The thalamo-cortico-thalamic loop was investigated in adult rats exposed to ethanol during the last week of fetal life. Animals underwent either cortical or thalamic injections of lectin-conjugated horseradish peroxidase. Results demonstrate that prenatal exposure to ethanol causes permanent changes in the thalamocortical circuits. Alterations of thalamo-cortical and cortico-thalamic projections are concentrated at the level of axon terminal fields. The most severe thalamic damage is observed in the anterior intralaminar and midline nuclei; crossed cortico-thalamic projections also appear to be severely impaired. In the cortex, the damage to thalamic terminals displays a medio-lateral gradient of increasing severity through sensori-motor areas, with the lateral fields more impaired. Cells of origin of thalamo-cortical and cortico-thalamic projections are less affected by prenatal ethanol exposure: in the thalamus and layer 5 of sensori-motor cortex labeled cells exhibit normal values of areal numeric density. Conversely, cortico-thalamic neurons of layer 6, especially in the lateral agranular sensori-motor field, display smaller values of areal density than those of normal animals. Possible mechanisms underlying the establishment of these abnormalities are discussed.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/BF00215293 | DOI Listing |
Nat Commun
February 2024
Center for Neural Informatics, Krasnow Institute for Advanced Studies and Bioengineering Department, College of Engineering & Computing, George Mason University, Fairfax, VA, USA.
We present a quantitative strategy to identify all projection neuron types from a given region with statistically different patterns of anatomical targeting. We first validate the technique with mouse primary motor cortex layer 6 data, yielding two clusters consistent with cortico-thalamic and intra-telencephalic neurons. We next analyze the presubiculum, a less-explored region, identifying five classes of projecting neurons with unique patterns of divergence, convergence, and specificity.
View Article and Find Full Text PDFAging Cell
February 2024
The Jackson Laboratory, Bar Harbor, Maine, USA.
The disconnection of neuronal circuitry through synaptic loss is presumed to be a major driver of age-related cognitive decline. Age-related cognitive decline is heterogeneous, yet whether genetic mechanisms differentiate successful from unsuccessful cognitive decline through maintenance or vulnerability of synaptic connections remains unknown. Previous work using rodent and primate models leveraged various techniques to imply that age-related synaptic loss is widespread on pyramidal cells in prefrontal cortex (PFC) circuits but absent on those in area CA1 of the hippocampus.
View Article and Find Full Text PDFCell Rep
December 2023
Department of Neurosurgery, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China; Frontier Science Center of Immunology and Metabolism, Wuhan University, Wuhan 430071, China. Electronic address:
Appropriate histone modifications emerge as essential cell fate regulators of neuronal identities across neocortical areas and layers. Here we showed that NSD1, the methyltransferase for di-methylated lysine 36 of histone H3 (H3K36me2), controls both area and layer identities of the neocortex. Nsd1-ablated neocortex showed an area shift of all four primary functional regions and aberrant wiring of cortico-thalamic-cortical projections.
View Article and Find Full Text PDFbioRxiv
October 2024
Department of Neurobiology, Duke University, Durham, NC 27710, USA.
bioRxiv
August 2023
The Jackson Laboratory, Bar Harbor, ME 04609, USA.
The disconnection of neuronal circuits through synaptic loss is presumed to be a major driver of age-related cognitive decline. Age-related cognitive decline is heterogeneous, yet whether genetic mechanisms differentiate successful from unsuccessful cognitive decline through synaptic structural mechanisms remains unknown. Previous work using rodent and primate models leveraged various techniques to suggest that age-related synaptic loss is widespread on pyramidal cells in prefrontal cortex (PFC) circuits but absent on those in area CA1 of the hippocampus.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!