Prism adaptation and aftereffect: specifying the properties of a procedural memory system.
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Prism adaptation, a form of procedural learning, is a phenomenon in which the motor system adapts to new visuospatial coordinates imposed by prisms that displace the visual field. Once the prisms are withdrawn, the degree and strength of the adaptation can be measured by the spatial deviation of the motor actions in the direction opposite to the visual displacement imposed by the prisms, a phenomenon known as aftereffect. This study was designed to define the variables that affect the acquisition and retention of the aftereffect. Subjects were required to throw balls to a target in front of them before, during, and after lateral displacement of the visual field with prismatic spectacles. The diopters of the prisms and the number of throws were varied among different groups of subjects. The results show that the adaptation process is dependent on the number of interactions between the visual and motor system, and not on the time spent wearing the prisms. The results also show that the magnitude of the aftereffect is highly correlated with the magnitude of the adaptation, regardless of the diopters of the prisms or the number of throws. Finally, the results suggest that persistence of the aftereffect depends on the number of throws after the adaptation is complete. On the basis of these results, we propose that the system underlying this kind of learning stores at least two different parameters, the contents (measured as the magnitude of displacement) and the persistence (measured as the number of throws to return to the baseline) of the learned information. (+info)
Common inhibitory mechanism in human inferior prefrontal cortex revealed by event-related functional MRI.
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Inhibition of an ongoing reaction tendency for adaptation to changing environments is a major function of the human prefrontal cortex. This function has been investigated frequently using the go/no-go task and set-shifting tasks such as the Wisconsin Card Sorting Test (WCST). Studies in humans and monkeys suggest the involvement of the dorsolateral prefrontal cortex in the two task paradigms. However, it remains unknown where in the dorsolateral prefrontal cortex this function is localized, whether a common inhibitory mechanism is used in these task paradigms and how this inhibitory function acts on two different targets, i.e. the go response in the go/no-go task and the cognitive set in the WCST. In the go/no-go task of this study, subjects were instructed to either respond (go trial) or not respond (no-go trial), depending on the cue stimulus presented. The signals of functional MRI (fMRI) related to the inhibitory function should be transient by nature. Thus, we used the temporal resolution of fMRI (event-related fMRI) by which transient signals in go and no-go trials can be analysed separately and compared with each other. We found a focus that showed transient no-go dominant activity in the posterior part of the inferior frontal sulcus in the right hemisphere. This was true irrespective of whether the subjects used their right or left hands. These results suggest that the transient activation in the right inferior prefrontal area is related to the neural mechanism underlying the response inhibition function. Furthermore, this area was found to be overlapped spatially with the area that was activated transiently during cognitive set shifting in the WCST. The transient signals in the go/no-go task peaked 5 s after the transient expression of the inhibitory function, and the transient signals in the WCST peaked 7s after the transient expression, reflecting different durations of neuronal activity in the two inhibitory task paradigms. These results imply that the right inferior prefrontal area is commonly involved in the inhibition of different targets, i.e. the go response during performance of the go/no-go task and the cognitive set during performance of the WCST. (+info)
An fMRI version of the Farnsworth-Munsell 100-Hue test reveals multiple color-selective areas in human ventral occipitotemporal cortex.
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Studies of patients with cerebral achromatopsia have suggested that ventral occipitotemporal cortex is important for color perception. We created a functional magnetic resonance imaging (fMRI) version of a clinical test commonly used to assess achromatopsia, the Farnsworth-Munsell 100-Hue test. The test required normal subjects to use color information in the visual stimulus to perform a color sequencing task. A modification of the test requiring ordering by luminance was used as a control task. Subjects were also imaged as they passively viewed colored stimuli. A limited number of areas responded more to chromatic than achromatic stimulation, including primary visual cortex. Most color-selective activity was concentrated in ventral occipitotemporal cortex. Several areas in ventral cortex were identified. The most posterior, located in posterior fusiform gyrus, corresponded to the area activated by passive viewing of colored stimuli. More anterior and medial color-selective areas were located in the collateral sulcus and fusiform gyrus. These more anterior areas were not identified in previous imaging studies which used passive viewing of colored stimuli, and were most active in our study when visual color information was behaviorally relevant, suggesting that attention influences activity in color-selective areas. The fMRI version of the Farnsworth-Munsell test may be useful in the study of achromatopsia. (+info)
Nutritionally-directed compensatory growth enhances mammary development and lactation potential in rats.
