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PubMed1995

Excitatory responses evoked in prefrontal cortex by mediodorsal thalamic nucleus stimulation: influence of anaesthesia.

The prefrontal cortex and the mediodorsal thalamic nucleus are reciprocally connected through excitatory amino acid pathways. Cortical excitatory responses resulting from activation of either the mediodorsal thalamic nucleus-prefrontal cortex pathway (short latency) or the recurrent collaterals of prefrontal cortex-mediodorsal thalamic nucleus neurons (long latency) can be discriminated mainly by their latency. The present study was undertaken to compare the effects of halothane and ketamine anaesthesia on these cortical excitatory responses and to establish their pharmacological characteristics using microiontophoretic application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D,L-2-amino-5-phosphonovaleric acid (APV), the specific antagonists of D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptors respectively. The number of prefrontal cortex cells which presented short or long latency excitatory responses was smaller in halothane- than in ketamine-anaesthetized rats. Whatever the anaesthetic used, short latency responses were blocked by CNQX and not affected by APV. Long latency responses were mainly blocked by APV and occasionally by CNQX in halothane-anaesthetized rats, while they were only blocked by CNQX in ketamine-anaesthetized animals. Therefore, halothane seems to preferentially reduce evoked responses mediated by AMPA receptors while ketamine completely abolishes evoked responses involving NMDA receptors. Moreover, the present data confirm that excitatory responses resulting from the activation of the mediodorsal thalamic nucleus-prefrontal cortex pathway are mainly mediated by AMPA receptors. In addition, they demonstrate that cortical responses linked to the activation of recurrent collaterals from prefrontal cortex-mediodorsal thalamic nucleus neurons involve both AMPA and NMDA receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1985

The prefrontal "cortex" in the pigeon catecholamine histofluorescence.

The prefrontal cortex of mammals is densely innervated with dopaminergic fibers. We report a comparable, dense network of catecholamine (probably dopamine)-containing fluorescent fibers in the posterodorsolateral neostriatum of the pigeon. This region is clearly separable from paleostriatum augmentatum, lobus parolfactorius, posterior archistriatum, posteromedial corticoid and septum, all of which also show strong catecholamine fluorescence. Parallel biochemical, anatomical and neurobehavioral data support the suggestion that posterodorsolateral neostriatum in the pigeon may be comparable to the mammalian prefrontal cortex. Thus the telencephalic tissue represented as the prefrontal cortex in mammals and the posterodorsolateral neostriatum in the pigeon, may turn out to be a phylogenetically ancient neural device.

Animals↗
PubMed2005

Prefrontal cortex, thalamus, and cerebellar volumes in adolescents and young adults with adolescent-onset alcohol use disorders and comorbid mental disorders.

BACKGROUND: In adults, prefrontal, thalamic, and cerebellar brain injury is associated with excessive ethanol intake. As these brain structures are actively maturing during adolescence, we hypothesized that subjects with adolescent-onset alcohol use disorders, compared with control subjects, would have smaller brain volumes in these areas. Thus, we compared prefrontal-thalamic-cerebellar measures of adolescents and young adults with adolescent-onset alcohol use disorders (AUD, defined as DSM-IV alcohol dependence or abuse) with those of sociodemographically similar control subjects. METHODS: Magnetic resonance imaging was used to measure prefrontal cortex, thalamic, and cerebellar volumes in 14 subjects (eight males, six females) with an AUD (mean age, 17.0+/-2.1 years) and 28 control subjects (16 males, 12 females; 16.9+/-2.3 years). All AUD subjects were recruited from substance abuse treatment programs and had comorbid mental disorders. RESULTS: Subjects with alcohol use disorders had smaller prefrontal cortex and prefrontal cortex white matter volumes compared with control subjects. Right, left, and total thalamic, pons/brainstem, right and left cerebellar hemispheric, total cerebellar, and cerebellar vermis volumes did not differ between groups. There was a significant sex-by-group effect, indicating that males with an adolescent-onset AUD compared with control males had smaller cerebellar volumes, whereas the two female groups did not differ in cerebellar volumes. Prefrontal cortex volume variables significantly correlated with measures of alcohol consumption. CONCLUSIONS: These findings suggest that a smaller prefrontal cortex is associated with early-onset drinking in individuals with comorbid mental disorders. Further studies are warranted to examine if a smaller prefrontal cortex represents a vulnerability to, or a consequence of, early-onset drinking.

Adolescent↗
PubMed1995

Lesions of the medial prefrontal cortex and sexual behavior in the male rat.

