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PubMed2004

The contribution of spatial remapping impairments to unilateral visual neglect.

Left visual neglect following right hemisphere damage is a heterogeneous phenomenon, in which several underlying impairments have been identified. Despite recent advances in understanding the neural and cognitive bases of these impairments, current theories of neglect, particularly those that emphasise attentional deficits, do not explain a number of phenomena, including: 'Ipsilesional' neglect after left orienting. Positive or 'productive' manifestations. Spatial transposition errors. Mislocalisations. Revisiting behaviour during visual search. Lack of awareness for objects toward the contralesional side of space. We propose that these manifestations of neglect can be accounted for by an additional underlying disorder of spatial remapping due to parietal dysfunction. In primary visual areas, retinotopic maps are renewed and thus overwritten at each new ocular fixation. Remapping processes operating in higher-level oculocentric visual maps of the parietal cortex ensure visual integration of these successive retinal images over time and space, by creating a constantly updated representation of stimulus locations in terms of distance and direction from the fovea. They consist in the storage, refreshment and re-localization of the different components of the visual scene that are successively attended during its exploration, and provide spatial constancy of visual perception and a spatial buffer for working memory [Cereb Cortex 5 (1995) 470; Visual Cogn 7 (2000) 17]. We begin this article by reviewing theoretical and experimental arguments that have highlighted the importance of parietal remapping processes in maintaining an accurate representation of space across saccadic shifts. We then focus on findings from the double-step saccade task, [Ann Neurol 38 (1995) 739] as a basis for our model of the role of remapping impairments in many of the symptoms of neglect. From these results, remapping impairments would be demonstrated when a saccade has to be guided across the midline after having fixated an object in either the left or right visual field for patients with either left- or right-side parietal lesions. In addition, patients with right-side lesions will have remapping impairments within the left visual field following a saccade to a left-side target (see Fig. 5). In a large part of the article, we seek to build our hypothesis based on this basic model and more speculative assumptions supported with extensive evidence from the literature.

Attention↗
PubMed2004

The challenges of understanding mammalian cognition and memory-based behaviours: an interactive learning and memory systems approach.

Various research problems are presented to illustrate the utility of using the interactive multiple learning and memory systems view to better understand normal and abnormal manifestations of mammalian behaviour. Evidence for incidental learning and memory processes is presented and various implications of this work are discussed. Empirical and theoretical work directed at understanding the cognitive and non-cognitive processes associated with place learning in the water task and context conditioning during aversive events is also presented.

Amnesia, Retrograde↗
PubMed2005

Applications of prism adaptation: a tutorial in theory and method.

Data and theory from prism adaptation are reviewed for the purpose of identifying control methods in applications of the procedure. Prism exposure evokes three kinds of adaptive or compensatory processes: postural adjustments (visual capture and muscle potentiation), strategic control (including recalibration of target position), and spatial realignment of various sensory-motor reference frames. Muscle potentiation, recalibration, and realignment can all produce prism exposure aftereffects and can all contribute to adaptive performance during prism exposure. Control over these adaptive responses can be achieved by manipulating the locus of asymmetric exercise during exposure (muscle potentiation), the similarity between exposure and post-exposure tasks (calibration), and the timing of visual feedback availability during exposure (realignment).

Adaptation, Physiological↗
PubMed2003

Spatial learning is delayed and brain-derived neurotrophic factor mRNA expression inhibited by administration of MK-801 in rats.

Brain-derived neurotrophic factor (BDNF) is involved in activity-dependent plasticity and interacts with the neurotransmitter glutamate. Glutamate N-methl-D-aspartate (NMDA) receptor activation increases BDNF expression, while BDNF facilitates NMDA activity, with both involved in spatial learning. Administration of the NMDA receptor antagonist MK-801 can impair this leaning. The interaction between NMDA and BDNF in learning is examined in this study. Adult male Sprague-Dawley rats received either i.p. MK-801 or saline and were trained to locate a submerged water maze platform. Sedentary and activity yoked groups were included for biochemical comparisons. Control rats quickly learned the platform location while MK-801-treated rats learned at a significantly slower rate (P < 0.0001). In situ hybridization for hippocampal BDNF mRNA indicated significant increases in the yoked and learning groups. However, MK-801 attenuated the BDNF mRNA increase in the learning and activity-yoked conditions (P < 0.05). Administration of MK-801 to the sedentary group did not alter baseline mRNA levels. These data suggest that BDNF expression is important for NMDA-dependent learning and memory. Interestingly, learning still occurs across trials independent of the NMDA and BDNF interaction. Increases in BDNF and NMDA activity may be significant components in learning and memory, and modulation of these systems may be beneficial for developing strategies to improve cognitive function.

Animals↗
PubMed2004

Positive effects of deprenyl and estradiol on spatial memory and oxidant stress in aged female rat brains.