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A nutritionally-regulated compensatory growth regimen imposed during a growing period from prepuberty to gestation can significantly affect mammary development and subsequent lactation performance. The objectives of this study were as follows: 1) to determine whether a compensatory nutrition regimen enhances lactation potential for the first and second lactation cycles and 2) to determine the extent to which a compensatory nutrition regimen modulates cell proliferation, differentiation, and apoptosis and expression of genes in mammary tissues of female rats. Female Sprague-Dawley rats (n = 122, 35 d of age) were randomly assigned either to the control group, with free access to diet, or to a stair-step compensatory nutrition feeding regimen, with an alternating 2-2-3-3-wk schedule. The regimen began with an energy-restricted diet (40% restriction) for 2 wk, followed by the control diet for 2 wk; this step was then repeated at 3-wk intervals. Pups of dams from the compensatory nutrition regimen group gained more during mid-lactation than did control group pups. Mammary tissues were obtained from early (d 2) and late (d 19) lactating rats. Mammary tissue from the compensatory nutrition group exhibited increased cell proliferation and greater gamma-glutamyltranspeptidase and ornithine decarboxylase gene expressions than did tissue from the control group during early lactation of both cycles. Mammary tissue from the compensatory nutrition group also had fewer apoptotic cells than tissue from the control group during late lactation of the first lactation cycle. These results suggest that the compensatory nutrition regimen imposed during the peripubertal developmental phase stimulated mammary growth and enhanced lactation performance by affecting the expression of genes that regulate the cell cycle. (+info)
Primary hypoxic tolerance and chemical preconditioning during estrus cycle in mice.
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BACKGROUND AND PURPOSE: Exogenous application of estrogens or progesterone ameliorates hypoxic/ischemic cell damage. This study investigates whether values of primary and induced hypoxic tolerance vary endogenously during the estrus cycle in female mice. METHODS: Population spike amplitude (PSA) and NADH were measured during hypoxic hypoxia and recovery in hippocampal slices from untreated control animals (C slices) and slices prepared from animals pretreated in vivo with a single intraperitoneal injection of 3-nitropropionate (3NP) (3NP slices) or acetylsalicylate (ASA) (ASA slices). RESULTS: Posthypoxic recovery of PSA was dose dependent in 3NP slices from males, with maximal recovery on pretreatment attained with 20 mg/kg 3NP (82+/-32% [mean+/-SD]; C slices, 38+/-29%; P<0.01). PSA recovered to 17+/-12% in C slices during proestrus, 43+/-23% during estrus, and 63+/-44% during diestrus. In 3NP slices, recovery of PSA increased to 57+/-36% (P<0. 05) during proestrus. Hypoxic tolerance was not increased in other stages of the estrus cycle. Hypoxic NADH increase during proestrus declined from 212+/-76% in C slices to 133+/-11% in 3NP slices (P<0. 05). Recovery of PSA in ASA slices was 75+/-36% (P<0.01 versus control) in males and 48+/-34% during proestrus (P<0.05 versus ASA slices from males). CONCLUSIONS: Primary and induced hypoxic tolerance are endogenously modulated during the estrus cycle. Differences in hypoxic oxidative energy metabolism mediate part of the differential tolerance. Experimental and clinical therapeutic strategies against cerebral ischemia/hypoxia need to consider sex-related dependence. (+info)
Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting.
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Prolonged deprivation of food induces dramatic changes in mammalian metabolism, including the release of large amounts of fatty acids from the adipose tissue, followed by their oxidation in the liver. The nuclear receptor known as peroxisome proliferator-activated receptor alpha (PPARalpha) was found to play a role in regulating mitochondrial and peroxisomal fatty acid oxidation, suggesting that PPARalpha may be involved in the transcriptional response to fasting. To investigate this possibility, PPARalpha-null mice were subjected to a high fat diet or to fasting, and their responses were compared with those of wild-type mice. PPARalpha-null mice chronically fed a high fat diet showed a massive accumulation of lipid in their livers. A similar phenotype was noted in PPARalpha-null mice fasted for 24 hours, who also displayed severe hypoglycemia, hypoketonemia, hypothermia, and elevated plasma free fatty acid levels, indicating a dramatic inhibition of fatty acid uptake and oxidation. It is shown that to accommodate the increased requirement for hepatic fatty acid oxidation, PPARalpha mRNA is induced during fasting in wild-type mice. The data indicate that PPARalpha plays a pivotal role in the management of energy stores during fasting. By modulating gene expression, PPARalpha stimulates hepatic fatty acid oxidation to supply substrates that can be metabolized by other tissues. (+info)
Dissociated vertical deviation: an exaggerated normal eye movement used to damp cyclovertical latent nystagmus.
