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PubMed1987

Reciprocal functional connections of the olfactory bulbs and other olfactory related areas with the prefrontal cortex.

Reciprocal putative connections of the prefrontal cortex (PFC) (agranular insular, ventral and lateral orbital region) with the ipsi and contralateral main olfactory bulb (IOB; COB), the mediodorsal thalamic nucleus (MD), the basolateral amygdaloid nucleus (BLA) and the piriform cortex (PC) were investigated with electrophysiological techniques. Evoked field responses and orthodromic unit driving, generated in PFC following electrical stimulation of the above mentioned structures, were abolished following topical application of KCl, except for COB evoked mass potentials. Thus, locally generated activity was elicited in agranular insular cortex following IOB activation, the same region where recently, the taste cortex in the rat was localized. Since gustatory-visceral afferent information reaches insular cortex via 2-3 synaptic relays, autonomic, olfactory and gustatory inputs may interact at this level, and, as suggested previously for the mouse, play a key integrative role in flavor perception. Antidromically invaded neurons, 47% of which were identified by the collision-extinction technique, were also found in PFC areas which overlapped to a considerable extent with those from which orthodromic unit responses were obtained. In particular, closely spaced neurons in ventrolateral orbital (VLO) and lateral orbital (LO) regions were antidromically invaded following IOB and PC shocks; some neurons antidromically discharged by IOB were also transsynaptically activated following PC stimulation. These findings are in agreement with recent neuroanatomical studies which demonstrate axonal projections from PFC neurons to the IOB and COB in the rat and South American armadillo. In addition, stimulation of PFC regions dorsal to the rhinal fissure mostly inhibited spontaneous unit discharges recorded at the mitral cell layer of the IOB, suggesting that this effect may be partially mediated by excitatory inputs of prefrontal axons onto granule cells. The conduction properties, antidromic thresholds and activity-dependent variations in conduction velocity (CV) of bulbopetal neurons in prefrontal cortex were found to be similar to those exhibited by cells projecting to the IOB from olfactory peduncle regions, but not to those present in bulbopetal neurons of the horizontal limb of diagonal band, indicating that the OB may be subjected to centrifugal control by at least two cell groups differing in both histochemical and electrophysiological properties.

Afferent Pathways↗
PubMed1991

Supersensitivity to the reinforcing effects of cocaine following 6-hydroxydopamine lesions to the medial prefrontal cortex in rats.

The effects of neurotoxic lesions to the medial prefrontal cortex on both the acquisition and maintenance of intravenous cocaine self-administration were examined. In one experiment, acquisition of intravenous cocaine self-administration (0.25, 0.5 or 1.0 mg/kg/infusion) was measured in separate groups of rats 14 days following either a sham or 6-hydroxydopamine lesion to the medial prefrontal cortex. For sham rats, the 1.0 and 0.5 mg/kg dose supported reliable self-administration as indicated by discriminative responding. These rats reliably chose a lever that resulted in the delivery of these doses of cocaine over an inactive lever. Reinforced response rates were reduced when 0.25 mg/kg was the available dose and there was a loss of discriminative responding for some of the rats suggesting that it was close to threshold for self-administration. For rats that sustained a 70% depletion of dopamine in the medial prefrontal cortex, the dose-response curve was an inverse function across the entire dose range tested. In contrast to the data from the control rats, lesioned rats had a high rate of reinforced responses and demonstrated good discrimination for all doses including 0.25 mg/kg/infusion, suggesting a supersensitive response to the initial reward effect of cocaine. Another group of rats was first screened for reliable cocaine self-administration (0.5 mg/kg/infusion) and then subjected to either the prefrontal cortical 6-hydroxydopamine or sham lesion. Dose-response curves for cocaine self-administration were compared 14 days following the infusions. The lesioned rats responded reliably for low doses of cocaine that were unable to maintain responding in sham rats. These data support the hypothesis that the medial prefrontal cortex plays an important role in cocaine self-administration.

Animals↗
PubMed2002

Stimulation of 5-hydroxytryptamine (5-HT(2C) ) receptors in the ventrotegmental area inhibits stress-induced but not basal dopamine release in the rat prefrontal cortex.

