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Early researchers of radiocarbon levels in Southern Hemisphere tree rings identified a variable North-South hemispheric offset, necessitating construction of a separate radiocarbon calibration curve for the South. We present here SHCal20, a revised calibration curve from 0–55,000 cal BP, based upon SHCal13 and fortified by the addition of 14 new tree-ring data sets in the 2140–0, 3520–3453, 3608–3590 and 13,140–11,375 cal BP time intervals. We detail the statistical approaches used for curve construction and present recommendations for the use of the Northern Hemisphere curve (IntCal20), the Southern Hemisphere curve (SHCal20) and suggest where application of an equal mixture of the curves might be more appropriate. Using our Bayesian spline with errors-in-variables methodology, and based upon a comparison of Southern Hemisphere tree-ring data compared with contemporaneous Northern Hemisphere data, we estimate the mean Southern Hemisphere offset to be 36 ± 27 14C yrs older.

Deficits following stroke are classically attributed to focal damage, but recent evidence suggests a key role of distributed brain network disruption. We measured resting functional connectivity (FC), lesion topography, and behavior in multiple domains (attention, visual memory, verbal memory, language, motor, and visual) in a cohort of 132 stroke patients, and used machine-learning models to predict neurological impairment in individual subjects. We found that visual memory and verbal memory were better predicted by FC, whereas visual and motor impairments were better predicted by lesion topography. Attention and language deficits were well predicted by both. Next,we identified a general pattern of physiological network dysfunction consisting of decrease of interhemispheric integration and intrahemispheric segregation, which strongly related to behavioral impairment in multiple domains. Network-specific patterns of dysfunction predicted specific behavioral deficits, and loss of interhemispheric communication across a set of regions was associated with impairment across multiple behavioral domains. These results link key organizational features of brain networks to brain–behavior relationships in stroke.

The corpus callosum (CC) is the largest fiber tract in the human brain, allowing interhemispheric communication by connecting homologous areas of the two cerebral hemispheres. In adults, CC size shows a robust allometric relationship with brain size, with larger brains having larger callosa, but smaller brains having larger callosa relative to brain size. Such an allometric relationship has been shown in both males and females, with no significant difference between the sexes. But there is some evidence that there are alterations in these allometric relationships during development. However, it is currently not known whether there is sexual dimorphism in these allometric relationships from birth, or if it only develops later. We study this in neonate data. Our results indicate that there are already sex differences in these allometric relationships in neonates: male neonates show the adult‐like allometric relationship between CC size and brain size; however female neonates show a significantly more positive allometry between CC size and brain size than either male neonates or female adults. The underlying cause of this sexual dimorphism is unclear; but the existence of this sexual dimorphism in neonates suggests that sex‐differences in lateralization have prenatal origins. In adults, corpus callosum (CC) size shows a robust allometric relationship with brain size, with larger brains having larger callosa, but smaller brains having larger callosa relative to brain size. Such an allometric relationship has been shown in both males and females, with no significant difference between the sexes. But there is some evidence that there are alterations in these allometric relationships during development. Our results indicate that there are already sex differences in these allometric relationships in neonates: male neonates show the adult‐like allometric relationship between CC size and brain size; however, female neonates show a significantly more positive allometry between CC size and brain size than either male neonates or female adults.

Background Interhemispheric communication of olfactory information is crucial for accurate odor perception and odor source localization in animals. However, the underlying structural basis for this communication in mammals remains poorly understood. Using electrophysiological recordings and virus-mediated tracing, we systematically dissected the neural circuits involved in interhemispheric transmission between the bilateral olfactory bulbs (OBs). Results We identified the anterior olfactory nucleus (AON) as a central hub that facilitates direct communication between the OBs via three distinct pathways: the excitatory inter-bulbar pathway, the inhibitory inter-bulbar pathway, and the bi-bulbar co-innervation pathway. Notably, our results highlight the differential roles of AON subregions in these pathways: the pars externa (AONpE) primarily mediates the inhibitory pathway, while the pars principalis (AONpP) participates in all three pathways. These pathways recruit CaMKIIα-positive neurons in specific AON regions, which in turn project to distinct neuronal populations within the OBs.  Conclusions This study provides novel anatomical insights into the neural circuits underlying interhemispheric olfactory communication. The differential connectivity patterns of AON subregions contribute to a better understanding of how bilateral olfactory information is processed and transferred between the two OBs.

