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 145 records · Page 8Linked to original sources

PubMed1989

An anterograde tracer study on the development of corticospinal projections from the medial prefrontal cortex in the rat.

The aim of the present study is to investigate, both qualitatively and quantitatively, the development of corticospinal (CS) projections from the medial prefrontal cortex of the rat. This study was carried out with the use of anterogradely transported wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) after iontophoretic injections in the medial prefrontal cortex. For comparison similar injections are made in the sensorimotor cortex. The CS axons of neurons situated in the medial prefrontal cortex have reached the first thoracic segment (T1) at postnatal day 3 (P3) and reach their most caudal extension in the spinal cord sixth thoracic segment (T6) at postnatal day 7 (P7) and then gradually disappear during the second postnatal week. Quantitative results revealed that after labelling of the medial prefrontal cortex no peaks in labelling density, neither at the cervical nor at the lumbar intumescence, were present. Furthermore, the CS axons of medial prefrontal neurons never showed any outgrowth into the spinal grey matter at any age studied. Concludingly, the extension and subsequent elimination of CS axons originating in the medial prefrontal cortex follow a similar time course as those from the occipital cortex (Dev. Brain Res., 36 (1987) 121-130).

Animals↗

PubMed1986

6-Hydroxydopamine and excitotoxin lesions of medial prefrontal cortex fail to affect schedule-induced drinking in the rat.

Schedule-induced drinking was examined in rats following 6-hydroxydopamine and N-methyl-D-aspartate lesions of the medial prefrontal cortex. 6-Hydroxydopamine reduced the concentrations of dopamine and noradrenaline in the medial prefrontal cortex to 17 and 37% of control values respectively, while changes were not observed in the nucleus accumbens. Lesions with N-methyl-D-aspartate were confined to the medial prefrontal cortex. Schedule-induced water consumption, determined over 11 consecutive 1 h/day testing sessions, was not significantly altered by either lesion. These results suggest that the mesocortical dopaminergic projection to the medial prefrontal cortex, and reciprocal projections from medial prefrontal cortex to the nucleus accumbens and the ventral tegmental area, are not essential for the acquisition of schedule-induced drinking.

Animals↗

PubMed1995

Localized alterations in pre- and postsynaptic serotonin binding sites in the ventrolateral prefrontal cortex of suicide victims.

Altered serotonin indices have been reported in the brain of suicide victims. We sought to localize the changes in presynaptic and postsynaptic serotonin receptors and identify an area of prefrontal cortex that may influence suicide risk. Quantitative autoradiography was performed in coronal sections of prefrontal cortex to determine whether serotonin 5-HT1A receptor (postsynaptic in cortex) and serotonin transporter (presynaptic) binding are different in suicide victims compared to matched controls. 5-HT1A receptor binding was higher in 85 of the 103 sampled areas in the suicide group (n = 18 pairs; P < 0.0001). The increase ranged from 17 to 30%. The increase was more pronounced in the ventrolateral prefrontal cortex. Serotonin transporter binding was found to be lower in the suicide group in all but one of the 43 sampled regions (n = 22 pairs; P < 0.0001). The reduction in binding was most pronounced in the ventrolateral prefrontal cortex, where the difference between suicides and controls ranged between 15 and 27%. Serotonin transporter and 5-HT1A binding were negatively correlated (r = -0.35 to -0.44, P = 0.04 to 0.007) within the same brain areas, suggesting common regulatory factors with opposite effects on binding to the two receptors. We conclude that suicide victims have an abnormality in the serotonin system involving predominantly the ventrolateral prefrontal cortex, and hypothesize that the serotonergic dysfunction in this brain region contributes to the risk for suicidal behavior.

Adult↗

PubMed1990

Dopaminergic modulation of cholinergic responses in rat medial prefrontal cortex: an electrophysiological study.