The present study investigated whether 5-HT(2C) receptors in the ventrotegmental area and prefrontal cortex regulate basal and stimulus-evoked dopamine release in the prefrontal cortex. Using the in vivo microdialysis technique in conscious rats, we studied the effect of a selective 5-HT(2C) receptor agonist, Ro60-0175, on basal and immobilization stress-induced dopamine release in the prefrontal cortex. Ro60-0175 intraperitoneally (2.5 mg/kg) and into the ventrotegmental area (10 microg/0.5 microL) completely antagonized the effect of stress on extracellular dopamine without altering basal levels. Infusion of 10 microm Ro60-0175 through the cortical probe had no significant effect on basal and stress-induced dopamine release. SB242084 (10 mg/kg), a selective antagonist of 5-HT(2C) receptors, significantly increased basal extracellular dopamine and completely prevented the effect of intraperitoneal and intraventrotegmental Ro60-0175 on the stress-induced rise of extracellular dopamine, but had no effect itself in stressed rats. The results show that Ro60-0175 suppresses cortical dopamine release induced by immobilization stress through the stimulation of 5-HT(2C) receptors in the ventrotegmental area. While confirming that endogenous 5-HT acting on 5-HT(2C) receptors tonically inhibit basal dopamine release in the prefrontal cortex, the present findings suggest that the stimulation of 5-HT(2C) receptors with an exogenous agonist preferentially inhibit stimulated release.

Aminopyridines↗
PubMedDate not supplied

Effects of medial prefrontal cortex stimulation on the spontaneous activity of the ventral pallidal neurons in the rat.

The neural connections from the medial prefrontal cortex to the ventral pallidum were investigated in urethane-anesthetized rats. Extracellular recordings were made from 124 spontaneously firing neurons in the ventral pallidum while the medial prefrontal cortex was electrically stimulated. The most frequent response to prefrontal cortex stimulation was inhibition of the firing rate of 72.3% of the neurons with orthodromic response (mean latency: 14.4 +/- 1.6 ms). Excitatory responses were found in 27.7% of the neurons with orthodromic response (mean latency: 8.5 +/- 1.4 ms). Frequency histograms of latencies were unimodal in both types of responses. Fifty-nine neurons (47.6% of the total tested) showed no change in spontaneous firing after medial prefrontal cortex stimulation. The electrophysiological results support previous anatomical findings of connections between the medial prefrontal cortex and the ventral pallidum. These projections play a predominantly inhibitory role in the spontaneous activity of ventropallidal neurons, and show topographical organization. This inhibition may modulate the motor performance of motivated behaviors.

Action Potentials↗
PubMed1993

Chronic infusions of GABA into the medial prefrontal cortex induce spatial alternation deficits in aged rats.

It has been proposed that functions associated with the prefrontal cortex could change as a consequence of aging. Previous experiments in young rats have demonstrated that anatomical lesions or chronic GABA infusions into this area produce deficits in spatial delayed alternation tasks. The present study examines the effect of chronic (7 days) GABA or saline infusion into the prefrontal cortex on the performance of delayed alternation task in old rats (24 months). The results suggested that aged rats needed more sessions to acquire the delayed alternation task. GABA infusions into the prefrontal cortex produced deficits in spatial alternation tasks similar to those previously observed in young rats. Performance rapidly recovered after the infusion period. Histological analysis showed similar lesion size in both groups. The results suggest that aged prefrontal cortex and/or related areas participating in the acquisition of the delayed alternation task are more sensitive to aging processes. Furthermore, the prefrontal cortex is important for the retention of a previously learned spatial delayed alternation task. The structures involved in functional recovery from these deficits appear to be fully functional in aged rats.

Aging↗
PubMed1993

Local circuit neurons of developing and mature macaque prefrontal cortex: Golgi and immunocytochemical characteristics.

