Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
The human amygdala paralaminar nucleus (PL) contains many immature excitatory neurons that undergo prolonged maturation from birth to adulthood. We describe a previously unidentified homologous PL region in mice that contains immature excitatory neurons and has previously been considered part of the amygdala intercalated cell clusters or ventral endopiriform cortex. Mouse PL neurons are born embryonically, not from postnatal neurogenesis, despite a subset retaining immature molecular and morphological features in adults. During juvenile-adolescent ages (P21-P35), the majority of PL neurons undergo molecular, structural, and physiological maturation, and a subset of excitatory PL neurons migrate into the adjacent endopiriform cortex. Alongside these changes, PL neurons develop responses to aversive and appetitive olfactory stimuli. The presence of this homologous region in both humans and mice points to the significance of this conserved mechanism of neuronal maturation and migration during adolescence, a key time period for amygdala circuit maturation and related behavioral changes.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10922384 | PMC |
| http://dx.doi.org/10.1016/j.neuron.2023.11.010 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
ABCA7 variants impact phosphatidylcholine and mitochondria in neurons.
Nature
September 2025
Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, USA.
Loss-of-function variants in the lipid transporter ABCA7 substantially increase the risk of Alzheimer's disease, yet how they impact cellular states to drive disease remains unclear. Here, using single-nucleus RNA-sequencing analysis of human brain samples, we identified widespread gene expression changes across multiple neural cell types associated with rare ABCA7 loss-of-function variants. Excitatory neurons, which expressed the highest levels of ABCA7, showed disrupted lipid metabolism, mitochondrial function, DNA repair and synaptic signalling pathways.
View Article and Find Full Text PDFGluN2A-NMDA receptor inhibition disinhibits the prefrontal cortex, reduces forced swim immobility, and impairs sensorimotor gating.
Acta Pharmacol Sin
September 2025
Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong-Hong Kong Joint Laboratory for Psychiatric Disorders, Guangdong Province Key Laboratory of Psychiatric Disorders, Guangdong Bas
Recent investigations into the rapid antidepressant effects of ketamine, along with studies on schizophrenia-related susceptibility genes, have highlighted the GluN2A subunit as a critical regulator of both emotion and cognition. However, the specific impacts of acute pharmacological inhibition of GluN2A-containing NMDA receptors on brain microcircuits and the subsequent behavioral consequences remain poorly understood. In this study, we first examined the effects of MPX-004, a selective GluN2A NMDA receptor inhibitor, on behavior within the dorsomedial prefrontal cortex (dmPFC).
View Article and Find Full Text PDFDentate granule cell capacitance is stable across the light-dark cycle.
eNeuro
September 2025
Department of Neurobiology and McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, AL35294 and.
The plasma membrane acts as a capacitor that plays a critical role in neuronal excitability and signal propagation. Neuronal capacitance is proportional to the area of the cell membrane, thus is often used as a measure of cell size that is assumed to be relatively stable. Recent work proposes that the capacitance of dentate granule cells and cortical pyramidal cells changes across the light-dark cycle in a manner that alters synaptic integration.
View Article and Find Full Text PDFExploring the potential pathogenesis of migraine using glutamatergic neuron models derived from induced pluripotent stem cells (iPSCs) of migraine patients.
Brain Res
September 2025
Department of Neurology, Shanghai Sixth People's Hospital, Shanghai 200233, China. Electronic address:
Migraine is a complex neurological disorder influenced by multiple genetic susceptibility factors, yet current animal models fail to fully recapitulate its human-specific pathophysiology. In this study, we explored the potential mechanisms underlying migraine by examining functional abnormalities and molecular dysregulation in glutamatergic neurons derived from induced pluripotent stem cells (iPSCs) of migraine patients. As key excitatory cells in the central nervous system, glutamatergic neurons are implicated in migraine through altered excitability, ion channel dysfunction, and dysregulation of nociceptive signaling molecules.
View Article and Find Full Text PDFExcitatory cortical neurons from CDKL5 deficiency disorder patient-derived organoids show early hyperexcitability not identified in neurogenin2 induced neurons.
Neurobiol Dis
September 2025
F.M. Kirby Neurobiology Department, Boston Children's Hospital, Boston, MA, USA; Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA; Human Neuron Core, Rosamund Stone Zander Translational Neuroscience Center, Boston Children's Hospital, Boston, MA, USA.
CDKL5 deficiency disorder (CDD) is a rare developmental and epileptic encephalopathy resulting from variants in cyclin-dependent kinase-like 5 (CDKL5) that lead to impaired kinase activity or loss of function. CDD is one of the most common genetic etiologies identified in epilepsy cohorts. To study how CDKL5 variants impact human neuronal activity, gene expression and morphology, CDD patient-derived induced pluripotent stem cells and their isogenic controls were differentiated into excitatory neurons using either an NGN2 induction protocol or a guided cortical organoid differentiation.
View Article and Find Full Text PDF