Increasing age decreases spatial learning and memory. Spatial learning is coordinated with different brain regions. Since the oxidative damage may play a role in the aging process, including the associated cognitive decline, age-related impairment in spatial learning and memory may be alleviated by antioxidant treatment. The present study examined the effects of the monoamine oxidase B inhibitor L-deprenyl, alone and in combination with estradiol, on spatial memory using the Morris water maze and oxidant stress in aged female rat brains. We demonstrated that co-administration of deprenyl and estradiol caused a synergistic effect on spatial memory. However, use of either deprenyl or estradiol alone increased antioxidant enzyme activities in brain and reduced lipid peroxidation. Therefore, positive effects of deprenyl and estradiol on spatial memory may occur due not only to their antioxidant activities but also to the different actions.

Age Factors↗
PubMed2004

Choline pivaloyl esters improve in rats cognitive and memory performances impaired by scopolamine treatment or lesions of the nucleus basalis of Meynert.

The effects of two choline pivaloyl esters, [2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium iodide (1) and [2-(2,2-dimethylpropionyloxy)ethyl]trimethylammonium 2,2-dimethylpropionate (2), on learning and memory impairments induced in rats by scopolamine or lesions of nucleus basalis magnocellularis (NBM) have been evaluated by object recognition and Morris water maze tests in comparison with Tacrine (THA). Both 1 and 2 restored discrimination in object recognition test for assessing working-episodic memory and improved spatial memory in scopolamine or NBM-lesioned rats as well. The positive effects produced by 1 and 2 on cognitive and memory deficits were well comparable with those evoked by THA, used as reference compound.

Acetylcholinesterase↗
PubMed2006

A decreased survival of proliferated cells in the hippocampus is associated with a decline in spatial memory in aged rats.

In aged rats, although learning and memory impairment is prominent, both the number of granular cells and the degree of neuronal progenitor proliferation in the hippocampus are known to be preserved. We examined the association between the survival of newly generated neurons in the hippocampus and the learning ability in aged rats. By using BrdU, a cell proliferation marker to determine neurogenesis and contextual fear conditioning to determine learning ability, we found that in aged rats, along with memory impairment, the survival of both the proliferated cells at baseline and those enhanced by contextual fear conditioning decreased remarkably. These results suggest that the integration of newly generated neurons into hippocampal circuitry is decreased with aging, this phenomenon may, in part, explain the decline in learning and memory in aged rats.

Aging↗
PubMed2005

Differential generators for N20m and P35m responses to median nerve stimulation.

To study the spatial and behavioral dynamics of cortical sources for N20m and P35m at varying stimulus intensities, we measured neuromagnetic cortical responses to left electric median nerve stimulation at the wrist in 17 male healthy adults. The stimulus intensity levels were individually determined according to sensory threshold (ST) for perceiving electric pulses. Using equivalent current dipole (ECD) modeling, we analyzed the peak latencies, amplitudes, and locations of ECDs from 14 subjects for N20m and P35m elicited at 2 ST, 3 ST, and 4 ST. Compared with N20m, P35m was localized 3.3 +/- 0.6 mm more superiorly at 2-4 ST, and 2.9 +/- 1.2 mm more medially at 3-4 ST. Superimposed over subjects' own MR images, N20m ECDs were localized in the area of 3b contralateral to stimulus side in all 17 subjects at 3 ST, whereas P35m ECDs were localized either in the postcentral (in 14 subjects) or in the precentral areas (in 3 subjects). We found no clear correlation between N20m and P35m in terms of peak latencies as well as the corresponding growth of activation strengths along with stepwise increase in stimulus intensity. Our results imply that the two early SEF components, N20m and P35m, have differential cortical generators, with distinctive neurophysiological behaviors in response to varying stimulus intensity levels.

Adult↗
PubMed2004

Are spatial memories strengthened in the human hippocampus during slow wave sleep?

In rats, the firing sequences observed in hippocampal ensembles during spatial learning are replayed during subsequent sleep, suggesting a role for posttraining sleep periods in the offline processing of spatial memories. Here, using regional cerebral blood flow measurements, we show that, in humans, hippocampal areas that are activated during route learning in a virtual town are likewise activated during subsequent slow wave sleep. Most importantly, we found that the amount of hippocampal activity expressed during slow wave sleep positively correlates with the improvement of performance in route retrieval on the next day. These findings suggest that learning-dependent modulation in hippocampal activity during human sleep reflects the offline processing of recent episodic and spatial memory traces, which eventually leads to the plastic changes underlying the subsequent improvement in performance.

Adult↗
PubMed2006

Encoding new episodes and making them stick.