The neuromodulatory action of dopamine (DA) on acetylcholine (ACh)-evoked responses of prefrontal cortex (PFC) neurones were investigated electrophysiologically in rats anaesthetised with a combination of urethane and ketamine. Iontophoretic application of ACh-excited prefrontal cortex neurones. Concurrent application of DA (5-15 nA) resulted in complex changes in the ACh-evoked responses: (1) DA depressed spontaneous background discharges (designated as noise) proportionally more than the ACh-evoked discharges (designated as input signals), thus yielding an enhanced signal/noise ratio. This increase in signal/noise ratio by dopamine was reversed by iontophoretic application of the Da D2 antagonist sulpiride (20-50 nA). Nevertheless, iontophoretic application of D2 agonist quinpirole (5-35 nA) enhanced the ACh-evoked response, but was accompanied by some increase in spontaneous discharge, thus yielding no change in the signal/noise ratio. (2) DA also increased the signal/noise ratio by inducing a net increase of the ACh-evoked response but simultaneously suppressed the spontaneous activity of PFC neurones. This effect was more prominent following blockade of D1 receptors by SCH23390 (6 mg/kg, i.p.), suggesting that D1 receptors may normally inhibit D2 receptor function in the PFC. In addition, endogenous DA in the PFC did not play a significant part in modifying the ACh-evoked responses since the modulation of ACh-evoked response by DA or its D1 and D2 agonists was similar in both saline control and alpha-methyl-p-tyrosine-pretreated rats. (3) When ejected with larger iontophoretic current (16-35 nA), DA suppressed both the ACh-evoked and spontaneous discharge and this effect was mimicked by D1 agonist SKF38393 (5-15 nA). Taken together, these results suggest that complex dopaminergic modulation of the cholinergic responses of prefrontal cortex neurones are mediated by D1 and D2 receptors. This DA action may have a functional role in the cognitive-integrative processes occurring in the prefrontal cortex.

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

PubMed1993

The organization of projections from the mediodorsal nucleus of the thalamus to orbital and medial prefrontal cortex in macaque monkeys.

The organization of interconnections between the mediodorsal nucleus of the thalamus (MD) and the orbital and medial prefrontal cortex and the agranular insular cortex in the monkey was studied by retrograde and anterograde tracing techniques. In addition to the magnocellular and parvicellular divisions of MD, three other subdivisions can be recognized on the basis of myeloarchitecture, cytoarchitecture, and connections. The first two of these represent a parcellation of the magnocellular division into a lateral, fiber-rich MD pars fibrosa and a medial, poorly myelinated MD pars paramediana adjacent to the midline. The third is a small, poorly myelinated area located at the caudomedial and dorsal edges of MD; it is referred to as MD pars caudodorsalis. MD pars fibrosa is reciprocally interconnected primarily with areas 11, 12 and 13 in the central and lateral part of the orbital cortex. There is a general organization within this projection, with the rostrocaudal axis of the cortex represented from dorsal to ventral in the pars fibrosa, and the mediolateral cortical axis represented from medial to lateral. Cells that project to area 12 also extend laterally into the adjacent pars parvicellularis. MD pars paramediana is more heavily interconnected with the caudal and medial portions of the orbital region, particularly the agranular insular areas and the caudal parts of areas 13 and 14. Cells that project to two caudal areas, 13a and Iad, do not fit with the general organization, in that they are located in the dorsomedial parts of the pars fibrosa and pars paramediana, where they overlap with cells that project to area 14. The pars fibrosa and pars paramediana receive inputs from areas of the ventral forebrain such as the amygdala, piriform (olfactory) cortex, and entorhinal cortex, which project directly to the orbital and agranular insular cortex, as well as from the ventral pallidum. MD pars caudodorsalis is reciprocally interconnected with areas 14, 24, and 32 on the medial surface of the prefrontal cortex. In this part of the nucleus the dorsoventral axis of the medial prefrontal cortex is represented from caudal to rostral in the thalamus. The amygdala and other ventral forebrain structures do not send fibers into the pars caudodorsalis, even though some of these structures project directly to the medial prefrontal cortex. Ventral to MD, and separated from it by the internal medullary lamina, a small region was recognized that appears to be comparable to the anteroventral part of the submedial nucleus previously defined in the rat and cat.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1998

Human prefrontal cortex is not specific for working memory: a functional MRI study.

Lesion studies in monkeys have provided evidence that lateral prefrontal cortex is necessary for working memory, the cognitive processes involved in the temporary maintenance and manipulation of information. Monkey electrophysiological studies, however, have also observed prefrontal neuronal activity associated with cognitive processes that are nonmnemonic. We tested the hypothesis that the same regions of human prefrontal cortex that demonstrate activity during working memory tasks would also demonstrate activity during tasks without working memory demands. During echoplanar fMRI imaging, subjects performed a three-condition experiment (working memory task, nonworking memory task, rest). In the working memory task, subjects observed serially presented stimuli and determined if each stimulus was the same as that presented two stimuli back. The nonworking memory task in Experiment 1 required subjects to identify a single predetermined stimulus; in Experiment 2, subjects were required to make a button press to every stimulus. In all subjects in both experiments, the working memory task exhibited greater prefrontal cortical activity compared to either nonworking memory task. In these same prefrontal regions, greater activation was also observed during both nonworking memory tasks compared to rest. We conclude that human lateral prefrontal cortex supports processes in addition to working memory. Thus, reverse inference of the form "if prefrontal cortex is active, working memory is engaged" is not supported.

