for two weeks, in both cases by intraperitoneal (ip) route. Citalopram given at a single dose of 20 mg/kg, but not 10 mg/kg, significantly inhibited release of glutamate and aspartate induced by sodium channel activator, veratridine (100 microM). Glutamate and aspartate release was also diminished in animals treated chronically with citalopram. Citalopram did not affect extracellular level of 5-hydroxytryptamine (5-HT) after acute doses, but increased it after chronic administration. On the other hand, single and repeated doses of the drug inhibited veratridine-evoked 5-HT release. Neither single nor chronic treatment with citalopram influenced spontaneous and evoked dopamine (DA) release. The results suggest that in the presence of depolarizing agent, e.g. under conditions resembling a disturbed homeostasis of neuronal network, antidepressant drugs with profile of SSRI may influence excitatory systems in the brain. This effect does not seem to be dependent on the interaction with 5-HT or DA neurotransmission, but rather some inhibitory modulators stimulated in stress situations may contribute to the observed results.

Animals↗

PubMed2006

Injection of l-glutamate into medial prefrontal cortex induces cardiovascular responses through NMDA receptor - nitric oxide in rat.

We have reported that l-glutamate (l-glu) microinjections into ventral portion of medial prefrontal cortex (vMPFC) caused tachycardia and blood pressure increase in unanesthetized rats. In the present study, we report the subtype of vMPFC glutamatergic receptor mediating the response as well as the possible involvement of nitric oxide (NO) in these cardiovascular responses. Microinjection of 200nL of l-glu (81nmol) into the vMPFC of unanesthetized rats caused long-lasting pressor and tachycardic responses which were abolished by pretreatment with 4nmol of the specific NMDA receptor antagonist AP7. The response was not affected by 4nmol of the non-NMDA receptor antagonist NBQX. Local pretreatment with 80nmol of the unspecific nitric oxide synthase (NOS) inhibitor NG-nitro-l-arginine methyl ester (l-NAME) or 0.08nmol of the specific neuronal NOS (nNOS) inhibitor N(omega)-Propyl-l-arginine (N-Propyl) blocked l-glu effects. Microinjection of the NO donor sodium nitroprusside (SNP: 3, 9, 27 or 81nmol) in the vMPFC caused dose-related long-lasting pressor and tachycardic responses in unanesthetized rats, which were similar to those caused by l-glu. These results suggest that cardiovascular responses evoked by local injection of l-glu into the vMPFC of unanesthetized rats are caused by activation of a local NMDA receptor-NO pathway.

Animals↗

PubMed2001

The release of noradrenaline in the locus coeruleus and prefrontal cortex studied with dual-probe microdialysis.

The present study was undertaken to investigate and compare the properties of noradrenaline release in the locus coeruleus (LC) and prefrontal cortex (PFC). For that aim the dual-probe microdialysis technique was applied for simultaneous detection of noradrenaline levels in the LC and PFC in conscious rats. Calcium omission in the LC decreased noradrenaline levels in the LC, but increased its levels in the PFC. Novelty increased noradrenaline levels in both structures. Infusion of the alpha(2)-adrenoceptor agonist clonidine decreased extracellular noradrenaline in the LC as well as in the PFC. Infusion of the alpha(2A)-adrenoceptor antagonist BRL44408, or the alpha(1)-adrenoceptor agonist cirazoline into the LC or PFC caused a similar dose-dependent increase in both structures. When BRL44408 or cirazoline were infused into the LC, few effects were seen in the PFC. Infusion of the 5-HT(1A)-receptor agonist flesinoxan into the LC or the PFC decreased the release of noradrenaline in both structures. When flesinoxan was infused into the LC, no effects were seen in the PFC. When the GABA(A) antagonist bicuculline was applied to the LC, noradrenaline increased in the LC as well as in the PFC. It is concluded that the release of noradrenaline from somatodendritic sites and nerve terminals responded in a similar manner to presynaptic receptor modulation. The possible existence of dendritic noradrenaline release is discussed.

Adrenergic alpha-Agonists↗

PubMed2000

The effects of local application of D2 selective dopaminergic drugs into the medial prefrontal cortex of rats in a delayed spatial choice task.

The study examined the effects of modulation of dopamine D2 receptors-mediated neurotransmission in the rat's prefrontal cortex (PFC) on storage and executive components of working memory. Rats were trained on delayed (delay interval, 3 s) and non-delayed choice in a U-maze. The prominence of proactive interference was evaluated by sorting errors in a current trial on the basis of animal reactions in a preceding trial. The erroneous runs to the same arm of the maze as in the previous trial were identified as the repetitions (RE) and the erroneous runs to the other arm in comparison with the previous trial were classified as alternations (AE). The bilateral microinfusion of D2 agonists PPHT (0.004 microg, 0.04 microg, 0.4 microg/1 microl) into medial wall of the PFC produced a dose-dependent increase in the error rate of the delayed-response task and did not influence non-delayed choice. In delay condition PPHT enhanced the perseverative tendencies (the rate of RE was significantly higher than the rate of AE), in non-delayed choice the erroneous performance was mainly represented by AE. In contrast, the infusion of D2-receptor antagonist sulpiride (0.03 microg, 0.3 microg, 3 microg/1 microl) increased the accuracy of delayed choice and changed the mode of intertrial dependence-rats made significantly more AE than RE. The results are discussed in terms of the involvement of D2 receptor dependent transmission of the PFC in different cognitive processes related to the delayed performance in U-maze (within-trial short-term storage of information versus dynamic control of between-trials working memory processing).