Lesions of the cerebral cortex near the midline in the frontal region appearing to destroy most of the cingulate cortex and adjacent prefrontal areas had profound effects on male rat sexual behavior. At the first postoperative tests, one week after the lesion, the mount and intromission latencies were extremely long (> 60 min). They continued elevated at every fortnightly test until postlesion week 13, when they were no longer different from controls. However, the proportion of animals that intromitted or ejaculated was reduced at this time. The lesion had a slight effect on the number of intromissions and on the intromission ratio, but did not reliably modify other parameters of sexual behavior in those males that copulated after operation. These data suggest that the medial prefrontal cortex is important for the initiation of sexual behaviour but less so for its execution. It is proposed that the elaboration and/or interpretation of environmental stimuli are rendered deficient by the lesion. Consequently, sexual behavior is activated only with difficulty. This coincides with the arousal hypothesis proposed by Beach [8]. There appears to exist a spontaneous recovery of the mechanisms responsible for the activation of sex behavior because the lesioned group was not different from the sham or intact groups 13 weeks postlesion. Remaining cortical tissue or other brain structures may compensate for the initial deficiencies. However, the lesion's effect on intromission behavior did not diminish with time. This could suggest that possible motor deficiencies produced by the lesion are irreversible.

Animals↗
PubMed2002

Coding of objects in the prefrontal cortex in monkeys and humans.

The prefrontal cortex is an area of high-level association cortex that plays an important part in the processing of visual objects. In this update, we summarize recent experimental findings that have investigated object processing in the frontal cortex in monkeys and humans. We highlight several common themes that have emerged from the study of these different systems, including the short-term maintenance of object information in working memory and the processing of novel information. Together, these findings suggest that regions of the prefrontal cortex participate in the selection, maintenance, and evaluation of task-relevant attributes. At a larger level, the convergence of findings from monkey and human studies demonstrates that concurrent investigation of scientific questions in both species can be a fruitful approach and promises to lead to future advances.

Animals↗
PubMed2006

Changed morphine sensitivity of morphine-dependent rats after laser exposure of the cerebral prefrontal cortex.

We studied the effect of bilateral laser exposure of the cerebral prefrontal cortex in morphine-dependent rats on their sensitivity to positive reinforcing and toxic effect of morphine. Laser exposure led to partial deafferentation of the cingulum. Exposure of the anterior and central areas of the prefrontal cortex stimulated self-administration of low morphine doses and had no effect on self-administration of high concentrations. Exposure of the posterior area of the prefrontal cortex did not appreciably change self-administration of medium and low morphine doses, but self-administration of high doses significantly increased. Exposure of the anterior area of the prefrontal cortex significantly decreased the sensitivity to the positive reinforcing effect of morphine. Exposure of the posterior prefrontal cortex decreased the sensitivity to the toxic effect of morphine.

Animals↗
PubMed1997

The flexible use of multiple cue relationships in spatial navigation: a comparison of water maze performance following hippocampal, medial septal, prefrontal cortex, or posterior parietal cortex lesions.

Rats prepared with lesions of the prefrontal cortex, posterior parietal cortex, hippocampus, or medial septal area were tested for acquisition of a number of variations of the open-field water maze using a version of place learning assessment described by Eichenbaum, Stewart, and Morris (1991). Specifically, the individual role of the aforementioned cortical and subcortical structures in tasks with differing representational demands on navigation were assessed. The results suggest that the sham-operated control, posterior parietal cortex-lesioned rats, and medial septal area-lesioned rats were able to navigate effectively under changing task conditions. Conversely, the navigational performances of the prefrontal cortex- and hippocampal formation-lesioned rats were impaired when task demands changed. The results are discussed in terms of the flexible use of multiple distal cues to guide navigation and the resulting loss of this flexibility after lesions to either the prefrontal cortex or the hippocampus.

Animals↗
PubMed2002

Regulation of medial prefrontal cortex dopamine by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptors.