Adult↗

PubMed1996

Prefrontal cortex inputs of the nucleus accumbens-nigro-thalamic circuit.

The functional organization of the cortico-nucleus accumbens-substantia nigra pars reticulata circuit was investigated in the rat using combined anatomical and electrophysiological approaches. The nucleus accumbens neurons which project to the substantia nigra pars reticulata are located in a circumscribed region of the core immediately adjacent and extending dorsally to the anterior commissure. As shown by retrograde and anterograde transports of wheatgerm agglutinin conjugated to horseradish peroxidase, the region of the nucleus accumbens related to the substantia nigra was found to receive bilateral inputs from restricted areas of the medial and lateral prefrontal cortex, i.e., prelimbic/medial orbital and dorsal agranular insular areas. The electrical stimulation of these medial and lateral prefrontal cortical areas induced excitatory responses in nucleus accumbens neurons projecting to the dorsomedial substantia nigra pars reticulata. Interestingly, an important proportion (61%) of the nucleus accumbens-nigral cells responding to the stimulation of the lateral prefrontal cortex were also excited by the stimulation of the medial prefrontal cortex, demonstrating the existence of a convergent influence of these cortical areas on single nucleus accumbens cells. Furthermore, the present data also show that the stimulation of the medial prefrontal cortex results in a powerful inhibition of the tonic firing of the substantia nigra pars reticulata neurons. In conclusion, this study reveals the existence of a functional link between the prefrontal cortex (prelimbic/medial orbital and agranular insular areas) and the nucleus accumbens neurons which innervate the dorsomedial region of the substantia nigra pars reticulata. Since the dorsomedial region of substantia nigra pars reticulata is known to project to subfields of the mediodorsal and ventromedial thalamic nuclei related to the prefrontal cortex, the present data further demonstrate the existence of a prefrontal-nucleus accumbens-thalamo-cortical circuit involving the substantia nigra pars reticulata.

Animals↗

PubMed1983

Allocortical afferent connections of the prefrontal cortex in the cat.

Afferent connections of the prefrontal cortex of the cat arising in allocortical regions have been investigated using the horseradish peroxidase retrograde transport technique. Our results demonstrate the existence of projections from the olfactory peduncle, anterior and posterior prepiriform cortices, cortico-amygdaloid transition area, entorhinal cortex, ventral, caudal and dorsal subiculum and postsubiculum to the prefrontal cortex.

Afferent Pathways↗

PubMed1981

Delayed-alternation performance after selective lesions of the medial and sulcal prefrontal cortex of the guinea pig.

The sulcal or medial subdivision of the prefrontal cortex of the guinea pig was ablated after the animals had learned a spatial delayed-alternation task. Retention of this task was significantly impaired only after ablation of the medial prefrontal cortex. As the most critical cortical region for delayed-alternation performance in the rat is also situated in the medial prefrontal cortex, our findings suggest a close functional correspondence of the prefrontal cortices of these rodent species.

Afferent Pathways↗

PubMed1997

Dopamine-glutamate interactions in the prefrontal cortex of the conscious rat: studies on ageing.

The effects of apomorphine, a D1-D2 dopamine receptor agonist, on the extracellular concentration of glutamate were investigated in the medial prefrontal cortex of young, middle-aged and aged rats. In vivo intracerebral perfusions were undertaken in the conscious rat using a concentric push-pull cannula system. Glutamate concentration in the samples were determined by HPLC with fluorometric detection. Apomorphine produced an increase in extracellular concentration of glutamate in medial prefrontal cortex of young rats (178% of baseline) only at 10 microM, but not at 5 and 20 microM. This increase in glutamate concentration induced by apomorphine was significantly attenuated by blockade of D1-D2 dopamine receptors with haloperidol. Apomorphine, at 10 microM, failed to induce an increase in extracellular concentration of glutamate in the prefrontal cortex of middle-aged and aged rats. However, at 20 microM, apomorphine induced an increase in glutamate concentration in the prefrontal cortex of middle-aged rats, but not in aged rats. These data indicate that an interaction between dopamine and glutamate exists in the medial prefrontal cortex and that this interaction deteriorates with age.