Autism spectrum disorders (ASDs) represent a formidable challenge for psychiatry and neuroscience because of their high prevalence, lifelong nature, complexity and substantial heterogeneity. Facing these obstacles requires large-scale multidisciplinary efforts. Although the field of genetics has pioneered data sharing for these reasons, neuroimaging had not kept pace. In response, we introduce the Autism Brain Imaging Data Exchange (ABIDE)—a grassroots consortium aggregating and openly sharing 1112 existing resting-state functional magnetic resonance imaging (R-fMRI) data sets with corresponding structural MRI and phenotypic information from 539 individuals with ASDs and 573 age-matched typical controls (TCs; 7–64 years) (http://fcon_1000.projects.nitrc.org/indi/abide/). Here, we present this resource and demonstrate its suitability for advancing knowledge of ASD neurobiology based on analyses of 360 male subjects with ASDs and 403 male age-matched TCs. We focused on whole-brain intrinsic functional connectivity and also survey a range of voxel-wise measures of intrinsic functional brain architecture. Whole-brain analyses reconciled seemingly disparate themes of both hypo- and hyperconnectivity in the ASD literature; both were detected, although hypoconnectivity dominated, particularly for corticocortical and interhemispheric functional connectivity. Exploratory analyses using an array of regional metrics of intrinsic brain function converged on common loci of dysfunction in ASDs (mid- and posterior insula and posterior cingulate cortex), and highlighted less commonly explored regions such as the thalamus. The survey of the ABIDE R-fMRI data sets provides unprecedented demonstrations of both replication and novel discovery. By pooling multiple international data sets, ABIDE is expected to accelerate the pace of discovery setting the stage for the next generation of ASD studies.

BackgroundMultiple sclerosis is a neurodegenerative disease that damages the myelin sheath within the central nervous system. Axonal demyelination, particularly in the corpus callosum, impacts communication between the brain’s hemispheres in persons with multiple sclerosis (PwMS). Changes in interhemispheric communication may impair gait coordination which is modulated by communication across the corpus callosum to excite and inhibit specific muscle groups. To further evaluate the functional role of interhemispheric communication in gait and mobility, this study assessed the ipsilateral silent period (iSP), an indirect marker of interhemispheric inhibition and how it relates to gait adaptation in PwMS.MethodsUsing transcranial magnetic stimulation (TMS), we assessed interhemispheric inhibition differences between the more affected and less affected hemisphere in the primary motor cortices in 29 PwMS. In addition, these same PwMS underwent a split-belt treadmill walking paradigm, with the faster paced belt moving under their more affected limb. Step length asymmetry (SLA) was the primary outcome measure used to assess gait adaptability during split-belt treadmill walking. We hypothesized that PwMS would exhibit differences in iSP inhibitory metrics between the more affected and less affected hemispheres and that increased interhemispheric inhibition would be associated with greater gait adaptability in PwMS.ResultsNo statistically significant differences in interhemispheric inhibition or conduction time were found between the more affected and less affected hemisphere. Furthermore, SLA aftereffect was negatively correlated with both average percent depth of silent period (dSP%AVE) (r = -0.40, p = 0.07) and max percent depth of silent period (dSP%MAX) r = -0.40, p = 0.07), indicating that reduced interhemispheric inhibition was associated with greater gait adaptability in PwMS.ConclusionThe lack of differences between the more affected and less affected hemisphere indicates that PwMS have similar interhemispheric inhibitory capacity irrespective of the more affected hemisphere. Additionally, we identified a moderate correlation between reduced interhemispheric inhibition and greater gait adaptability. These findings may indicate that interhemispheric inhibition may in part influence responsiveness to motor adaptation paradigms and the need for further research evaluating the neural mechanisms underlying the relationship between interhemispheric inhibition and motor adaptability.

