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EN
Deposits of somatopetal tracers, that filled the entire dorsolateral cortex of one hemisphere, labelled only a few cell bodies in the thalamic mediodorsal nucleus (MD). Further experiments served to confirm the existence of strong projections from MD to the mesial and suprarhinal areas ofthe frontal cortex. Thus, only a very small proportion of the MD neurones in the rat projects outside the cortical areas described first by Leonard (1969). We conclude that at least in the rat, cortical projections of the MD are selective enough to be used as the basis for definition of the prefrontal cortex.
EN
Lesions of the medial prefrontal cortex strongly impaired rats delayed alternation behaviour in a T-maze, both when the lesion was inflicted after the initial acquisition of the task and when the lesion was added after criterion performance had been reattained following an of the parietal cortex. Lesions of the parietal cortex did not impair this behaviour, either when the parietal lesion was inflicted after the initial acquisition of the task or when it was added to a prefrontal lesion after criterion performance had beed reattained. Combined, one stage, parietal and prefrontal lesions did not have a stronger effect on delayed alternation than did prefrontal lesions alone. These results indicate that in spite of the strong anatomical connectivity between the prefrontal and parietal "association" cortex the latter is not necessary for the recovery of delayed alternation after prefrontal lesions. In comparison with the parietal cortex, the prefrontal cortex seems to be uniquely involved in mediation of delayed alternation.
EN
Our work assesses the effects of ? opioid receptor activation on high-threshold Ca2+/Ba2+ currents in freshly dispersed pyramidal neurons of the medial prefrontal cortex in rats. Application of the specific ? receptor agonist (D-Ala2, N-Me-Phe4, Gly5-ol)-enkephalin (DAMGO) at 1 muM decreased Ca2+ current amplitudes from 0.72 to 0.49 nA. The effect was abolished by naloxone and ?-Conotoxin GVIA. Inhibition was not abolished by strong depolarisation of the cell membrane. In addition, a macroscopic Ba2+ current recorded in cell-attached configuration was inhibited when DAMGO was applied outside the patch pipette. An adenylyl cyclase inhibitor (SQ 22536) and a protein kinase A inhibitor (H-89) decreased Ca2+ current amplitude. Moreover, the inhibitory effect of mu opioid receptors on Ca2+ currents required the activation of protein kinase A. We conclude that activation of mu opioid receptors in medial prefrontal cortex pyramidal neurons inhibits N type Ca2+ channel currents, and that protein kinase A is involved in this transduction pathway.
EN
Verbal phonological and semantic fluencies were investigated in 24 patients with unilateral prefrontal lesions and 10 normal control subjects. Lesions were limited to small areas within either the dorsolateral (Brodmann?s area 46/9) or ventromedial (posterior part of the gyrus rectus) cortices. In a phonological fluency task, patients with lesions to the left dorsolateral region were impaired. In semantic fluency, not only the left dorsolateral group but also the two right frontal damaged groups performed worse than the control group. In agreement with previous studies, our results show that the phonological fluency is mediated by the left dorsolateral prefrontal cortex. In contrast to this, performance on the semantic fluency task depends on a wider portion of the prefrontal cortex involving the left and right dorsolateral and the right ventromedial areas.
EN
In the present study we evaluated the effects of early social isolation and re-socialization on dendritic development and the expression of the vasoactive intestinal peptide (VIP) in the medial prefrontal cortex (mPFC) of the rat. Sprague-Dawley male rats were reared either in isolation (IC) or social (SC) conditions from postnatal day 18 to 32. Rats were then behaviorally evaluated in the open field test, and approximately half of the animals were sacrificed. Their brains were processed either for immunocytochemical labeling against VIP or for the Golgi-Cox-Sholl staining. The remaining IC rats were resocialized during 30 additional days. The results demonstrated that early social isolation impair neuronal dendritic arborization and increase the number of VIP-immunoreactive neurons. Furthermore, animals displayed hyperlocomotion in the open-field test. According to our structural, immunocytochemical and open-field data, the resocialization experience was unable to reverse neuronal and behavioral abnormalities.
EN
It has been reported that periodic maternal separation in rats leads to a variety of endure behavioral, neurochemical and microstructural sequelae associated with the pathophysiology of anxiety disorders. Since it has been proposed that these changes might be permanent, we examined whether environmental complexity aid to recover the structural dendritic impairment induced by neonatal maternal deprivation in the medial prefrontal cortex of the rat. In addition, the anxiety-like behavior was assessed in the elevated plus-maze. Repeated maternal separation between postnatal days 6-21 (3 hours daily) significantly reduced the dendritic material in layer II/III pyramidal neurons and induced anxiety-like behaviors in the elevated plus maze. Furthermore, environmental stimulation (twice a day, 1 h each) during 12 consecutive days (postnatal days 23-35) failed to recover the neuronal and behavioral disorders induced by neonatal maternal separation. The results demonstrated that (i) neonatal maternal separation severely altered pyramidal dendritic outgrowth in close association with anxiety-like behavior assessed in the elevated plus maze, and (ii) postweaning environmental complexity was unable to recover neither the prefrontocortical neuronal impairment nor the novelty-induced anxiety-like behavior triggered by early maternal deprivation.
EN
Sham operated controls and four groups of subjected to of various parts of their were compared in food and water intake and four behavioural tasks. The ablations were aimed at removing the ventral prefrontal cortex, the dorsal part of the medial prefrontal cortex, the total medial prefrontal cortex, and the anterior dorsolateral (non-prefrontal) cortex. Only two groups had a significantly impaired food and water intake: the ventral prefrontal and the non-prefrontal anterolateral. The Latter group was not adipsic. Two variants of spontaneous alternation were administered in a T-maze: a non-cued version in which both arms were grey and a sued version in which one arm was white and the other black. While all ablated groups behaved like the control group on the non-aued test, the number of perseverative responses of the total anteromedial group was significantly increased in the cued version of the test. Significant group differences could be seen neither in a test of conditioned taste aversion nor in extinction of operantly conditioned bar presses. Finally, in a vertical hole-board exploration test the only significant group difference was a prolongation of the mean visit duration of the ventrally lesioned animals in comparision with all other groups. The results of the present study further indicate functional differentiation within the prefrontal cortex of the rat.
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