scholarly journals Chandelier Cartridge Density Is Reduced in the Prefrontal Cortex in Autism

2021 ◽  
Author(s):  
Sarwat Amina ◽  
Carmen Falcone ◽  
Tiffany Hong ◽  
Marisol Wendy Wolf-Ochoa ◽  
Gelareh Vakilzadeh ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Prefrontal Cortex ◽  
Protein Expression ◽  
Postnatal Development ◽  
Cell Number ◽  
Cortical Circuitry ◽  
Patient Cohort ◽  
Cell Somata

Abstract An alteration in the balance of excitation-inhibition has been proposed as a common characteristic of the cerebral cortex in autism, which may be due to an alteration in the number and/or function of the excitatory and/or inhibitory cells that form the cortical circuitry. We previously found a decreased number of the parvalbumin (PV)+ interneuron known as Chandelier (Ch) cell in the prefrontal cortex in autism. This decrease could result from a decreased number of Ch cells, but also from decreased PV protein expression by Ch cells. To further determine if Ch cell number is altered in autism, we quantified the number of Ch cells following a different approach and different patient cohort than in our previous studies. We quantified the number of Ch cell cartridges—rather than Ch cell somata—that expressed GAT1—rather than PV. Specifically, we quantified GAT1+ cartridges in prefrontal areas BA9, BA46, and BA47 of 11 cases with autism and 11 control cases. We found that the density of GAT1+ cartridges was decreased in autism in all areas and layers. Whether this alteration is cause or effect remains unclear but could result from alterations that take place during cortical prenatal and/or postnatal development.

Neuronal and glial cell number is altered in a cortical layer-specific manner in autism

Autism ◽  
2021 ◽  
pp. 136236132110144
Author(s):  
Carmen Falcone ◽  
Natalie-Ya Mevises ◽  
Tiffany Hong ◽  
Brett Dufour ◽  
Xiaohui Chen ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Cerebral Cortex ◽  
Prefrontal Cortex ◽  
Glial Cells ◽  
Cell Types ◽  
Cell Number ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Specific Cell ◽  
Human Brains

Autism spectrum disorder is a neurodevelopmental condition characterized by impaired social communication and repetitive behaviors. Changes in the number of specific cell types in the cerebral cortex could produce a dramatic alteration in the regulation of cortical circuits, and thus an alteration of behavior. We investigated whether there are layer-specific changes in the number of neurons, astrocytes, and oligodendrocytes in the prefrontal cortex in postmortem human brains from autism spectrum disorder subjects. We quantified the number of specific cell types in the prefrontal cortex (Brodmann areas 9, 46, and 47) of 10 cases with autism spectrum disorder and 10 age-matched control cases. We found that the number of neurons was increased and the number of astrocytes was decreased in layer II of all three prefrontal areas. Area BA47 was most widely affected presenting with an increased number of neurons and a decreased number of astrocytes in layer II and deeper layers of the cortex. Among other possibilities, the alterations in neuron and glial cell number we report here are consistent with a failure of radial glial cells to shift daughter cell production from neurons to astrocytes during prenatal cortical development in autism spectrum disorder. The data provided here are key anatomical findings that shed light on autism spectrum disorder pathogenesis. Lay abstract The cerebral cortex affected with autism spectrum disorder presents changes in the number of neurons and glia cells, possibly leading to a dysregulation of brain circuits and affecting behavior. However, little is known about cell number alteration in specific layers of the cortex in autism spectrum disorder. We found an increase in the number of neurons and a decrease in the number of astrocytes in specific layers of the prefrontal cortex in postmortem human brains from autism spectrum disorder cases. We hypothesize that this may be due to a failure in neural stem cells to shift differentiation from neurons to glial cells during prenatal brain development. These data provide key anatomical findings that contribute to the bases of autism spectrum disorder pathogenesis.

scholarly journals Postnatal development of synaptic structure proteins in pyramidal neuron axon initial segments in monkey prefrontal cortex

2009 ◽  
Vol 514 (4) ◽  
pp. 353-367 ◽  
Author(s):  
Dianne A. Cruz ◽  
Emily M. Lovallo ◽  
Steven Stockton ◽  
Matthew Rasband ◽  
David A. Lewis
Keyword(s):  
Prefrontal Cortex ◽  
Postnatal Development ◽  
Pyramidal Neuron ◽  
Synaptic Structure ◽  
Monkey Prefrontal Cortex ◽  
Axon Initial Segments

Expression of super cervical ganglion-10 (SCG-10) mRNA in the monkey cerebral cortex during postnatal development

2002 ◽  
Vol 323 (3) ◽  
pp. 199-202 ◽  
Author(s):  
Takao Oishi ◽  
Noriyuki Higo ◽  
Keiji Matsuda ◽  
Motoharu Hayashi
Keyword(s):  
Cerebral Cortex ◽  
Postnatal Development ◽  
Cervical Ganglion

Age-related and photoperiodic variation of the DAZ gene family in the testis of the Syrian hamster (Mesocricetus auratus)

Zygote ◽  
2018 ◽  
Vol 26 (2) ◽  
pp. 127-134 ◽  
Author(s):  
Candela Rocío González ◽  
Luciana Moverer ◽  
Ricardo Saúl Calandra ◽  
Silvia Inés González-Calvar ◽  
Alfredo Daniel Vitullo
Keyword(s):  
Protein Expression ◽  
Gene Family ◽  
Syrian Hamster ◽  
Mesocricetus Auratus ◽  
Cell Number ◽  
The Novel ◽  
Age Related ◽  
Mrna And Protein Expression ◽  
Long Photoperiod ◽  
Daz Gene

SummaryThe Deleted in AZoospermia (DAZ) gene family regulates the development, maturation and maintenance of germ cells and spermatogenesis in mammals. The DAZ family consists of two autosomal genes, Boule and Dazl (Daz-like), and the Daz gene on chromosome Y. The aim of this study was to analyze the localization of DAZL and BOULE during testicular ontogeny of the seasonal-breeding Syrian hamster, Mesocricetus auratus. We also evaluated the testicular expression of DAZ family genes under short- or long-photoperiod conditions. In the pre-pubertal and adult testis, DAZL protein was found mainly in spermatogonia. BOULE was found in the spermatogonia from 20 days of age and during the pre-pubertal and adult period it was also detected in spermatocytes and round spermatids. DAZL and BOULE expression in spermatogonia was strictly nuclear only in 20-day-old hamsters. We also detected the novel mRNA and protein expression of BOULE in Leydig cells. In adult hamsters, Dazl expression was increased in regressed testis compared with non-regressed testis and DAZL protein expression was restricted to primary spermatocytes in regressed testis. These results show that DAZL and BOULE are expressed in spermatogonia at early stages in the Syrian hamster, then both proteins translocate to the cytoplasm when meiosis starts. In the adult regressed testis, the absence of DAZL in spermatogonia might be related to the decrease in germ cell number, suggesting that DAZ gene family expression is involved in changes in seminiferous epithelium during photoregression.

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