New Pachygyria Syndrome Linked to Actin Regulation Identified: When mutated, CTNNA2 leads to a new form of pachygyria that has a diffuse anterior-posterior gradient with cerebellar hypoplasia, thinning corpus callosum, and absent anterior commissure

2018 ◽  
Vol 176 (11) ◽  
pp. 2234-2235
1993 ◽  
Vol 10 (1) ◽  
pp. 159-171 ◽  
Author(s):  
Robert Desimone ◽  
Jeffrey Moran ◽  
Stanley J. Schein ◽  
Mortimer Mishkin

AbstractThe classically defined receptive fields of V4 cells are confined almost entirely to the contralateral visual field. However, these receptive fields are often surrounded by large, silent suppressive regions, and stimulating the surrounds can cause a complete suppression of response to a simultaneously presented stimulus within the receptive field. We investigated whether the suppressive surrounds might extend across the midline into the ipsilateral visual field and, if so, whether the surrounds were dependent on the corpus callosum, which has a widespread distribution in V4. We found that the surrounds of more than half of the cells tested in the central visual field representation of V4 crossed into the ipsilateral visual field, with some extending up to at least 16 deg from the vertical meridian. Much of this suppression from the ipsilateral field was mediated by the corpus callosum, as section of the callosum dramatically reduced both the strength and extent of the surrounds. There remained, however, some residual suppression that was not further reduced by addition of an anterior commissure lesion. Because the residual ipsilateral suppression was similar in magnitude and extent to that found following section of the optic tract contralateral to the V4 recording, we concluded that it was retinal in origin. Using the same techniques employed in V4, we also mapped the ipsilateral extent of surrounds in the foveal representation of VI in an intact monkey. Results were very similar to those in V4 following commissural or contralateral tract sections. The findings suggest that V4 is a central site for long-range interactions both within and across the two visual hemifields. Taken with previous work, the results are consistent with the notion that the large suppressive surrounds of V4 neurons contribute to the neural mechanisms of color constancy and figure-ground separation.


2020 ◽  
Vol 117 (19) ◽  
pp. 10554-10564 ◽  
Author(s):  
Annalisa Paolino ◽  
Laura R. Fenlon ◽  
Peter Kozulin ◽  
Elizabeth Haines ◽  
Jonathan W. C. Lim ◽  
...  

A unique combination of transcription factor expression and projection neuron identity demarcates each layer of the cerebral cortex. During mouse and human cortical development, the transcription factor CTIP2 specifies neurons that project subcerebrally, while SATB2 specifies neuronal projections via the corpus callosum, a large axon tract connecting the two neocortical hemispheres that emerged exclusively in eutherian mammals. Marsupials comprise the sister taxon of eutherians but do not have a corpus callosum; their intercortical commissural neurons instead project via the anterior commissure, similar to egg-laying monotreme mammals. It remains unknown whether divergent transcriptional networks underlie these cortical wiring differences. Here, we combine birth-dating analysis, retrograde tracing, gene overexpression and knockdown, and axonal quantification to compare the functions of CTIP2 and SATB2 in neocortical development, between the eutherian mouse and the marsupial fat-tailed dunnart. We demonstrate a striking degree of structural and functional homology, whereby CTIP2 or SATB2 of either species is sufficient to promote a subcerebral or commissural fate, respectively. Remarkably, we reveal a substantial delay in the onset of developmental SATB2 expression in mice as compared to the equivalent stage in dunnarts, with premature SATB2 overexpression in mice to match that of dunnarts resulting in a marsupial-like projection fate via the anterior commissure. Our results suggest that small alterations in the timing of regulatory gene expression may underlie interspecies differences in neuronal projection fate specification.


2004 ◽  
Vol 16 (3) ◽  
pp. 401-414 ◽  
Author(s):  
Sophie Bayard ◽  
Nadia Gosselin ◽  
Manon Robert ◽  
Maryse Lassonde

Interhemispheric differences of the N100 latency in visual evoked potentials have been used to estimate interhemispheric transfer time (e.g., Saron & Davidson, 1989). Recent work has also suggested that the P300 component could reflect the efficacy of interhemispheric transmission (Polich & Hoffman, 1998). The purpose of the present study was to study the differential role of the corpus callosum (CC) and anterior commissure (AC) in the interhemispheric propagation of these two electrophysiological components. Thus, the amplitude and latency distribution of the N100 and P300 components were analyzed using high-density electrical mapping in a subject with agenesis of CC but preservation of AC, a subject with agenesis of both CC and AC, and 10 neurologically intact control subjects. The task consisted of a modified visual oddball paradigm comprising one frequent and two rare stimuli, one presented on the same and the other on the opposite side of the frequent stimulus. Interhemispheric differences in latency were found for the N100 component in controls. However, in the acallosal subjects, this component was not identifiable in the indirectly stimulated hemisphere. In controls, no interhemispheric differences were observed in the distribution of the P300 latency and amplitude to rare and frequent stimuli. The distribution of the P300 amplitude in the acallosal subject with an AC was identical to that of the controls, whereas in the acallosal subject lacking the AC, the amplitude was greater in the hemisphere receiving the frequent stimuli, regardless of the visual hemifield in which the rare stimuli were presented. In both acallosal subjects, hemispheric differences in the P300 latency were observed, the latencies being shorter in the hemisphere directly stimulated for all categories of stimuli. These results suggest that the interhemispheric transfer of both the N100 and P300 components relies on the integrity of cortical commissures. Possible P300 generator sources are discussed.


1967 ◽  
Vol 45 (9) ◽  
pp. 1591-1596 ◽  
Author(s):  
Melvin Goldstein

A new pattern of colony differentiation was observed in a portion of a clone (5%) in the normally undifferentiated species, Eudorina elegans. The new form possesses somatic and generative cells arranged on opposite sides of the anterior–posterior axis of the colony and the somatic cells die gradually during colony maturation. The development and ultimate pattern of colony differentiation is described and compared with known patterns of differentiation in Eudorina illinoisensis and Eudorina (Pleodorina) californica. A possible mechanism to account for colony differentiation in Eudorina is discussed.


2019 ◽  
Author(s):  
Shruti Jain ◽  
Christina A. Watts ◽  
Wilson C.J. Chung ◽  
Kristy Welshhans

AbstractDown syndrome is the most common genetic cause of intellectual disability and occurs due to the trisomy of human chromosome 21. Adolescent and adult brains from humans with Down syndrome exhibit various neurological phenotypes including a reduction in the size of the corpus callosum, hippocampal commissure and anterior commissure. However, it is unclear when and how these interhemispheric connectivity defects arise. Using the Ts65Dn mouse model of Down syndrome, we examined interhemispheric connectivity in postnatal day 0 (P0) Ts65Dn mouse brains. We find that there is no change in the volume of the corpus callosum or anterior commissure in P0 Ts65Dn mice. However, the volume of the hippocampal commissure is significantly reduced in P0 Ts65Dn mice, and this may contribute to the impaired learning and memory phenotype of this disorder. Interhemispheric connectivity defects that arise during development may be due to disrupted axon growth. In line with this, we find that developing hippocampal neurons display reduced axon length in vitro, as compared to neurons from their euploid littermates. This study is the first to report the presence of defective interhemispheric connectivity at the time of birth in Ts65Dn mice, providing evidence that early therapeutic intervention may be an effective time window for the treatment of Down syndrome.


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