A study has been made of the nonpyramidal, local circuit neurons in developing and mature macaque monkey prefrontal cortex with Golgi and immunocytochemical techniques. The area chosen for study is located between the cingulate gyrus and the ventral bank of the principal sulcus, and contains areas 9 and 46 as described by Walker (J. Comp. Neurol. 73:59-86, '40). In Golgi studies, the unique axonal features of impregnated neurons made possible the identification of thirteen separate classes of local circuit neurons. Five of these cell types, in their general characteristics, resembled classes identified in human prefrontal cortex, as well as in other cortical areas of macaque monkeys and other species. Measurements of the scale of axon arbors and dendritic fields of the Golgi-stained local circuit neurons also suggested particular spatial relationships of certain classes to the scale of intrinsic lattice connections made by the axons of pyramidal neurons in the same region. Similarities in morphology between cells described in human prefrontal cortex and neuron varieties described in this study indicate that this region of monkey prefrontal cortex may serve as a useful model for neuron populations in human prefrontal cortex. Sufficient morphological detail was present in immunocytochemical studies to suggest one or more identifying biochemical characteristics for seven of the thirteen classes of local circuit neurons. The calcium binding proteins, parvalbumin, calbindin D-28K, and calretinin, were found in chandelier and wide arbor neurons, neurogliaform cells, and double bouquet neurons, respectively. In addition, cholecystokinin immunoreactivity was present in medium arbor neurons and in narrow arbor cells connecting layers 2 and 4. Somatostatin 28(1-12) immunoreactivity was detected in beaded axon neurons in layers 5 and 6. This biochemical characterization of local circuit neurons, although incomplete, confirms the separate identity of at least some of the varieties distinguished by Golgi morphology, and allows a start to be made on studies examining changes in their functional state. The general inhibitory nature of these interneurons suggests that they are likely to play a crucial role in determining patterns of neural activation in the prefrontal cortex.

Animals↗
PubMed2006

Evidence of altered neurogranin immunoreactivity in areas 9 and 32 of schizophrenic prefrontal cortex.

Schizophrenia is a complex and poorly understood neuropsychiatric disorder. Much research has begun to implicate the prefrontal cortex in the disease. Using immunocytochemistry we determined if neurogranin, a protein found in dendrites, spines and cell bodies and an upstream regulator of calcium was altered in areas 9 and 32 of schizophrenic prefrontal cortex. We examined its expression in pyramidal cells in layers III and V. Tissues from 7 controls and 7 schizophrenics (from our original MAP2 study, Jones, L., Johnson, N., Byne, W., 2002. Alterations in MAP2 staining in area 9 and 32 of schizophrenic prefrontal cortex. Psych. Res. 114, 137-148) matched for age, sex and postmortem interval were examined. Using area fraction analysis we quantified the immunostaining. Additionally, we counted the number of positively stained pyramidal cells in the same 7 pairs. Neurogranin immunostaining was dramatically reduced in both layers III (72%) and V (50%) in area 9. In area 32 there was a more modest reduction in both layers III (36%) and V (40%). There was no difference in either brain region or layer in the density of positively stained pyramidal cells. These data confirm mounting evidence suggesting dendritic loss in the prefrontal cortex and suggest that the loss of protein does not appear to be due to a change in the number of cells producing the protein but rather in the amount of protein being produced. Additionally, these data suggest that the loss of neurogranin may alter the calcium-calmodulin dependent pathways due to its role as a regulator of calmodulin suggesting a link between structural and functional alterations of the pyramidal cells in the prefrontal cortex.

Adult↗
PubMed1989

The role of the lateral cortico-cortical prefrontal pathway in self-stimulation of the medial prefrontal cortex in the rat.

Effects of electrolytic and kainic acid lesions at several stereotaxic planes of the lateral cortico-cortical prefrontal efferent pathway on self-stimulation of the medial prefrontal cortex were investigated. Electrolytic bilateral lesion of the sulcal prefrontal cortex, the first terminal area of this pathway, produced no effects on self-stimulation of the medial prefrontal cortex. However, bilateral electrolytic lesion of this pathway at the rostral part of the external capsule produced a permanent abolition of self-stimulation of the medial prefrontal cortex. These effects seemed selective since operant behaviour to obtain water, similar to that performed for self-stimulation and used as a control, was not affected by the lesion except on the 1st, 3rd (P less than 0.01) and 5th (P less than 0.05) days postlesion. Interestingly, bilateral microinjections of kainic acid (10 nmol in 0.8 microliters) at the same stereotaxic planes of the external capsule where electrolytic lesion was produced, had no effects on self-stimulation. These results suggest that fibres-of-passage through the external capsule are responsible for the abolition of self-stimulation. Bilateral electrolytic lesion of the entorhinal cortex, one of the caudal terminal areas of this descending set of fibres, produced a short transient decrease of self-stimulation of the medial prefrontal cortex. These results are discussed on the basis that complex, rather than single circuits are involved in maintaining self-stimulation in this neocortical area.

