Faculty Opinions recommendation of A spatial memory signal shows that the parietal cortex has access to a craniotopic representation of space.

Author(s):  
Maria Concetta Morrone ◽  
Paola Binda ◽  
Guido Marco Cicchini
eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Mulugeta Semework ◽  
Sara C Steenrod ◽  
Michael E Goldberg

Humans effortlessly establish a gist-like memory of their environment whenever they enter a new place, a memory that can guide action even in the absence of vision. Neurons in the lateral intraparietal area (LIP) of the monkey exhibit a form of this environmental memory. These neurons respond when a monkey makes a saccade that brings the spatial location of a stimulus that appeared on a number of prior trials, but not on the present trial, into their receptive fields (RFs). The stimulus need never have appeared in the neuron’s RF. This memory response is usually weaker, with a longer latency than the neuron’s visual response. We suggest that these results demonstrate that LIP has access to a supraretinal memory of space, which is activated when the spatial location of the vanished stimulus can be described by a retinotopic vector from the center of gaze to the remembered spatial location.


2017 ◽  
Author(s):  
Mulugeta Semework ◽  
Sara C. Steenrod ◽  
Michael E. Goldberg

Humans effortlessly establish a gist-like memory of their environment whenever they enter a new place. They can then use this memory to guide action even in the absence of vision. Neurons in the lateral intraparietal area (LIP) of the monkey exhibit a form of this environmental memory, responding when a monkey makes a saccade that brings the spatial location of a stimulus that appeared on a number of prior trials, but not on the present trial into their receptive fields. The stimulus need never have appeared in the receptive field of the neuron. This response is usually weaker with a longer latency than the neuron's visual response. We suggest that these results demonstrate that LIP has access to a craniotopic memory of space, which is activated when the spatial location of the vanished stimulus can be described by a retinotopic vector from the center of gaze to the stimulus.


1993 ◽  
Vol 5 (6) ◽  
pp. 869-884 ◽  
Author(s):  
David S. Touretzky ◽  
A. David Redish ◽  
Hank S. Wan

O'Keefe (1991) has proposed that spatial information in rats might be represented as phasors: phase and amplitude of a sine wave encoding angle and distance to a landmark. We describe computer simulations showing that operations on phasors can be efficiently realized by arrays of spiking neurons that recode the temporal dimension of the sine wave spatially. Some cells in motor and parietal cortex exhibit response properties compatible with this proposal.


Cortex ◽  
2002 ◽  
Vol 38 (5) ◽  
pp. 854-859 ◽  
Author(s):  
Gereon R. Fink ◽  
John C. Marshall ◽  
Peter H. Weiss ◽  
Thomas Stephan ◽  
Nadim J. Shah ◽  
...  

1997 ◽  
Vol 352 (1360) ◽  
pp. 1437-1448 ◽  
Author(s):  
Alain Berthoz

This paper reviews the involvement of the parietal cortex and the hippocampus in three kinds of spatial memory tasks which all require a memory of a previously experienced movement in space. The first task compared, by means of positron emission tomography (PET) scan techniques, the production, in darkness, of self–paced saccades (SAC) with the reproduction, in darkness, of a previously learned sequence of saccades to visual targets (SEQ). The results show that a bilateral increase of activity was seen in the depth of the intraparietal sulcus and the medial superior parietal cortex (superior parietal gyrus and precuneus) together with the frontal sulcus but only in the SEQ task, which involved memory of the previously seen targets and possibly also motor memory. The second task is the vestibular memory contingent task, which requires that the subject makes, in darkness, a saccade to the remembered position of a visual target after a passively imposed whole–body rotation. Deficits in this task, which involves ‘vestibular memory’, were found predominantly in patients with focal vascular lesions in the parieto–insular (vestibular) cortex, the supplementary motor area–supplementary eye field area, and the prefrontal cortex. The third task requires mental navigation from the memory of a previously learned route in a real environment (the city of Orsay in France). A PET scan study has revealed that when subjects were asked to remember visual landmarks there was a bilateral activation of the middle hippocampal regions, left inferior temporal gyrus, left hippocampal regions, precentral gyrus and posterior cingulate gyrus. If the subjects were asked to remember the route, and their movements along this route, bilateral activation of the dorsolateral cortex, posterior hippocampal areas, posterior cingulate gyrus, supplementary motor areas, right middle hippocampal areas, left precuneus, middle occipital gyrus, fusiform gyrus and lateral premotor area was found. Subtraction between the two conditions reduced the activated areas to the left hippocampus, precuneus and insula. These data suggest that the hippocampus and parietal cortex are both involved in the dynamic aspects of spatial memory, for which the name ’topokinetic memory’ is proposed. These dynamic aspects could both overlap and be different from those involved in the cartographic and static aspects of ‘topographic’ memory.


2020 ◽  
Vol 13 (1) ◽  
Author(s):  
Xiao-fei He ◽  
Ge Li ◽  
Li-li Li ◽  
Ming-yue Li ◽  
Feng-yin Liang ◽  
...  

Abstract Background Cerebral microinfarcts (MIs) lead to progressive cognitive impairments in the elderly, and there is currently no effective preventative strategy due to uncertainty about the underlying pathogenic mechanisms. One possibility is the dysfunction of GABAergic transmission and ensuing excitotoxicity. Dysfunction of GABAergic transmission induces excitotoxicity, which contributes to stroke pathology, but the mechanism has kept unknown. The secreted leucine-rich repeat (LRR) family protein slit homologue 2 (Slit2) upregulates GABAergic activity and protects against global cerebral ischemia, but the neuroprotective efficacy of Slit2 against MIs has not been examined. Methods Middle-aged Wild type (WT) and Slit2-Tg mice were divided into sham and MI treatment groups. MIs were induced in parietal cortex by laser-evoked arteriole occlusion. Spatial memory was then compared between sham and MI groups using the Morris water maze (MWM) task. In addition, neuronal activity, blood brain barrier (BBB) permeability, and glymphatic clearance in peri-infarct areas were compared using two-photon imaging, while GABAergic transmission, microglial activation, neuronal loss, and altered cortical connectivity were compared by immunofluorescent staining or western blotting. Results Microinfarcts increased the amplitude and frequency of spontaneous intracellular Ca2+ signals, reduced neuronal survival and connectivity within parietal cortex, decreased the number of GABAergic interneurons and expression of vesicular GABA transporter (VGAT), induced neuroinflammation, and impaired both glymphatic clearance and spatial memory. Alternatively, Slit2 overexpression attenuated dysfunctional neuronal Ca2+ signaling, protected against neuronal death in the peri-infarct area as well as loss of parietal cortex connectivity, increased GABAergic interneuron number and VGAT expression, attenuated neuroinflammation, and improved both glymphatic clearance and spatial memory. Conclusion Our results strongly suggest that overexpression of Slit2 protected against the dysfunction in MIs, which is a potential therapeutic target for cognition impairment in the elderly.


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