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Ionic Mechanisms Involved in β3-Adrenoceptor-Mediated Augmentation of GABAergic Transmission Onto Pyramidal Neurons in Prefrontal Cortex.
J Neurochem
January 2025
School of Life Science, Nanchang University, Nanchang, China.
Activation of the brain-penetrant beta3-adrenergic receptor (Adrb3) is implicated in the treatment of depressive disorders. Enhancing GABAergic inputs from interneurons onto pyramidal cells of prefrontal cortex (PFC) represents a strategy for antidepressant therapies. Here, we probed the effects of the activation of Adrb3 on GABAergic transmission onto pyramidal neurons in the PFC using in vitro electrophysiology.
View Article and Find Full Text PDFDetection of Insulin in Insulin-Deficient Islets of Patients with Type 1 Diabetes.
Life (Basel)
January 2025
Laboratory of Nervous System Development, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution "Petrovsky National Research Centre of Surgery", Tsurupi Street, 3, 117418 Moscow, Russia.
Type 1 diabetes (T1D) is related to the autoimmune destruction of β-cells, leading to their almost complete absence in patients with longstanding T1D. However, endogenous insulin secretion persists in such patients as evidenced by the measurement of plasma C-peptide. Recently, a low level of insulin has been found in non-β islet cells of patients with longstanding T1D, indicating that other islet cell types may contribute to persistent insulin secretion.
View Article and Find Full Text PDFAlterations in Prefrontal Cortical Somatostatin Neurons in Schizophrenia: Evidence for Weaker Inhibition of Pyramidal Neuron Dendrites.
Biol Psychiatry
January 2025
Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pittsburgh; Department of Neuroscience, Dietrich School of Arts and Sciences, University of Pittsburgh; Center for the Neural Basis of Cognition, Carnegie Mellon University. Electronic address:
Background: Certain cognitive processes require inhibition provided by the somatostatin (SST) class of gamma-aminobutyric acid (GABA) neurons in the dorsolateral prefrontal cortex (DLPFC). This inhibition onto pyramidal neuron dendrites depends on both SST and GABA signaling. Although SST mRNA levels are lower in the DLPFC in schizophrenia, it is not known if SST neurons exhibit alterations in the capacity to synthesize GABA, principally via the 67-kilodalton isoform of glutamic acid decarboxylase (GAD67).
View Article and Find Full Text PDFMapping the cellular etiology of schizophrenia and complex brain phenotypes.
Nat Neurosci
January 2025
Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA.
Psychiatric disorders are multifactorial and effective treatments are lacking. Probable contributing factors to the challenges in therapeutic development include the complexity of the human brain and the high polygenicity of psychiatric disorders. Combining well-powered genome-wide and brain-wide genetics and transcriptomics analyses can deepen our understanding of the etiology of psychiatric disorders.
View Article and Find Full Text PDFAbsolute number of three populations of interneurons and all GABAergic synapses in the human hippocampus.
J Neurosci
January 2025
Laboratory of Cerebral Cortex Research, HUN-REN Institute of Experimental Medicine, Budapest, Hungary
The human hippocampus, essential for learning and memory, is implicated in numerous neurological and psychiatric disorders, each linked to specific neuronal subpopulations. Advancing our understanding of hippocampal function requires computational models grounded in precise quantitative neuronal data. While extensive data exist on the neuronal composition and synaptic architecture of the rodent hippocampus, analogous quantitative data for the human hippocampus remain very limited.
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