In the medial prefrontal cortex, repeated cocaine produces tolerance of the extracellular dopamine response to subsequent cocaine injection. These studies characterized the influence of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptors on the medial prefrontal cortex dopamine response to acute cocaine, amphetamine and potassium chloride as a first step to assess whether these receptor subtypes may be candidates for mediating dopamine tolerance after repeated cocaine. Local infusion of 10 microM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) produced an approximate 40% increase in dopamine levels in the medial prefrontal cortex, while a 30 microM dose did not alter basal levels infused over a 3-h period. Thus, 30 microM CNQX was chosen for the remaining experiments, and was infused for 1 h prior to and during all in vivo treatments. Local medial prefrontal cortex infusion of the 30 microM dose blocked the small increase in dopamine levels elicited by systemic saline injection (maximum of 26%), as well as the much larger increase in response to acute cocaine injection (maximum of 340%). Local infusion of D-amphetamine (3 and 30 microM) through the probe increased dopamine to 300 and 600% of basal levels, respectively. Co-infusion of CNQX partially blocked the response for the first 40 min, but dopamine levels recovered by 60 min later. Local infusion of 100 mM potassium chloride elicited a 600% increase in dopamine levels, which was attenuated approximately 50% by CNQX co-infusion. Potassium-stimulated release of dopamine was also measured in vitro in medial prefrontal cortical and striatal tissue. By 30 s after potassium addition, dopamine levels increased to 800% above baseline in the medial prefrontal cortex, and this increase was blocked by the presence of 30 microM CNQX. In contrast, potassium-stimulated dopamine release in striatal tissue was approximately 250% above basal levels, with no effect of CNQX on dopamine release. Locomotor behavior collected during dialysis experiments demonstrated that increased activity induced by local infusion of potassium chloride was severely attenuated by co-infusion of 30 microM CNQX, while no effects of this drug were found for cocaine-elicited behavior. These results suggest a potent influence of glutamate via alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate/kainate receptors on extracellular dopamine in the medial prefrontal cortex, and these receptors may regulate dopamine release through a presynaptic mechanism. The findings may help elucidate the role of medial prefrontal cortex dopamine-glutamate interactions in drug abuse and stress- and drug-precipitated psychosis.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1986

Development of connections between the mediodorsal nucleus of the thalamus and the prefrontal cortex in the rat.

The postnatal ingrowth of thalamocortical fibers from the mediodorsal nucleus to the prefrontal cortex was investigated in relation to the development of cortical lamination. Like the dopaminergic fibers in the prefrontal cortex and the thalamic fibers in the visual cortex, the mediodorsal fibers have entered the prefrontal cortex at birth. Most of the fibers are found in the developing layer VI, but, in contrast to the above-mentioned systems, a considerable number of mediodorsal fibers have already penetrated into the upper, most immature part of the cortical plate on postnatal day 1. From day 1 to day 7 an increasing number of mediodorsal fibers reach the upper cortical plate, which by then is developing layer III, the terminal layer of these fibers. The reciprocal connection from the layer VI cells of the prefrontal cortex to the mediodorsal nucleus develops between day 4 and day 9. Finally, the projection from the contralateral prefrontal cortex to the mediodorsal nucleus is established around day 10. The early presence of the mediodorsal fibers in the upper, differentiating cortical plate might indicate an important role for the mediodorsal fibers in the laminar development of the prefrontal cortex.

Animals↗
PubMed1998

Increase of extracellular glutamate and expression of Fos-like immunoreactivity in the ventral tegmental area in response to electrical stimulation of the prefrontal cortex.

Electrical stimulation of the medial prefrontal cortex caused glutamate release in the ventral tegmental area (VTA) of freely moving animals. Cathodal stimulation was given through monopolar electrodes in 0.1-ms pulses at an intensity of 300 microA and frequencies of 4-120 Hz. Glutamate was measured in 10-min perfusate samples by HPLC coupled with fluorescence detection following precolumn derivatization with o-phthaldialdehyde/beta-mercaptoethanol. The stimulation-induced glutamate release was frequency dependent and was blocked by the infusion of the sodium channel blocker tetrodotoxin (10 microM) through the dialysis probe. The stimulation also induced bilateral Fos-like immunoreactivity in ventral tegmental neurons, with a significantly greater number of Fos-positive cells on the stimulated side. These findings add to a growing body of evidence suggesting that the medial prefrontal cortex regulates dopamine release in the nucleus accumbens via its projection to dopamine cell bodies in the VTA.

Animals↗
PubMed1990

Vertical and horizontal coding of space in the monkey dorsolateral prefrontal cortex.

Single cell activity in the dorsolateral prefrontal cortex was recorded in a monkey performing a delayed alternation (DA) task in 3 directions, to the left, to the right, and upwards. Among the 127 units studied in all three directions, 18 neurons were spatially selective in one direction (to the left, to the right or upwards), 37 neurons in two directions and 8 neurons in each 3 directions during the performance of the DA task. Of the 9 neurons that were spatially selective upwards, 8 had a specific pattern of activity during the delay period and one during the response period. When several spatial directions are studied in a DA task, as in this work, it becomes evident that the prefrontal cortex contains a large number of spatially selective neurons. The results of this study suggest that there is a spatial memory map in the prefrontal cortex which is needed not only when a DA task is performed to the left and to the right but also in the upward direction.