Aging↗

PubMed1997

Short- and long-term plasticity of the hippocampus to nucleus accumbens and prefrontal cortex pathways in the rat, in vivo.

The pathways from the hippocampal formation to the nucleus accumbens and the prefrontal cortex are likely to play a role in several aspects of learning and memory. In the present study we addressed the question of how plastic changes in these structures may occur simultaneously. This question can be studied in an appropriate way in the hippocampal/fornix-fimbria to prefrontal cortex/nucleus accumbens system, since electrical stimulation of the fornix-fimbria fibre bundle evokes characteristic field potentials in the two target areas simultaneously. First, we examined the termination field in the nucleus accumbens (medial shell and core region with an extension into the ventro-medial caudate-putamen) and the prefrontal cortex (deeper layers of the ventral prelimbic and ventral infralimbic areas) by recording single unit activity evoked by stimulation of fornix-fimbria fibres in halothane anaesthetized rats. Second, we studied short-term plasticity, namely paired pulse facilitation, in these two areas upon stimulation of the fornix-fimbria fibres. In the nucleus accumbens, paired pulse facilitation was encountered for double pulse intervals between 25 and 500 ms, peaking around 100 ms. In the medial prefrontal cortex it was confined to intervals between 25 and 200 ms, with a peak around 75 ms. Third, we investigated whether LTP could be elicited simultaneously in the two target structures by a single tetanic stimulation (50 Hz, 2 s) of the fornix-fimbria fibres. LTP that was sustained for more than 90 min in the medial prefrontal cortex, reached levels of 130% of control values. In the nucleus accumbens, however, only a transient form of potentiation was found which lasted no more than 60 min. These data show that synaptic weights can be changed in several target structures of the hippocampal formation, simultaneously, in a distributed way.

Animals↗

PubMed1996

Differential effects of prenatal exposure to cocaine and amphetamine on growth parameters and morphometry of the prefrontal cortex in the rat.

The purpose of this study was to investigate the differential effects of prenatal exposure to psychostimulants, e.g., cocaine or amphetamine, on basic growth parameters and morphometry of the medial prefrontal cortex of the rat. A group of pregnant Wistar rats was given 60 mg/kg body weight/day of cocaine hydrochloride and another group 10 mg/kg body weight/day of d-amphetamine sulfate, subcutaneously, from gestational days 8 to 22. Control groups of pregnant rats were pair-fed; litters were culled to eight pups (4 males and 4 females) weighed every other day until postnatal day 30 and every week until day 90. The body weight growth patterns modelled by a Gompertz curve were different in rats prenatally exposed to the two psychostimulants. Rats exposed to amphetamine had on average a slower growth than those exposed to cocaine, reaching an identical estimated adult weight. Allometric relationships between forebrain and body weight and cerebellum and body weight were described by two distinct postnatal growth phases that are different among the experimental groups. In the comparison of the two psychostimulants the relative cerebellum/body growth is lower in the offspring of the cocaine group than in the amphetamine group between PND14-PND30; between PND30-PND90 the relative growth rate is considerably higher in the offspring of the cocaine dams compared to that of the amphetamine dams. Groups of perfused animals were selected at postnatal days 14 and 30 to analyze the morphometric organization of the medial prefrontal cortex. In serial celloidin sections the volumes of the prefrontal cortex were determined; the number of neurons per unit volume of reference area was calculated using the stereological technique of the disector. The changes found in the morphometric parameters show a catch-up at postnatal day 30 of the "increased" density of neurons of the medial prefrontal cortex found at postnatal day 14. These data show differential growth patterns of offspring from cocaine- and amphetamine-exposed rats; a delayed development in the achievement of normal morphometric parameters of neurons in the prelimbic subarea of the medial prefrontal cortex occurs in the prenatally amphetamine-exposed offspring at early ages, and a catch-up is found after the first month of life. Complementary studies are needed to assess whether these changes have functional implications in the rats exposed prenatally to psychostimulants.

Amphetamine↗

PubMed1998

Involvement of gamma-aminobutyric acid neurotransmission in phencyclidine-induced dopamine release in the medial prefrontal cortex.