Background Transcranial magnetic stimulation (TMS) has attracted plenty of attention as it has been proved to be effective in facilitating motor recovery in patients with stroke. The aim of this study was to systematically review the effects of repetitive TMS (rTMS) and theta burst stimulation (TBS) protocols in modulating cortical excitability after stroke. Methods A literature search was carried out using PubMed, Medline, EMBASE, CINAHL, and PEDro, to identify studies that investigated the effects of four rTMS protocols—low and high frequency rTMS, intermittent and continuous TBS, on TMS measures of cortical excitability in stroke. A random-effects model was used for all meta-analyses. Results Sixty-one studies were included in the current review. Low frequency rTMS was effective in decreasing individuals’ resting motor threshold and increasing the motor-evoked potential of the non-stimulated M1 (affected M1), while opposite effects occurred in the stimulated M1 (unaffected M1). High frequency rTMS enhanced the cortical excitability of the affected M1 alone. Intermittent TBS also showed superior effects in rebalancing bilateral excitability through increasing and decreasing excitability within the affected and unaffected M1, respectively. Due to the limited number of studies found, the effects of continuous TBS remained inconclusive. Motor impairment was significantly correlated with various forms of TMS measures. Conclusions Except for continuous TBS, it is evident that these protocols are effective in modulating cortical excitability in stroke. Current evidence does support the effects of inhibitory stimulation in enhancing the cortical excitability of the affected M1.

The corpus callosum is the largest axonal tract in the human brain, connecting the left and right cortical hemipheres. This structure is affected in myriad human neurodevelopmental disorders, and can be entirely absent as a result of congenital or surgical causes. The age when callosal loss occurs, for example via surgical section in cases of refractory epilepsy, correlates with resulting brain morphology and neuropsychological outcomes, whereby an earlier loss generally produces relatively improved interhemispheric connectivity compared to a loss in adulthood (known as the “Sperry’s paradox”). However, the mechanisms behind these age-dependent differences remain unclear. Perhaps the best documented and most striking of the plastic changes that occur due to developmental, but not adult, callosal loss is the formation of large, bilateral, longitudinal ectopic tracts termed Probst bundles. Despite over 100 years of research into these ectopic tracts, which are the largest and best described stereotypical ectopic brain tracts in humans, much remains unclear about them. Here, we review the anatomy of the Probst bundles, along with evidence for their faciliatory or detrimental function, the required conditions for their formation, patterns of etiology, and mechanisms of development. We provide hypotheses for many of the remaining mysteries of the Probst bundles, including their possible relationship to preserved interhemispheric communication following corpus callosum absence. Future research into naturally occurring plastic tracts such as Probst bundles will help to inform the general rules governing axon plasticity and disorders of brain miswiring.

[This corrects the article DOI: 10.3389/fnins.2024.1424746.].

Transcallosal projections within the corpus callosum allow for the transfer of information between bilateral primary motor cortices (M1). Interhemispheric inhibition (IHI) is one approach to probe transcallosal communication using transcranial magnetic stimulation (TMS) whereby the motor evoked potential (MEP) elicited by TMS is reduced in amplitude when preceded by a conditioning TMS pulse delivered to the opposite M1. In a double-blinded, placebo-controlled study, 24 participants received 2.5 mg of lorazepam (GABA agonist), 50 mg of baclofen (GABA agonist) and a placebo in separate sessions. Short-interval interhemispheric inhibition (SIHI) and long-interval interhemispheric inhibition (LIHI) recorded from the first dorsal interosseous muscle were quantified before and at peak plasma concentration following drug ingestion. Baclofen significantly reduced SIHI and LIHI while lorazepam had no effect. These findings advance our understanding of the pharmacological basis of transcallosal inhibition in humans.