Supernumerary neurons within the cerebral cortical subplate in autism spectrum disorders

Avino, Thomas A.; Hutsler, Jeffrey J.

doi:10.1016/j.brainres.2021.147350

Cited by 10 publications

(11 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Variations in the density of WMICs have been reported in specific psychiatric disorders and behavioral deficits (Kubo, 2020) such as schizophrenia (Akbarian et al, 1996;Connor et al, 2011;Fung et al, 2014), autism spectrum disorder (ASD) (Amaral et al, 2008;Avino & Hutsler, 2021;Bailey et al, 1998;Hutsler & Casanova, 2016), depression (Beasley et al, 2002), and Alzheimer's disease (Kowall & Beal, 1988). Despite the potential clinical aspects associated with changes to the WMICs, studies dealing with the total number, distribution, and density of WMICs in primates are limited.…”

Section: Introductionmentioning

confidence: 99%

The distribution, number, and certain neurochemical identities of infracortical white matter neurons in a chimpanzee (Pan troglodytes) brain

Swiegers

Bhagwandin

Williams

et al. 2021

J of Comparative Neurology

View full text Add to dashboard Cite

We examined the number, distribution, and immunoreactivity of the infracortical white matter neuronal population, also termed white matter interstitial cells (WMICs), throughout the telencephalic white matter of an adult female chimpanzee. Staining for neuronal nuclear marker (NeuN) revealed WMICs throughout the infracortical white matter, these cells being most numerous and dense close to the inner border of cortical layer VI, decreasing significantly in density with depth in the white matter. Stereological analysis of NeuN-immunopositive cells revealed an estimate of approximately 137.2 million WMICs within the infracortical white matter of the chimpanzee brain studied. Immunostaining revealed subpopulations of WMICs containing neuronal nitric oxide synthase (nNOS, approximately 14.4 million in number), calretinin (CR, approximately 16.7 million), very few WMICs containing parvalbumin (PV), and no calbindin-immunopositive neurons. The nNOS, CR, and PVimmunopositive WMICs, possibly all inhibitory neurons, represent approximately 22.6% of the total WMIC population. As the white matter is affected in many cognitive conditions, such as schizophrenia, autism, epilepsy, and also in neurodegenerative diseases, understanding these neurons across species is important for the translation of findings of neural dysfunction in animal models to humans. Furthermore, studies of WMICs in species such as apes provide a crucial phylogenetic context for understanding the evolution of these cell types in the human brain.

show abstract

Section: Introductionmentioning

confidence: 99%

The distribution, number, and certain neurochemical identities of infracortical white matter neurons in a chimpanzee (Pan troglodytes) brain

Swiegers

Bhagwandin

Williams

et al. 2021

J of Comparative Neurology

View full text Add to dashboard Cite

show abstract

“…SPNs outlived their normal lifespan in these cases, and in fact, surgical removal of these cortical malformations resulted in significant improvement in patients, suggesting SPNs are the epileptic focus (Luhmann et al, 2009 , 2018 ; Richter et al, 2016 ). Frozen human postmortem tissue samples showed a large average density of NeuN (a neuronal marker)-positive neurons in layer 6 of patients with autism spectrum disorder, with cell morphologies consistent with SPNs, suggesting an abnormal initial population or a partial failure of apoptosis in SPNs aids atypical neural development in these patients (Avino and Hutsler, 2021 ). Moreover, there is evidence that hypoxia that occurs in most preterm infants leads to higher rate of programmed cell death (Hargitai et al, 2001 ).…”