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PURPOSE: Dissociated vertical deviation (DVD) has eluded explanation for more than a century. The purpose of this study has been to elucidate the etiology and mechanism of DVD. METHODS: Eye movement recordings of six young adults with DVD were made with dual-coil scleral search coils under various conditions of fixation, illumination, and head tilt. Horizontal, vertical, and torsional eye movements were recorded for both eyes simultaneously. Analyses of the simultaneous vertical and torsional movements occurring during the DVD response were used to separate and identify the component vergence and version eye movements involved. RESULTS: Typically, both horizontal and cyclovertical latent nystagmus developed upon occlusion of either eye. A cycloversion then occurred, with the fixing eye intorting and tending to depress, the covered eye extorting and elevating. Simultaneously, upward versions occurred for the maintenance of fixation, consisting variously of saccades and smooth eye movements, leading to further elevation of the eye behind the cover. The cyclovertical component of the latent nystagmus became partially damped as the DVD developed. CONCLUSIONS: In patients with an early-onset defect of binocular function, the occlusion of one eye, or even concentration on fixing with one eye, produces unbalanced input to the vestibular system. This results in latent nystagmus, sometimes seen only with magnification. The cyclovertical component of the latent nystagmus, when present, is similar to normal vestibular nystagmus induced by dynamic head tilting about an oblique axis. Such vestibular nystagmus characteristically produces a hyperdeviation of the eyes. In the case of cyclovertical latent nystagmus, the analogous hyperdeviation will persist unless corrected by a vertical vergence. A normal, oblique-muscle-mediated, cycloversion/vertical vergence is called into play. This occurs in the proper direction to correct the hyperdeviation, but it occurs in an exaggerated form in the absence of binocular vision, probably as a learned response. The cycloversion/vertical vergence helps damp the cyclovertical nystagmus (a cyclovertical "nystagmus block-age" phenomenon), aiding vision in the fixing eye. But this mechanism also produces unavoidable and undesirable elevation and extortion of the fellow eye, which we call DVD. (+info)
Role of central AT1 and V1 receptors in cardiovascular adaptation to hemorrhage in SD and renin TGR rats.
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In acute experiments, intracranially applied angiotensin II and vasopressin elicit significant cardiovascular effects. The purpose of the present study was to find out whether chronic intrabrain elevation of these peptides, occurring in the renin transgenic TGR(mRen2)27 (TGR) rats, results in an alteration of the cardiovascular control. Mean arterial blood pressure (MAP) and heart rate responses to hypovolemia were examined in hypertensive TGR and normotensive Sprague-Dawley (SD) rats under control conditions and during blockade of central AT1 or V1 receptors. Both groups received cerebroventricular infusions of either 1) cerebrospinal fluid (series 1), 2) AT1 receptors antagonist (AT1ANT, series 2), or 3) V1 receptors antagonist (V1ANT, series 3). Blockade of AT1 and V1 receptors decreased MAP in TGR but not in SD rats. In SD rats, bleeding elicited a similar decrease of MAP in each series and a transient increase of heart rate in series 3. In TGR, hemorrhage caused bradycardia and decrease of MAP, which was greater than in SD rats. Hemorrhagic hypotension in TGR was abolished by V1ANT and bradycardia by V1ANT or AT1ANT. The results demonstrate remarkable differences in cardiovascular adjustment to hemorrhage in SD and TGR rats and provide evidence for enhanced involvement of central V1 and AT1 receptors in the regulation of blood pressure during hypovolemia in TGR. Central V1 vasopressin receptors play a crucial role in eliciting posthemorrhagic hypotension and bradycardia in this strain. (+info)