Animals↗
PubMed2004

Hippocampal place cells show increased sensitivity to changes in the local environment following prefrontal cortex lesions.

It has been proposed that the prefrontal cortex modulates neural activity in posterior cortex via inhibitory mechanisms. As a result, damage to the former area may produce disinhibition in posterior regions and increase sensitivity to extraneous information. This hypothesis was investigated by examining how prefrontal cortex lesions affected the firing of hippocampal place cells in freely moving rats. In experiment 1, the positional firing of lesion-group cells was altered to a greater extent than that of control-group cells when objects were introduced into the recording environment. This suggested that place cell firing was overly influenced by local cues in the prefrontal-lesioned animals. In experiment 2 place cells were recorded while rats foraged on a circular track with access to both local and distal multimodal cues. Although the position of place fields in lesion-group cells was not excessively tied to local cues, a greater proportion of the fields lost their spatial selectivity following a rotation of these cues. The cue-related effects were associated with larger extracellular action-potential amplitudes and a greater incidence of burst-firing in lesion-group cells. This finding is consistent with the hypothesis that lesions of the prefrontal cortex result in a disinhibition of posterior cortex.

Action Potentials↗
PubMed2005

Medial prefrontal cortex lesions inhibit reflex micturition in anethetized rats.

The medial prefrontal cortex is thought to participate in the control of micturition and urinary continence, based on evidence from clinical reports, but its exact role is not fully understood. This study investigated whether ibotenic acid lesions of the medial prefrontal cortex would influence volume-evoked micturition in urethane-anesthetized rats. The incidence and amplitude of bladder contractions were recorded during continuous saline infusion (0.1 ml/min) immediately before and 1 week after ibotenic acid (0.5 microg) or vehicle (0.5 microl) was injected into the medial prefrontal cortex. Vehicle injection did not change the incidence or amplitude of bladder contractions compared to pre-injection values. Ibotenic acid lesions prolonged the time interval between bladder contractions significantly although it did not affect the amplitude of bladder contractions. Histological analysis revealed that ibotenic acid lesions were restricted primarily to the anterior cingulate and prelimbic cortices. Larger ibotenic acid lesions extending ventrally into the infralimbic cortex produced a variable response but did not change the overall incidence or amplitude of bladder contractions significantly. These data indicate that the medial prefrontal cortex influences the timing of bladder contractions but does not affect contraction amplitudes.

Anesthesia↗
PubMed2006

Organization of mnemonic and response operations within prefrontal cortex.

There is mounting evidence that prefrontal cortex (PFC) is activated during mnemonic operations such as working memory maintenance and also during response-related operations. In the current study, we examine the neural organization of mnemonic and response operations with respect to each other within PFC. Stimulus-evoked and sustained functional MRI activity was recorded during performance of a mental calculation task. The presence or absence of mnemonic and response demands was manipulated in a 2 x 2 factorial design with conditions requiring: (1) memory encoding and maintenance (M+); (2) response selection and execution (R+); (3) encoding, maintenance, and response execution (M+R+); (4) neither mnemonic nor response-related processes (M-R-). The first step of the analyses identified PFC voxels exhibiting differential activity during (M+) vs. (R+) trials. Within these voxels, we then examined activity during multiple phases of (M+R+) trials. Greater stimulus-evoked and sustained activity was observed within the anterior extent of dorsolateral prefrontal cortex (BA 46) during R+ vs. M+ trials. In contrast, greater activity was observed in the posterior extent of dorsolateral PFC during M+ vs. R+ trials. Importantly, both regions were activated during (M+R+) trials. Activity levels during all of these conditions exceeded levels observed during (M-R-) control trials. These results suggest that integrative functions of PFC that allow past information to guide future actions may emerge from communication between discrete subregions supporting mnemonic and response operations.

Adolescent↗
PubMed2003

Daily injections alter spine density in rat medial prefrontal cortex.

Apical dendrites of pyramidal neurons in medial prefrontal cortex are reorganized after chronic corticosterone treatment. In this study, we assessed the effects of chronic corticosterone administration on dendritic spines. Adult male rats received sc injections of either corticosterone or vehicle daily for 3 weeks or were left untreated. Layer II-III neurons in medial prefrontal cortex were stained using a Golgi-Cox procedure and spines were counted on the portions of apical dendrites where maximal corticosterone-induced dendritic changes occur. In vehicle- and corticosterone-treated rats, spine density proximal to the soma was increased relative to untreated rats, while spine density in the distal portion of the apical arbor was unchanged, suggesting that daily handling alone altered spine density. This stress-induced change in spine density likely reflects important functional changes in excitatory synaptic inputs in prefrontal cortex.

