The comparative effects of frontal, parietal, occipitotemporal, and limbic forebrain lesions in weanling rats on learning☆

Thompson, Robert; Yü, Jen

doi:10.1016/0031-9384(85)90141-6

Cited by 15 publications

(4 citation statements)

References 24 publications

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“…Apoptosis, also known as programmed cell death, is a crucial biological process involved in maintaining development and tissue homeostasis. Inappropriate stimulation or inhibition of apoptosis can lead to several physiological imbalances and disorders (Thompson and Yu 1985). The consequences of apoptosis in Pb-induced damage to brain may reflect in behavioral, motor, and cognitive impairments.…”

Section: Discussionmentioning

confidence: 99%

“…Melatonin, which influences the cell differentiation and growth in a number of cell culture systems, has been shown to prevent in vitro and in vivo apoptosis in thymocytes (Sainz et al 1995;Roth, Rabin, and Agenello 1997;Mayo et al 1998). Melatonin alone has no effect on the of apoptosis can lead to several physiological imbalances and disorders (Thompson and Yu 1985). The consequences of apoptosis in Pb-induced damage to brain may reflect in behavioral, motor, and cognitive impairments.…”

Section: Figurementioning

confidence: 99%

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Melatonin Protection against Lead-Induced Changes in Human Neuroblastoma Cell Cultures

et al. 2006

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The nervous system is the primary target for low-levels of lead (Pb) exposure and the developing brain appears to be especially vulnerable to Pb neurotoxicity. Chronic low-level Pb exposure causes growth retardation and intellectual impairment. In the present study the protective effect of melatonin during exposure to low-levels of Pb in human SH-SY5Y neuroblastoma cell cultures was assessed. The cells were exposed to Pb (0.01 to 10 microM) for 48 h. Pb inhibited the proliferation of neuroblastoma cells significantly in a concentration-dependent manner. A 50% inhibition (IC50) of cell proliferation was observed at about 5 microM Pb. Pb decreased (16% to 62%) the levels of total cellular glutathione (GSH) in a concentration (0.1 to 10 microM)-dependent manner. Exposure of cells to Pb (5 microM) for 48 h resulted in an eightfold increase in caspase-3 activity and prostaglandin E2 (PGE2) level. Pretreatment with melatonin (10 microM) blocked the effects of Pb on GSH content and caspase-3 activity, and showed significant improvement in reducing the level of PGE2. The results suggest that some of the neurotoxic effects of Pb may be partly mediated by apoptosis and pretreatment with melatonin can prevent these effects. The present study asserts the neuroprotective effect of melatonin in conditions of Pb-induced toxicity in neuroblastoma cell cultures.

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Section: Discussionmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Melatonin Protection against Lead-Induced Changes in Human Neuroblastoma Cell Cultures

et al. 2006

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“…Whether this observation relates to differences in lesion size or, rather, regional location and lateral extent of the injury awaits further experimentation. Because ofthe variety of instrumental tasks disrupted by extensive parietallesions, Thompson and his co11eagues (Thompson, Huestis, Crine11a, & Yu, 1986;Thompson & Yu, 1985) have classified the parietal neocortex as part ofthe brain's "general learning system." Also, Kesner, DiMattia, and Crutcher (1987), using radial maze methodologies that dissociate working-from reference-memory dysfunctions, have reported that an impainnent of reference memory, but not working memory, accompanies large parietallesions.…”

Section: Discussionmentioning

confidence: 99%

Visuospatial functions in the rat following injuries to striate, peristriate, and parietal neocortical sites