Animals↗
PubMed2000

Developmental depersonalization: the prefrontal cortex and self-functions in autism.

The human self model suggests that the construct of self involves functions such as agency, body-centered spatial perspectivity, and long-term unity. Vogeley, Kurthen, Falkai, and Maieret (1999) suggest that agency is subserved by the prefrontal cortex and other association areas of the cortex, spatial perspectivity by the prefrontal cortex and the parietal lobes, and long-term unity by the prefrontal cortex and the temporal lobes and that all of these functions are impaired in schizophrenia. Exploring the connections between the prefrontal cortex and the construct of self, the present article extends the application of the self model to autism. It suggests that in contrast to schizophrenia, agency and spatial perspectivity are probably preserved in autism, but that, similarly to schizophrenia, long-term unity is probably impaired. This hypothesis is compatible with a model of neuropsychological dysfunction in autism in a neural network including parts of the prefrontal cortex, the temporal lobes, and the cerebellum.

Autistic Disorder↗
PubMedDate not supplied

[Serotonergic control of prefrontal cortex].

INTRODUCTION AND DEVELOPMENT: The prefrontal cortex (PFC) plays a crucial role in higher brain functions such as working memory or cognition and controls, via the excitatory axons of pyramidal neurons, the activity of many subcortical motor and limbic areas. It receives a dense innervation from the brainstem aminergic nuclei, including the serotonergic raphe nuclei. Prefrontal function and metabolism is altered in patients with severe psychiatric disorders, like major depression or schizophrenia. Although the exact role of serotonergic neurotransmission in PFC remains largely unknown, the PFC contains a very large density or serotonin 5-HT1A (inhibitory) and 5-HT2A (excitatory) receptors. In addition, hallucinogens like LSD or DOI are agonists and atypical antipsychotics are antagonists at 5-HT2A receptors. In this review we focus on the main excitatory and inhibitory mechanisms through which serotonin modulates pyramidal and GABAergic neuron activity in the PFC. CONCLUSIONS: We report on the presence of 5-HT1A and 5-HT2A receptor-mediated responses in pyramidal neurons of the PFC that exert opposite effects on their activity when recorded in vivo in the anesthetized rat. Despite the large co-expression of both receptors in pyramidal neurons of the PFC, physiological amounts of 5-HT mainly inhibit pyramidal neurons. This is probably due to the distinct location of 5-HT1A and 5-HT2A in pyramidal neurons. Thus, 5-HT1A receptors are mainly localized in the axon hillock, where they may have a prominent inhibitory role in the control of pyramidal activity given their coupling to GIRK channels. Moreover, 5-HT can inhibit pyramidal neurons indirectly through the activation of 5-HT2A and 5-HT3 receptors localized in GABAergic interneurons and a subsequent increase in synaptic GABA inputs.

Animals↗
PubMed2003

The medial prefrontal cortex in the rat: evidence for a dorso-ventral distinction based upon functional and anatomical characteristics.

The prefrontal cortex in rats can be distinguished anatomically from other frontal cortical areas both in terms of cytoarchitectonic characteristics and neural connectivity, and it can be further subdivided into subterritories on the basis of such criteria. Functionally, the prefrontal cortex of rats has been implicated in working memory, attention, response initiation and management of autonomic control and emotion. In humans, dysfunction of prefrontal cortical areas with which the medial prefrontal cortex of the rat is most likely comparable is related to psychopathology including schizophrenia, sociopathy, obsessive-compulsive disorder, depression, and drug abuse. Recent literature points to the relevance of conducting a functional analysis of prefrontal subregions and supports the idea that the area of the medial prefrontal cortex in rats is characterized by its own functional heterogeneity, which may be related to neuroanatomical and neurochemical dissociations. The present review covers recent findings with the intent of correlating these distinct functional differences in the dorso-ventral axis of the rat medial prefrontal cortex with anatomical and neurochemical patterns.