Section: Early Environmental Insult and Pathophysiology Of The Subpla...mentioning

confidence: 99%

Changing subplate circuits: Early activity dependent circuit plasticity

Mukherjee

2023

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Early neural activity in the developing sensory system comprises spontaneous bursts of patterned activity, which is fundamental for sculpting and refinement of immature cortical connections. The crude early connections that are initially refined by spontaneous activity, are further elaborated by sensory-driven activity from the periphery such that orderly and mature connections are established for the proper functioning of the cortices. Subplate neurons (SPNs) are one of the first-born mature neurons that are transiently present during early development, the period of heightened activity-dependent plasticity. SPNs are well integrated within the developing sensory cortices. Their structural and functional properties such as relative mature intrinsic membrane properties, heightened connectivity via chemical and electrical synapses, robust activation by neuromodulatory inputs—place them in an ideal position to serve as crucial elements in monitoring and regulating spontaneous endogenous network activity. Moreover, SPNs are the earliest substrates to receive early sensory-driven activity from the periphery and are involved in its modulation, amplification, and transmission before the maturation of the direct adult-like thalamocortical connectivity. Consequently, SPNs are vulnerable to sensory manipulations in the periphery. A broad range of early sensory deprivations alters SPN circuit organization and functions that might be associated with long term neurodevelopmental and psychiatric disorders. Here we provide a comprehensive overview of SPN function in activity-dependent development during early life and integrate recent findings on the impact of early sensory deprivation on SPNs that could eventually lead to neurodevelopmental disorders.

show abstract

“…27 Recent neuropathological studies suggested that the development of the cortical subplate is also altered since the frontal, temporal, and parietal cortices of adults with ASD contain an excess of subplate neurons, especially white matter interstitial neurons. 10,28,29 Neuroimaging studies in young children with high and low familial risk revealed that brain development in children with ASD is characterized by aberrant growth: early overgrowth is followed by regression. 30 This is best documented for the frontal, temporal, and cingulate cortices.…”

Section: What This Paper Addsmentioning

confidence: 99%

Section: Pathophysiology Of the Early Signs Of Asdmentioning

confidence: 99%

“… 10 These neurons play a role in finding the optimal balance between glutamatergic (excitatory) and GABAergic (inhibitory) neural activity, thus allowing for a modulation of the afferent input to the deep cortical layers. 10 Increasing evidence suggests that (1) in ASD altered subplate dissolution in the frontal, temporal, and parietal areas results in an excess of white matter interstitial neurons, 28 , 29 and (2) ASD is characterized by an altered glutamatergic–GABAergic balance. 65 , 66 Thus, the following sequence of events is conceivable.…”

Section: Pathophysiology Of the Early Signs Of Asdmentioning

confidence: 99%

See 1 more Smart Citation

Emerging signs of autism spectrum disorder in infancy: Putative neural substrate

Hadders‐Algra

2022

Develop Med Child Neuro

View full text Add to dashboard Cite

Autism spectrum disorder (ASD) is characterized by altered development of the social brain with prominent atypical features in the fronto‐temporo‐parietal cortex and cerebellum. Early signs of ASD emerge between 6 and 12 months: reduced social communication, slightly less advanced motor development, and repetitive behaviour. The fronto‐temporo‐parietal cortex and cerebellum play a prominent role in the development of social communication, whereas fronto‐parietal‐cerebellar networks are involved in the planning of movements, that is, movement selection. Atypical sensory responsivity, a core feature of ASD, may result in impaired development of social communication and motor skills and/or selection of atypical repetitive behaviour. In the first postnatal year, the brain areas involved are characterized by gradual dissolution of temporary structures: the fronto‐temporo‐parietal cortical subplate and cerebellar external granular layer. It is hypothesized that altered dissolution of the transient structures opens the window for the expression of early signs of ASD arising in the impaired developing permanent networks. What this paper adds The early social and motor signs of autism spectrum disorder emerge between the ages of 6 and 12 months. Altered dissolution of transient brain structures in the fronto‐temporo‐parietal cortex and cerebellum may underlie the emergence of these early signs.

show abstract

Supernumerary neurons within the cerebral cortical subplate in autism spectrum disorders

Cited by 10 publications

References 86 publications

The distribution, number, and certain neurochemical identities of infracortical white matter neurons in a chimpanzee (Pan troglodytes) brain

The distribution, number, and certain neurochemical identities of infracortical white matter neurons in a chimpanzee (Pan troglodytes) brain

Changing subplate circuits: Early activity dependent circuit plasticity

Emerging signs of autism spectrum disorder in infancy: Putative neural substrate

Contact Info

Product

Resources

About