Animals↗

PubMed2000

Intra-medial prefrontal cortex injection of quinpirole, but not SKF 38393, blocks the acute motor-stimulant response to cocaine in the rat.

RATIONALE: Considerable evidence suggests that the medial prefrontal cortex (mPFC) is an important region in mediating certain behavioral and neurochemical responses to cocaine. However, a role for cortical dopamine (DA) receptor subtypes in modulating these responses has yet to be elucidated. OBJECTIVES: This study investigated the effects of intra-mPFC administration of DA agonists on the acute motor-stimulant response to cocaine. In addition, in vivo microdialysis techniques were employed to determine the effects of intracortical injection on cocaine-induced extracellular DA concentrations in the nucleus accumbens (NAC). METHODS: One week following bilateral cannulae implantation over the mPFC and the NAC (for dialysis experiments), male Sprague-Dawley rats received an intra-mPFC injection of saline, the DA D2-like agonist quinpirole (0.015, 0.05, 0.15, 0.5, 1.5, or 5.0 nmol per side) or the partial DA D1-like agonist SKF 38393 (0.5, 1.5, or 5.0 nmol per side) approximately 5 min before peripheral administration of saline or cocaine (15 mg/kg, i.p.). For dialysis experiments, only the highest dose of quinpirole was examined. RESULTS: Pretreatment with quinpirole produced a dose-dependent decrease in cocaine-induced motor activity, with the highest doses resulting in a complete abolition of the acute motor-stimulant response to cocaine. In contrast, intra-mPFC administration of SKF 38393 was not shown, at the doses tested, to alter cocaine-induced motor activity. In agreement with the behavioral effects, intra-mPFC quinpirole injection (5 nmol per side) significantly blocked cocaine-induced DA overflow in the NAC. CONCLUSIONS: The results of the present study provide additional support that the mPFC is a neural substrate through which cocaine, in part, produces its motor-stimulant effects. In addition, these data suggest that modulation of cortical DA D2 receptors can block acute cocaine-induced behavioral (locomotor activity) and neurochemical (DA concentrations in the NAC) responses in the rat.

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

PubMed2000

Altered responsiveness of medial prefrontal cortex neurons to glutamate and dopamine after withdrawal from repeated amphetamine treatment.

Using in vivo extracellular single-cell recording and microiontophoresis, we compared the responsiveness of medial prefrontal cortex (mPFC) neurons (layers V-VI) to dopamine and glutamate in rats that had received repeated amphetamine or saline injections. Neurons from amphetamine-pretreated rats showed increased responsiveness to glutamate and decreased responsiveness to dopamine after three days of withdrawal, suggesting that the mPFC is transiently hyperexcitable during amphetamine withdrawal. Published 2000 Wiley-Liss, Inc.

Amphetamine↗

PubMed1999

Perseveration, inhibition and the prefrontal cortex: a new look.

Perseverative actions are often the result of inhibitory problems; however, inhibitory problems do not always lead to perseverative actions. Some problems of inhibition have been attributed to immaturity of, or severe damage to, the prefrontal cortex. Research in this area has generally failed both to take into account species differences in prefrontal function that lead to different perseverative errors and to distinguish between perseverative errors that arise from a failure to inhibit salient emotions or motivational drives and errors that arise from an inability to engage in conceptual change. Recent studies on humans, chimpanzees, rhesus macaques, Japanese macaques, cotton-top tamarins and marmosets support this notion.

Affective Symptoms↗

PubMed2004

Selectivity for the spatial and nonspatial attributes of auditory stimuli in the ventrolateral prefrontal cortex.

Spatial and nonspatial auditory processing is hypothesized to occur in parallel dorsal and ventral pathways, respectively. In this study, we tested the spatial and nonspatial sensitivity of auditory neurons in the ventrolateral prefrontal cortex (vPFC), a cortical area in the hypothetical nonspatial pathway. We found that vPFC neurons were modulated significantly by both the spatial and nonspatial attributes of an auditory stimulus. When comparing these responses with those in anterolateral belt region of the auditory cortex, which is hypothesized to be specialized for processing the nonspatial attributes of auditory stimuli, we found that the nonspatial sensitivity of vPFC neurons was poorer, whereas the spatial selectivity was better than anterolateral neurons. Also, the spatial and nonspatial sensitivity of vPFC neurons was comparable with that seen in the lateral intraparietal area, a cortical area that is a part of the dorsal pathway. These data suggest that substantial spatial and nonspatial processing occurs in both the dorsal and ventral pathways.

Action Potentials↗

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