Animals↗
PubMed2000

Effects of footshock stress on superoxide dismutase and glutathione peroxidase enzyme activities and thiobarbituric acid reactive substances levels in the rat prefrontal cortex and striatum.

Mild footshock stress results in an increase dopamine metabolism in the prefrontal cortex. Increases in either the intensity or duration of stress enhance dopamine metabolism in the nucleus accumbens and striatum, as well as in the prefrontal cortex. Dopamine is metabolized by monoamine oxidase with hydrogen peroxide as a product. In this study we have demonstrated that while very mild (0.2 mA) footshock stress did not change glutathione peroxidase activity in the rat prefrontal cortex and striatum, more intense (1.6 mA) footshock stress increased glutathione peroxidase activity at 0, 15, 30 and 60 min after the footshock in the prefrontal cortex and at 30 min after the footshock in the striatum. Stress did not change superoxide dismutase activity and thiobarbituric acid reactive substances levels. These results indicate that increased dopamine metabolism induced by footshock stress is probably responsible for the increase of glutathione peroxidase activity.

Animals↗
PubMed2006

Reversible inactivations of rat medial prefrontal cortex impair the ability to wait for a stimulus.

In simple reaction time tasks, lesions of rat dorsomedial prefrontal cortex impair the ability to wait for trigger stimuli and result in increased premature responding. This effect could be due to impairments in attending to trigger stimuli, estimating the timing of trigger stimuli, or inhibitory control of the motor response. Here, we examined these issues by reversibly inactivating dorsomedial prefrontal cortex during simple reaction time tasks with variable or fixed foreperiods. There were three consistent effects of dorsomedial prefrontal cortex inactivation: 1) increased premature responding, 2) increased variability in the timing of premature responses, and 3) speeded response latencies, especially on trials with short foreperiods in tasks with variable foreperiods. We observed these effects independent of differences in foreperiod duration, foreperiod variability, and stimulus probabilities. Therefore, dorsomedial prefrontal cortex appears not to be involved in attending to the trigger stimulus or in time estimation. Instead, we suggest that dorsomedial prefrontal cortex is critical for inhibiting responses before the maximum foreperiod duration, i.e. the "deadline" [Ollman RT, Billington MJ (1972) The deadline model for simple reaction times. Cognit Psychol 3:311-336], after which the rat should respond even if the trigger stimulus has not occurred.

Animals↗
PubMed1996

Antagonism of NMDA receptors but not AMPA/kainate receptors blocks bursting in dopaminergic neurons induced by electrical stimulation of the prefrontal cortex.

Evidence suggests that the prefrontal cortex (PFC) plays an important role in the burst activity of midbrain dopaminergic (DA) neurons. In particular, electrical stimulation of the PFC elicits patterns of activity in DA neurons, closely time-locked to the stimulation, which resemble natural bursts. Given that natural bursts are produced by the activity of excitatory amino acid (EAA)-ergic afferents, if PFC-induced time-locked bursts are homologues of natural bursts, EAA antagonists should attenuate them. Hence, the NMDA (N-methyl-D-aspartate) antagonist CPP (3-((+/-)-2-carboxypiperazin-4-yl)propyl-1-phosphonic acid) and the AMPA (D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid)/kainate antagonist CNQX (6-cyano-7-nitroquinoxaline-2,3-dione) were applied by iontophoresis to DA neurons exhibiting time-locked bursts during PFC stimulation. CPP produced a significant reduction in time-locked bursting. In contrast, CNQX (at currents which antagonised AMPA responses) did not. These effects of CPP and CNQX on time-locked bursting mirror the effects previously reported for these drugs on natural bursting. Since natural bursting and bursting induced by PFC stimulation are both blocked selectively by CPP, the present results increase the degree of analogy between the two burst phenomena, thereby adding extra support to the contention that the cortex is involved in producing the natural bursting in DA neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1996

Effect of conditioned fear stress on dopamine release in the rat prefrontal cortex.