How do we encode, store, and retrieve new episodic memories, and what are the computations performed by the hippocampus during this process? One system that has been used to model the brain basis of episodic memory in humans is the study of spatial navigation by path integration in rodents. Here I discuss three exciting new findings focused on encoding or replay of spatial sequences in the rat hippocampus. These findings not only provide important new insight into the computations associated with encoding and consolidation of spatial trajectories, but may also have implications for understanding key aspects of human episodic memory.

Animals↗
PubMed2006

CaMKII activation in the entorhinal cortex disrupts previously encoded spatial memory.

To investigate the role of the entorhinal cortex in memory at a molecular level, we developed transgenic mice in which transgene expression was inducible and limited to the superficial layers of the medial entorhinal cortex, pre- and parasubiculum. We found that expression of a constitutively active mutant form of CaMKII in these structures disrupted spatial memory formation. Immediate post-training activation of the transgene disrupted previously established memory while transgene activation 3 weeks following the training was ineffective. These results demonstrate that, similar to the hippocampus, the entorhinal cortex plays a time-limited role in spatial memory formation but is not a final cortical repository of long-term memory. Moreover, these results suggest that the indiscriminate activation of CaMKII is able to disrupt preexisting memories, possibly by altering the pattern of synaptic weight changes that are thought to form the basis of the memory trace.

Animals↗
PubMed2006

Inducible and cell-type restricted manipulation in the entorhinal cortex.

The entorhinal cortex functions as the gateway to the hippocampal formation. However, its role in formation and consolidation of hippocampus-dependent memory remains relatively unexplored. In this issue of Neuron, Yasuda and Mayford report an elegant cell-type restricted inducible transgenic mouse overexpressing a mutant form of CaM kinase II selectively in superficial layers of medial entorhinal cortex and its upstream regions. These animals display a selective spatial memory deficit during the immediate posttraining period as well as during acquisition in the Morris water maze. Similar to the hippocampus, this time-limited involvement of entorhinal cortex in spatial memory processing suggests a crucial role for hippocampal-entorhinal circuitry in spatial memory formation.

Animals↗
PubMed2005

GABAB receptor antagonist SGS742 improves spatial memory and reduces protein binding to the cAMP response element (CRE) in the hippocampus.

Memory storage in the brain requires protein synthesis initiated through signaling pathways that control transcription. Such mechanisms are under active investigation for therapies in disorders involving cognitive dysfunction. Long-term memory can be improved by inhibiting activation or reducing expression of transcription factors such as ATF4/CREB2 and some C/EBP family members which appear to serve as memory suppressors. Here, we provide evidence that GABAB receptor antagonists may enhance cognition, at least in part, by this mechanism. We tested a GABAB receptor antagonist, SGS742 (CGP36742), on hippocampal-dependent memory and hippocampal nuclear CRE-binding activity in rats. As a result, acute in vivo administration of SGS742 both improved memory and reduced total hippocampal CRE-binding activity of which a large proportion in the basal state could be immunoneutralized with CREB2 antibodies. Consistent with its activity on information storage mechanisms, acute SGS742 effectively improved long-term memory in retrograde protocols, in which drug was given at times when memory formation can be interrupted by blocking new protein production. In conclusion, GABAB antagonists may provide a pharmacological therapy for cognitive impairment, sharing mechanistic features with genetic approaches to reduce CREB2 activity and to augment long-term memory.

Animals↗
PubMed2006

Metabotropic glutamate subtype 5 receptors modulate fear-conditioning induced enhancement of prepulse inhibition in rats.

Non-startling acoustic events presented shortly before an intense startling sound can inhibit the acoustic startle reflex. This phenomenon is called prepulse inhibition (PPI), and is widely used as a model of sensorimotor gating. The present study investigated whether PPI can be modulated by fear conditioning, whose acquisition can be blocked by the specific antagonist of metabotropic glutamate receptors subtype 5 (mGluR5), 2-methyl-6-(phenylethynyl)-pyridine (MPEP). The results show that a gap embedded in otherwise continuous noise sounds, which were delivered by two spatially separated loudspeakers, could inhibit the startle reflex induced by an intense sound that was presented 50 ms after the gap. The inhibitory effect depended on the duration of the gap, and was enhanced by fear conditioning that was introduced by temporally pairing the gap with footshock. Intraperitoneal injection of MPEP (0.5 or 5mg/kg) 30 min before fear conditioning blocked the enhancing effect of fear conditioning on PPI, but did not affect either the baseline startle magnitude or PPI if no fear conditioning was introduced. These results indicate that PPI is enhanced when the prepulse signifies an aversive event after fear conditioning. Also, mGlu5Rs play a role in preserving the fear-conditioning-induced enhancement of PPI.

Analysis of Variance↗
PubMed2004

Gradients of detection in neglect: comparison of peripersonal and extrapersonal space.