Animals↗
PubMed2003

Synaptic influence of hippocampus on pyramidal cells of the rat prefrontal cortex: an in vivo intracellular recording study.

The hippocampus and prefrontal cortex are two structures implicated in learning and memory and are related through a direct excitatory pathway. The characteristics of the synaptic influence of the hippocampus on pyramidal cells of the prefrontal cortex were determined using intracellular recordings in anesthetized rats. Single-pulse stimulation of the hippocampus induced an early EPSP of fixed latency in most of the recorded pyramidal cells (n = 106/116) thereby demonstrating a monosynaptic connection between hippocampal neurons and pyramidal cells of the prefrontal cortex. Furthermore, the EPSP was followed by a prolonged IPSP and suggests a simultaneous engagement of pyramidal and non-pyramidal neurons that may ultimately constrain the spread of excitation in response to hippocampal input. Paired-pulse stimulation induced short-term modifications in the synaptic responses and this short-term plasticity may contribute to the temporal filtering of information. Finally, tetanic stimulation of the hippocampus produced long-term potentiation of the monosynaptic EPSP with a concomitant potentiation of the IPSP, indicating that the hippocampo-prefrontal network can participate in the formation and consolidation of memories. In conclusion, the characteristics of the synaptic transmission in the hippocampo-prefrontal cortex pathway further supports the existence of a cooperative relationship between two structures known to be involved in higher cognitive processes.

Adaptation, Physiological↗
PubMed1993

Neurotensin participates in self-stimulation of the medial prefrontal cortex in the rat.

The effects of intracerebral microinjections of neurotensin and xenopsin on self-stimulation of the medial prefrontal cortex of the rat were studied. Unilateral microinjections into the medial prefrontal cortex of neurotensin at doses of 0.625, 1.25, 2.5, 5 and 10 nmol produced a dose-related decrease of self-stimulation in the ipsilateral medial prefrontal cortex. Self-stimulation of the contralateral medial prefrontal contex, used as control, was not affected by the microinjections. Similar results were found with the neurotension-like octapeptide, xenopsin. Unilateral microinjections of xenoposin into the medial prefrontal cortex, at doses of 1.8, 3.6, 7.2 and 14.4 nmol produced a dose-related decrease of self-stimulation of the ipsilateral medial prefrontal cortex. Self-stimulation of the contralateral medial prefrontal cortex was not affected. These results suggest that neurotensin is part of the neurochemical substrate of self-stimulation in this cortical area.

Animals↗
PubMed2000

The effects of ibotenic acid lesions of the medial and lateral prefrontal cortex on latent inhibition, prepulse inhibition and amphetamine-induced hyperlocomotion.

Hypofunction of prefrontal cortical regions, such as dorsolateral and orbital regions, has been suggested to contribute to the symptomatology of schizophrenia. In the rat, the medial and the lateral prefrontal cortices are considered as homologs of the primate dorsolateral and orbital prefrontal cortices, respectively. The present study investigated in rats the effects of lesions of the medial and lateral prefrontal cortices on latent inhibition, prepulse inhibition and amphetamine-induced activity. These paradigms are known to be modulated by the mesolimbic dopaminergic system, a system that has been suggested to be involved in the symptomatology of schizophrenia. Latent inhibition and prepulse inhibition are disrupted in schizophrenic patients as well as in rats treated with amphetamine. Amphetamine-induced activity was tested under dim light (low stress) and bright light (high stress) because stressful situations selectively increase mesocortical dopamine activity. Lateral prefrontal cortex lesioned animals did not differ in their behavior from control animals in any of the paradigms used in this study. Medial prefrontal cortex lesions did not affect latent inhibition but increased prepulse inhibition. In the amphetamine-induced activity experiment, prior to drug administration, open field locomotion was reduced under bright illumination for all lesion groups. After amphetamine administration, medial prefrontal cortex lesions attenuated the hyperlocomotor effect of the drug under the dim light condition and potentiated it under the bright light condition. The results indicate that medial and lateral prefrontal cortex can be functionally differentiated by their involvement in the modulation of behavior requiring mesocorticolimbic dopamine activation. The results in amphetamine induced activity suggest that the behavioral outcomes associated with medial prefrontal cortex depend on the background (stress) against which the evaluation is made. The results also support the notion that prepulse inhibition may be a better model than latent inhibition of the symptoms of schizophrenia associated with dysfunctional prefrontal activity.

Amphetamine↗