The effects of conditioned fear stress (CFS) on dopamine release in the medial prefrontal cortex were studied by in vivo microdialysis in the rat. CFS (exposure to an environment in which foot-shock had been delivered previously) induced a marked suppression of motility, i.e., freezing behavior. Extracellular concentrations of dopamine in the medial prefrontal cortex were increased by CFS. The increase of dopamine returned to the pretreatment levels when rats were returned to the home cages. Diazepam (0.5 mg/kg, i.p.) suppressed both the CFS-induced freezing behavior and extracellular dopamine levels in the medial prefrontal cortex. These findings suggest that anxiety and dopamine release in the prefrontal cortex might be related.

Animals↗
PubMed2005

'Compulsive' lever pressing in rats is enhanced following lesions to the orbital cortex, but not to the basolateral nucleus of the amygdala or to the dorsal medial prefrontal cortex.

In a new rat model of obsessive-compulsive disorder (OCD), 'compulsive' behaviour is induced by attenuating a signal indicating that a lever-press response was effective in producing food. We have recently found that compulsive lever pressing is increased following lesions to the rat orbital cortex, in accordance with several lines of evidence implicating the orbitofrontal cortex in the pathophysiology of OCD. In view of the functional similarities between the orbital cortex, the basolateral nucleus of the amygdala and the medial prefrontal cortex, the present study compared the effects of lesions to these three regions. The present study replicated the finding that lesions to the rat orbital cortex enhance compulsive lever pressing. In contrast, lesions to the dorsal medial prefrontal cortex and to the basolateral amygdala did not affect compulsive lever pressing. A comparison of these findings to current knowledge regarding similarities and differences in the functioning of the three regions sheds light on the mechanism by which signal attenuation induces compulsive lever pressing and on the role played by the orbital cortex in compulsive behaviour.

Amygdala↗
PubMed2003

An MRI study of subgenual prefrontal cortex in patients with familial and non-familial bipolar I disorder.

BACKGROUND: Over the past few years there has been an interest in the use of magnetic resonance imaging (MRI) to study specific brain regions in bipolar disorder. The present study compared the grey matter volume in the subgenual prefrontal cortex in patients with familial and non-familial bipolar disorder and normal control subjects. METHODS: MRI brain scans were performed on 12 patients with bipolar I disorder including six patients with a positive family history of bipolar disorder as well as eight control subjects. RESULTS: There was a significant reduction in the grey matter volume in the right subgenual prefrontal cortex, but not in the left subgenual prefrontal cortex. A family history x sex interaction with right prefrontal cortex volume was also observed as a trend. For females, a positive family history was associated with reduced right prefrontal cortex volumes; for males, a positive family history was associated with increased right prefrontal cortex volumes. LIMITATIONS: Small sample size, reduced statistical power. CONCLUSION: These data add to the emerging literature on structural changes in the subgenual prefrontal cortex in bipolar disorder, especially in patients with a positive family history.

Adult↗
PubMed1993

Evoked extracellular dopamine in vivo in the medial prefrontal cortex.

The measurement of evoked extracellular dopamine in the medial prefrontal cortex by using fast-scan cyclic voltammetry with carbon-fiber microelectrodes was established and release characteristics of mesoprefrontal dopamine neurons were examined in vivo in anesthetized rats. Despite the sparse dopaminergic innervation and the presence of more dense noradrenergic and serotonergic innervations overall in the medial prefrontal cortex, the measurement of extracellular dopamine was achieved by selective recording in dopamine-rich terminal fields and selective activation of ascending dopamine neurons. This was confirmed by electrochemical, pharmacological, and anatomical evidence. An increased release capacity for mesoprefrontal dopamine neurons was also demonstrated by the slower decay of the evoked dopamine response after inhibition of catecholamine synthesis and the maintenance of the evoked dopamine response at higher levels in the medial prefrontal cortex compared with the striatum during supraphysiological stimulation.

Animals↗