The present study was designed to examine the possible involvement of gamma-aminobutyric acid (GABA) neurotransmission in the mechanism of phencyclidine (1-(1-phenylcyclohexyl)piperidine; PCP)-induced dopamine release in the medial prefrontal cortex, using in vivo microdialysis in awake, freely moving rats. Local perfusion via the dialysis probe into the medial prefrontal cortex with PCP (100 and 500 microM) and dizocilpine ((+)-5-methyl-10,11-dihydroxy-5-H-dibenzo(a,d)cyclo-heptan-5,10-im ine; MK-801, 10 and 50 microM), a selective non-competitive NMDA receptor antagonist, was found to increase extracellular dopamine levels. Co-perfusion with NMDA (1 mM) or the GABAA receptor agonist muscimol (50 microM) attenuated the effects of PCP (500 microM) and MK-801 (50 microM) on extracellular dopamine levels. The dopamine reuptake inhibitor nomifensine (50 microM) also produced an increase in extracellular dopamine levels in the medial prefrontal cortex, but this effect was not affected by co-perfusion with muscimol (50 microM). On the other hand, local perfusion with PCP (100 and 500 microM) and MK-801 (10 and 50 microM), but not nomifensine (50 microM), reduced extracellular GABA levels in the medial prefrontal cortex. Co-perfusion with NMDA (1 mM) reduced the effects of PCP (500 microM) and MK-801 (50 microM) on extracellular GABA levels. These results suggest that PCP may facilitate dopamine release in the medial prefrontal cortex, at least in part, by the inhibition of GABA release via the antagonism of NMDA receptors.

Animals↗

PubMed1997

Prefrontal cortex cognitive deficits in children treated early and continuously for PKU.

To begin to study the importance of dopamine for executive function abilities dependent on prefrontal cortex during early childhood, the present investigation studied children in whom we predicted reduced dopamine in prefrontal cortex but otherwise normal brains. These are children treated early and continuously for the metabolic disorder phenylketonuria (PKU). Untreated PKU is the most common biochemical cause of mental retardation. The root problem is an inability to convert one amino acid, phenylalanine (Phe), into another, tyrosine (Tyr), the precursor of dopamine. Phe levels in the bloodstream soar; Tyr levels fall. Treatment with a diet low in Phe reduces the Phe:Tyr imbalance but cannot eliminate it. We hypothesized that the resultant modest elevation in the ratio of Phe to Tyr in the blood, which results in slightly less Tyr reaching the brain, uniquely affects the cognitive functions dependent on prefrontal cortex because of the special sensitivity of prefrontally projecting dopamine neurons to small decreases in Tyr. In a 4-year longitudinal study, we found that PKU children whose plasma Phe levels were three to five times normal (6-10 mg/dl) performed worse than other PKU children with lower Phe levels, matched controls, their own siblings, and children from the general population on tasks that required the working memory and inhibitory control abilities dependent on dorsolateral prefrontal cortex. The impairment was as evident in our oldest age range (3 1/2-7 years) as it was in the youngest (6-12 months). The higher a child's Phe level, the worse that child's performance. Girls were more adversely affected than boys. The deficit appears to be selective, affecting principally one neural system, since even PKU children with Phe levels three to five times normal performed well on the 13 control tasks. Clinical implications for the treatment of PKU and other neurodevelopmental disorders are discussed.

Age Factors↗

PubMed1986

Prefrontal cortex neuron activity during a discriminative conditioning paradigm in unanesthetized rats.

Single neuron responses were recorded from the prefrontal cortex of unanesthetized, restrained rats trained to a discriminative conditioning paradigm. The animals were preconditioned to a tone paired with footshock (CS+) and a second tone presented unpaired (CS-). Only neurons with large amplitude, positive first deflection action potentials were studied. Eighty-five percent of the units (17 of 20) emitted conditioned responses in that the response to either one or both of the conditioned stimuli (CS) was significantly different from spontaneous activity. Thirty-five percent of the units emitted differential conditioned responses in that the responses to one of the CS was significantly different than the response to the other CS and that the response was subsequently shown to extinguish when the footshock was withheld. The neurons which emitted the differential conditioned responses appeared to be located in the deeper layers of the anteromedial prefrontal cortex while the remaining neurons were located either in more superficial layers or anterior aspects of the prefrontal cortex. The results suggest that the anteromedial prefrontal cortex may be involved in neural mechanisms related to discriminative conditioning.

