scholarly journals A pan-mammalian map of interhemispheric brain connections predates the evolution of the corpus callosum

2018 ◽  
Vol 115 (38) ◽  
pp. 9622-9627 ◽  
Author(s):  
Rodrigo Suárez ◽  
Annalisa Paolino ◽  
Laura R. Fenlon ◽  
Laura R. Morcom ◽  
Peter Kozulin ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Ex Vivo ◽  
Anterior Commissure ◽  
Egg Laying ◽  
Mammalian Brain ◽  
Brain Organization ◽  
Commissural Neurons ◽  
Interhemispheric Connectivity ◽  
Key Aspects ◽  
Brain Connections

The brain of mammals differs from that of all other vertebrates, in having a six-layered neocortex that is extensively interconnected within and between hemispheres. Interhemispheric connections are conveyed through the anterior commissure in egg-laying monotremes and marsupials, whereas eutherians evolved a separate commissural tract, the corpus callosum. Although the pattern of interhemispheric connectivity via the corpus callosum is broadly shared across eutherian species, it is not known whether this pattern arose as a consequence of callosal evolution or instead corresponds to a more ancient feature of mammalian brain organization. Here we show that, despite cortical axons using an ancestral commissural route, monotremes and marsupials share features of interhemispheric connectivity with eutherians that likely predate the origin of the corpus callosum. Based on ex vivo magnetic resonance imaging and tractography, we found that connections through the anterior commissure in both fat-tailed dunnarts (Marsupialia) and duck-billed platypus (Monotremata) are spatially segregated according to cortical area topography. Moreover, cell-resolution retrograde and anterograde interhemispheric circuit mapping in dunnarts revealed several features shared with callosal circuits of eutherians. These include the layered organization of commissural neurons and terminals, a broad map of connections between similar (homotopic) regions of each hemisphere, and regions connected to different areas (heterotopic), including hyperconnected hubs along the medial and lateral borders of the cortex, such as the cingulate/motor cortex and claustrum/insula. We therefore propose that an interhemispheric connectome originated in early mammalian ancestors, predating the evolution of the corpus callosum. Because these features have been conserved throughout mammalian evolution, they likely represent key aspects of neocortical organization.

scholarly journals Differential timing of a conserved transcriptional network underlies divergent cortical projection routes across mammalian brain evolution

2020 ◽  
Vol 117 (19) ◽  
pp. 10554-10564 ◽  
Author(s):  
Annalisa Paolino ◽  
Laura R. Fenlon ◽  
Peter Kozulin ◽  
Elizabeth Haines ◽  
Jonathan W. C. Lim ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Corpus Callosum ◽  
Anterior Commissure ◽  
Regulatory Gene ◽  
Brain Evolution ◽  
Projection Neuron ◽  
Egg Laying ◽  
Mammalian Brain ◽  
Transcriptional Networks ◽  
Cortical Projection

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.

scholarly journals Neurodevelopmental wiring deficits in the Ts65Dn mouse model of Down syndrome

2019 ◽  
Author(s):  
Shruti Jain ◽  
Christina A. Watts ◽  
Wilson C.J. Chung ◽  
Kristy Welshhans
Keyword(s):  
Down Syndrome ◽  
Corpus Callosum ◽  
Mouse Model ◽  
Hippocampal Neurons ◽  
Anterior Commissure ◽  
Axon Growth ◽  
Chromosome 21 ◽  
Ts65dn Mouse ◽  
Hippocampal Commissure ◽  
Interhemispheric Connectivity

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.

scholarly journals Neuroanatomy and behavior in mice with a haploinsufficiency of AT-rich interactive domain 1B (ARID1B) throughout development

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
J. Ellegood ◽  
S. P. Petkova ◽  
A. Kinman ◽  
L. R. Qiu ◽  
A. Adhikari ◽  
...  
Keyword(s):  
Corpus Callosum ◽  
Ex Vivo ◽  
Chromatin Modification ◽  
Autism Spectrum ◽  
Repetitive Behaviors ◽  
Social Deficits ◽  
Altered Expression ◽  
Developmental Growth ◽  
And Behavior

Abstract Background One of the causal mechanisms underlying neurodevelopmental disorders (NDDs) is chromatin modification and the genes that regulate chromatin. AT-rich interactive domain 1B (ARID1B), a chromatin modifier, has been linked to autism spectrum disorder and to affect rare and inherited genetic variation in a broad set of NDDs. Methods A novel preclinical mouse model of Arid1b deficiency was created and validated to characterize and define neuroanatomical, behavioral and transcriptional phenotypes. Neuroanatomy was assessed ex vivo in adult animals and in vivo longitudinally from birth to adulthood. Behavioral testing was also performed throughout development and tested all aspects of motor, learning, sociability, repetitive behaviors, seizure susceptibility, and general milestones delays. Results We validated decreased Arid1b mRNA and protein in Arid1b+/− mice, with signatures of increased axonal and synaptic gene expression, decreased transcriptional regulator and RNA processing expression in adult Arid1b+/− cerebellum. During neonatal development, Arid1b+/− mice exhibited robust impairments in ultrasonic vocalizations (USVs) and metrics of developmental growth. In addition, a striking sex effect was observed neuroanatomically throughout development. Behaviorally, as adults, Arid1b+/− mice showed low motor skills in open field exploration and normal three-chambered approach. Arid1b+/− mice had learning and memory deficits in novel object recognition but not in visual discrimination and reversal touchscreen tasks. Social interactions in the male–female social dyad with USVs revealed social deficits on some but not all parameters. No repetitive behaviors were observed. Brains of adult Arid1b+/− mice had a smaller cerebellum and a larger hippocampus and corpus callosum. The corpus callosum increase seen here contrasts previous reports which highlight losses in corpus callosum volume in mice and humans. Limitations The behavior and neuroimaging analyses were done on separate cohorts of mice, which did not allow a direct correlation between the imaging and behavioral findings, and the transcriptomic analysis was exploratory, with no validation of altered expression beyond Arid1b. Conclusions This study represents a full validation and investigation of a novel model of Arid1b+/− haploinsufficiency throughout development and highlights the importance of examining both sexes throughout development in NDDs.