McDaniel

Wall

1988

Psychobiology

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The influenee oflesions located generaIly within four regions of the rat's posterior neocortex upon the aequisition and retention of two-choiee visual discriminations was assessed using a Thompson-Bryant apparatus. The ability to distinguish visual patterns was tested by utilizing stimuli eomposed of 45° versus 135 0 alternating blaek and white stripes (both total and local luminanee eues were eontroIled). "Brightness" discrimination was assessed by using blaek and white eard discriminanda. Posterior parietal injuries resulted in a dysfunction on eaeh of the four tasks, but rats with this injury eventuaIly attained eriterion for eaeh ofthe habits. SmaIler, more anteromedial parietallesions failed to disturb pattern discrimination and were not studied in the other paradigms. The only defieit observed in rats with medial peristriate injuries was a slight retardation in aequisition of the pattern discrimination. Sinee the effects of lateral peristriate and striate injuries upon pattern vision have been weIl described previously, the effects of these lesions on the retention and aequisition of the blaek-white discrimination were studied. Lateral peristriate lesions, but not striate lesions, were associated with a retention loBS of the brightness problem. This loss was detected even with a recovery interval of 60 days. Both striate and lateral peristriate lesions retarded blaek-white discrimination aequisition. Discussion foeuses on the probable natures of the visual dysfunctions associated with these injuries.Ablation of the rat's posterior neocortex has been reported to produce an abolition of form vision (e.g.,

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“…Our choice of the term PAC was based on the limited neuroanatomical evidence (e.g., Lashley, 1941; and limited neurobehavioral evidence concerning the effects of small lesions in this .egion upon behavior (Boyd & Thomas, 1977;Thomas & Weir, 1975) av~ilable at the time. These studies, along with studies in other laboratories (e.g., Thompson, Huestis, Crinella, & Yu, 1986;Thompson & Yu, 1985), showed that bilateral PAC lesions resulted in disturbed spatial learning in a variety of mazes (e.g., Hebb-Williams, Lashley III mazes) or mazelike (e.g., Y-or T-maze spatial position reversal and spatial alternation; Kolb et aI., 1983;McDaniel, Davall, & Waters, 1989; tasks. Recently, the influences of similar lesions have been extended to the Maier 3-table task (Thinus-Blanc, Save, Poucet, & Foreman, 1996).…”

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confidence: 77%

Turn-signal utilization by rats with either unilateral or bilateral posterior parietal cortex injuries

et al. 1998

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Rats with sham, unilateral, or bilateral aspiration lesions of the posterior parietal cortex (PPC) were trained in a water T-maze to use flashing lights located along the starting alley (two each) and inner walls of the goal alleys (two each) to fmd a hidden escape platform. Thereafter, the performance of the spatial response was tested under several conditions. Rats with bilateral PPC lesions were significantly inferior to unilateral-and sham-iI\jured rats in learning the "turn-signal" cued spatial task. Also, left-PPC-iI\jured rats committed significantly more errors than did the control animals. After mastering the task, cue saliency was reduced and the amount of spatial discontiguity between the stimuli and escape site was increased in two stages. That is, the flashing light closest to the escape platform was turned off for one testing session. On the following day, animals were required to rely on information located within the starting alley to make the correct spatial response at the choice point. Animals with bilateral or left PPC lesions were significantly impaired on the task with cues located only in the starting alley. The animals were then tested with competing constant illumination of the lights on the side of the apparatus opposite the flashing-light cues. The performance of all animals dropped to chance and failed to improve with training. Finally, three of the sham-operated controls were retrained to criterion on the original discrimination and prepared with bilateral PPC iI\juries. Substantial savings was observed. The results reveal a greater role of the left PPC than the right in the use of local sensory cues for spatial navigation, and they show that the PPC is not the repository ofthe "engram" for this learned visuospatial behavior.Research conducted during the past 20 years has shown that the rat has a cortical territory similar in many respects to posterior parietal cortex (PPC) in humans and nonhuman primates (e.g.

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The comparative effects of frontal, parietal, occipitotemporal, and limbic forebrain lesions in weanling rats on learning☆

Cited by 15 publications

References 24 publications

Melatonin Protection against Lead-Induced Changes in Human Neuroblastoma Cell Cultures

Melatonin Protection against Lead-Induced Changes in Human Neuroblastoma Cell Cultures

Visuospatial functions in the rat following injuries to striate, peristriate, and parietal neocortical sites

Turn-signal utilization by rats with either unilateral or bilateral posterior parietal cortex injuries

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