Action Potentials↗

PubMed1996

Rapid-rate transcranial magnetic stimulation of left dorsolateral prefrontal cortex in drug-resistant depression.

BACKGROUND: Lesion and neuroimaging studies suggest that left prefrontal lobe dysfunction is pathophysiologically linked to depression. Rapid-rate transcranial magnetic stimulation (rTMS) to prefrontal structures has a lateralised effect on mood in normal volunteers, and several preliminary studies suggest a beneficial effect of rTMS on depression. However, adequately controlled studies have not been conducted. METHODS: We have studied the effects of focal rTMS on the depressive symptoms in 17 patients with medication-resistant depression of psychotic subtype. The study was designed as a multiple cross-over, randomised placebo-controlled trial. Sham rTMS and stimulation of different cortical areas were used as controls. FINDINGS: Left dorsolateral prefrontal cortex rTMS resulted in a significant decrease in scores on the Hamilton depression rating scale HDRS (from 25.2 to 13.8) and the self-rated Beck questionnaire BQ (from 47.9 to 25.7). 11 of the 17 patients showed pronounced improvement that lasted for about 2 weeks after 5 days of daily rTMS sessions. No patient experienced any significant undesirable side-effects. INTERPRETATION: Our findings emphasise the role of the left dorsolateral prefrontal cortex in depression, and suggest that rTMS of the left dorsolateral prefrontal cortex might become a safe, non-convulsive alternative to electroconvulsive treatment in depression.

Adult↗

PubMed1994

Deficient sensorimotor gating after 6-hydroxydopamine lesion of the rat medial prefrontal cortex is reversed by haloperidol.

The present study sought to test the hypothesis that dopamine in the prefrontal cortex exerts an inhibitory influence on subcortical dopamsine systems and that depletion of prefrontal dopamine may affect behaviour via an increase in dopamine release in the basal ganglia. We used prepulse inhibition of the acoustic startle response, i.e. the inhibition of the acoustic startle response by a preceding non-startling stimulus, as the behavioural test, because this phenomenon of sensorimotor gating is modified in opposite directions by dopamine in the prefrontal cortex and in the basal ganglia. Rats were tested for prepulse inhibition before and after injections of the neurotoxin 6-hydroxydopamine into the medial prefrontal cortex. We attempted to differentiate the contributions of prefrontal dopamine and noradrenaline by pretreating the animals with desipramine (6-OHDAMI rats) or bupropion (6-OHDABUP rats), selective inhibitors of noradrenaline and dopamine reuptake respectively. 6-Hydroxydopamine lesion reduced prefrontal dopamine by 90% and noradrenaline by 80% in 6-OHDADMI rats, while prefrontal dopamine was reduced by 54% and noradrenaline by 95% in 6-OHDABUP rats. The ability of an acoustic prepulse (75 dB, 10 kHz) to inhibit the response to a startle pulse (100 dB noise burst) was maintained in sham-lesioned rats and in 6-OHDABUP rats. However, there was a marked reduction of prepulse inhibition (by 26%) in the 6-OHDADMI rats. Systemic administration of the dopamine antagonist haloperidol (0.05 mg/kg), which did not affect prepulse inhibition in sham-lesioned and in 6-OHDABUP rats, antagonized the lesion-induced deficit in prepulse inhibition in 6-OHDADMI rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗

PubMed1996

Behavioural effects of ablations of the presumed 'prefrontal cortex' or the corticoid in pigeons.

This study further explored functional similarities of mammalian prefrontal cortex and its presumed equivalent in pigeons. Our results show that the performance of delayed alternation of pigeons in an Y-maze is impaired following ablations of the prefrontal equivalent together with the corticoid but not of the corticoid alone. In the same maze, discrimination between vertical and horizontal stripes was unimpaired regardless of the lesion. Our results added the following new information. (1) Corticoid is not essentially involved in mediation of delayed responding. (2) Like monkeys, pigeons take much fewer trials to learn delayed alternation in a maze than in an operant chamber. (3) Lesions of the pigeon equivalent of the prefrontal cortex impair delayed responding also in the new apparatus. (4) These lesions do not impair visual pattern discrimination. Our results do not contradict the hypothesis that the postero-dorso-lateral neostriatum in pigeons is comparable to the prefrontal cortex in mammals.

Animals↗