Previous studies of target-cancellation performance in visuospatial neglect patients have reported lateral (left-right) and radial (near-far) gradients of attentional ability. The purpose of the present study was to replicate the reported attentional gradients in peripersonal space (within arms reach) and to examine whether lateral gradients of detection also appear in extrapersonal space (beyond arms reach), using equivalent tasks with no manual requirement. The relationship between radial gradients in peripersonal space and neglect severity (degree of lateral gradient) in extrapersonal space was also of interest. Right-hemisphere stroke subjects, with and without neglect, and healthy control subjects named visual targets on scanning sheets placed in peripersonal and extrapersonal space. The neglect group showed lateral gradients of increasing target detection from left to right in both peripersonal and extrapersonal space, which were not evident in the performance of either of the control groups. Double dissociations of neglect severity in peripersonal and extrapersonal space were also found in analyses of individual performance. Lesion analyses showed that peripersonal neglect was related to dorsal stream damage and extrapersonal neglect was related to ventral stream damage. Group analyses showed no significant radial gradients in peripersonal space in the three groups. In addition, while analyses of some individuals found significant near-far and far-near radial gradients, there was no correlation between radial gradients in peripersonal space and neglect severity in extrapersonal space. These results are discussed in terms of theorised hemispheric mechanisms of spatial attention and the relationship of neglect in the two co-ordinate spaces to the extent and location of damaged neurons in the right hemisphere.

Adult↗
PubMed2004

Topographical memory impairments after unilateral lesions of the anterior thalamus and contralateral inferotemporal cortex.

Monkeys with crossed unilateral excitotoxic lesions of the anterior thalamus and unilateral inferotemporal cortex ablation were severely impaired at learning two tasks which required the integration of information about the appearance of objects and their positions in space. The lesioned monkeys were also impaired at learning a spatial task and a task which required the integration of information about the appearance of objects and the background on which the objects were situated. Monkeys with only one of the unilateral lesions were not impaired and previous work has shown that monkeys with bilateral lesions of the anterior thalamus were not impaired on these tasks. These results indicate that the whole of the inferotemporal cortex-anterior thalamic circuit, which passes via the hippocampus, fornix, mamillary bodies and mamillothalamic tract, is essential for the topographical analysis of information about specific objects in different positions in space. Together with previous work, the results show that a unilateral lesion may affect cognition in the presence of other brain damage when an equivalent bilateral lesion alone does not. The tasks required the slow acquisition of information into long term memory and therefore assessed semantic knowledge although other research has shown impairment on topographical processing within working or episodic memory following lesions of the hippocampal-diencephalic circuit. It is argued that the hippocampal-diencephalic circuit does not have a role in a specific form of memory such as episodic memory but rather is involved in topographical analysis of the environment in perception and across all types of declarative memory.

Animals↗
PubMed2004

Convergent and divergent effects of neck proprioceptive and visual motion stimulation on visual space processing in neglect.

Visual motion stimulation as well as neck muscle vibration are known to effectively modulate the subjective body orientation in spatial neglect. However, so far only motion stimulation has been demonstrated to substantially influence size and space distortion in neglect patients. The present study aimed to compare the two stimulation methods with respect to their potentially differential impact on subjective body orientation and on space and size distortion, in five neglect patients showing perceptual distortions. We found comparable beneficial effects during left motion stimulation and left neck vibration for the subjective straight ahead. Additionally, left motion stimulation significantly ameliorated the leftward overextension in size matching, line bisection and distance estimation in all five patients. In contrast, during neck vibration only two patients showed an improvement for line bisection and size estimation and none did so for distance estimation. Since these two patients differed from the others as they had either no visual field defects or a major visual field sparing, we suggest--based on recent anatomical and neuropsychological findings--that neck vibration only tends to improve pure neglect-related visuo-perceptual distortions whereas motion stimulation can additionally improve perceptual distortions in neglect associated with hemianopia.

Adult↗
PubMed2004

Processing biases towards the preferred hand: valid and invalid cueing of left- versus right-hand movements.

A Posner-like paradigm was employed to investigate the effects of valid and invalid cueing of each hand on reaction time, movement time and peak velocity in an aiming task. Given claims of left hemisphere superiority in movement selection and inhibition (and the privileged within-hemisphere access of the right hand to such systems), it was hypothesised that invalidly cueing the left hand (i.e. right-hand movement precued, left-handed movement required by a go signal) would result in increased reaction time relative to invalid right-hand cueing. The hypothesis was not confirmed as reaction times of both hands were slowed equivalently by invalid cueing. Nevertheless, it was found that the movement duration of the left hand was increased substantially by invalid cueing, while the right hand was unaffected on this measure, suggesting a possible intentional rather than attentional difference between the two hands. These results are discussed in terms of a possible asymmetry of intentional processes related to hand movement and the right-hand advantage in movement duration.

Adult↗