A role for the corpus callosum in visual area V4 of the macaque

1993 ◽  
Vol 10 (1) ◽  
pp. 159-171 ◽  
Author(s):  
Robert Desimone ◽  
Jeffrey Moran ◽  
Stanley J. Schein ◽  
Mortimer Mishkin
Keyword(s):  
Visual Field ◽  
Corpus Callosum ◽  
Anterior Commissure ◽  
Color Constancy ◽  
Receptive Fields ◽  
Optic Tract ◽  
Complete Suppression ◽  
Central Visual Field ◽  
Field Representation ◽  
Area V4

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.

Inter- and Intra-hemispheric Processing of Visual Event-related Potentials in the Absence of the Corpus Callosum

2004 ◽  
Vol 16 (3) ◽  
pp. 401-414 ◽  
Author(s):  
Sophie Bayard ◽  
Nadia Gosselin ◽  
Manon Robert ◽  
Maryse Lassonde
Keyword(s):  
Corpus Callosum ◽  
Anterior Commissure ◽  
Event Related Potentials ◽  
Interhemispheric Transfer ◽  
P300 Amplitude ◽  
Oddball Paradigm ◽  
P300 Latency ◽  
Hemispheric Differences ◽  
Visual Hemifield ◽  
Related Potentials

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.

scholarly journals Prediction of recovery from supplementary motor area syndrome after brain tumor surgery: preoperative diffusion tensor tractography analysis and postoperative neurological clinical course

2018 ◽  
Vol 44 (6) ◽  
pp. E3 ◽  
Author(s):  
Kazunori Oda ◽  
Fumio Yamaguchi ◽  
Hiroyuki Enomoto ◽  
Tadashi Higuchi ◽  
Akio Morita
Keyword(s):  
Diffusion Tensor Imaging ◽  
Corpus Callosum ◽  
Supplementary Motor Area ◽  
Diffusion Tensor ◽  
Motor Area ◽  
Primary Motor Area ◽  
Sma Syndrome ◽  
Interhemispheric Connectivity ◽  
Recovery Group ◽  
Diffusion Tensor Imaging Tractography

OBJECTIVEPrevious studies have suggested a correlation between interhemispheric sensorimotor networks and recovery from supplementary motor area (SMA) syndrome. In the present study, the authors examined the hypothesis that interhemispheric connectivity of the primary motor cortex in one hemisphere with the contralateral SMA may be important in the recovery from SMA syndrome. Further, they posited that motor cortical fiber connectivity with the SMA is related to the severity of SMA syndrome.METHODSPatients referred to the authors’ neurological surgery department were retrospectively analyzed for this study. All patients with tumors involving the unilateral SMA region, without involvement of the primary motor area, and diagnosed with SMA syndrome in the postoperative period were eligible for inclusion. Preoperative diffusion tensor imaging tractography (DTT) was used to examine the number of fiber tracts (NFidx) connecting the contralateral SMA to the ipsilateral primary motor area via the corpus callosum. Complete neurological examination had been performed in all patients in the pre- and postoperative periods. All patients were divided into two groups: those who recovered from SMA syndrome in ≤ 7 days (early recovery group) and those who recovered in ≥ 8 days (late recovery group). Differences between the two groups were assessed using the Student t-test and the chi-square test.RESULTSEleven patients (10 men, 1 woman) were included in the study. All patients showed transient postoperative motor deficits because of SMA syndrome. Tractography data revealed NFidx from the contralateral SMA to the ipsilateral primary motor area via the corpus callosum. The mean tumor volume (early 27.87 vs late 50.91 cm3, p = 0.028) and mean NFidx (early 8923.16 vs late 4726.4, p = 0.002) were significantly different between the two groups. Fisher exact test showed a significant difference in the days of recovery from SMA syndrome between patients with an NFidx > 8000 and those with an NFidx < 8000.CONCLUSIONSDiffusion tensor imaging tractography may be useful for predicting the speed of recovery from SMA syndrome. To the authors’ knowledge, this is the first DTT study to identify interhemispheric connectivity of the SMA in patients with brain tumors.

scholarly journals Models of tendon development and injury

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Sophia K. Theodossiou ◽  
Nathan R. Schiele
Keyword(s):  
Computational Models ◽  
Ex Vivo ◽  
Current Model ◽  
Stem Cell Differentiation ◽  
Tendon Injury ◽  
Model Systems ◽  
Tendon Development ◽  
Key Aspects

AbstractTendons link muscle to bone and transfer forces necessary for normal movement. Tendon injuries can be debilitating and their intrinsic healing potential is limited. These challenges have motivated the development of model systems to study the factors that regulate tendon formation and tendon injury. Recent advances in understanding of embryonic and postnatal tendon formation have inspired approaches that aimed to mimic key aspects of tendon development. Model systems have also been developed to explore factors that regulate tendon injury and healing. We highlight current model systems that explore developmentally inspired cellular, mechanical, and biochemical factors in tendon formation and tenogenic stem cell differentiation. Next, we discuss in vivo, in vitro, ex vivo, and computational models of tendon injury that examine how mechanical loading and biochemical factors contribute to tendon pathologies and healing. These tendon development and injury models show promise for identifying the factors guiding tendon formation and tendon pathologies, and will ultimately improve regenerative tissue engineering strategies and clinical outcomes.

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