Initial anatomical and physiological studies suggested that sensory information relayed from the periphery by the thalamus is serially processed in primary sensory cortical areas. It is thought to propagate from layer 4 (L4) up to L2/3 and down to L5, which constitutes the main output of the cortex. However, more recent experiments point toward the existence of a direct processing of thalamic input by L5 neurons. Therefore, the role of L2/3 neurons in the sensory processing operated by L5 neurons is now highly debated. Using cell type-specific and reversible optogenetic manipulations in the somatosensory cortex of both anesthetized and awake mice, we demonstrate that L2/3 pyramidal neurons play a major role in amplifying sensory-evoked responses in L5 neurons. The amplification effect scales with the velocity of the sensory stimulus, indicating that L2/3 pyramidal neurons implement gain control in deep-layer neurons.
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http://dx.doi.org/10.1016/j.celrep.2018.08.038 | DOI Listing |
Psychedelic Med (New Rochelle)
December 2024
Departments of Anesthesiology and Critical Care, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Introduction: Psychedelic-induced experiences are thought to play an important role in the therapeutic actions of rapid-acting antidepressants. General anesthesia is one scenario in which patients can be rendered unconscious and masked to the psychedelic treatment, providing a simple yet effective method to examine drug-induced changes in the brain devoid of experiences.
Methods: Chronically stressed adult C57/BL6 male mice were given subhypnotic ketamine alone or ketamine and GABAergic anesthetic isoflurane at sedative (0.
Heliyon
December 2024
Guangdong Institute of Intelligence Science and Technology, Hengqin, Zhuhai, 519031, Guangdong, China.
Introduction: Transcranial electrical stimulation (tES), including transcranial alternating current stimulation (tACS) and transcranial direct current stimulation (tDCS), is widely studied for its potential to modulate brain oscillations and connectivity, offering treatment options for neurological disorders like Alzheimer's, Parkinson's, and insomnia. In this study, we focus on investigating the efficacy of tACS and tDCS in entraining intrinsic cortical network oscillations through a computational model.
Materials And Methods: We developed a 2D computational cortical neuron model with 2000 neurons (1600 pyramidal and 400 inhibitory), based on the Izhikevich neuron model.
J Cell Biol
February 2025
Department of Cell Biology, Harvard Medical School, Boston, MA, USA.
Endocytosis, required for the uptake of receptors and their ligands, can also introduce pathological aggregates such as α-synuclein (α-syn) in Parkinson's Disease. We show here the unexpected presence of intrinsically perforated endolysosomes in neurons, suggesting involvement in the genesis of toxic α-syn aggregates induced by internalized preformed fibrils (PFFs). Aggregation of endogenous α-syn in late endosomes and lysosomes of human iPSC-derived neurons (iNs), seeded by internalized α-syn PFFs, caused the death of the iNs but not of the parental iPSCs and non-neuronal cells.
View Article and Find Full Text PDFCan the transcriptomic profile of a neuron predict its physiological properties? Using a Patch-seq dataset of the primary visual cortex, we addressed this question by focusing on spike rate adaptation (SRA), a well-known phenomenon that depends on small conductance calcium (Ca)-dependent potassium (SK) channels. We first show that in parvalbumin-expressing (PV) and somatostatin-expressing (SST) interneurons (INs), expression levels of genes encoding the ion channels underlying action potential generation are correlated with the half-width (HW) of spikes. Surprisingly, the SK encoding gene is not correlated with the degree of SRA (dAdap).
View Article and Find Full Text PDFFront Neural Circuits
December 2024
Department of Physiology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Functional recovery from brain damage, such as stroke, is a plastic process in the brain. The excitatory glutamate -amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) plays a crucial role in neuronal functions, and the synaptic trafficking of AMPAR is a fundamental mechanism underlying synaptic plasticity. We recently identified a collapsin response mediator protein 2 (CRMP2)-binding compound, edonerpic maleate, which augments rehabilitative training-dependent functional recovery from brain damage by facilitating experience-driven synaptic delivery of AMPARs.
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