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Direction-selective ganglion cells (DSGCs) are tuned to motion in one direction. Starburst amacrine cells (SACs) are thought to mediate this direction selectivity through precise anatomical wiring to DSGCs. Nevertheless, we previously found that visual adaptation can reverse DSGCs's directional tuning, overcoming the circuit anatomy. Here we explore the role of SACs in the generation and adaptation of direction selectivity. First, using pharmacogenetics and two-photon calcium imaging, we validate that SACs are necessary for direction selectivity. Next, we demonstrate that exposure to an adaptive stimulus dramatically alters SACs' synaptic inputs. Specifically, after visual adaptation, On-SACs lose their excitatory input during light onset but gain an excitatory input during light offset. Our data suggest that visual stimulation alters the interactions between rod- and cone-mediated inputs that converge on the terminals of On-cone BCs. These results demonstrate how the sensory environment can modify computations performed by anatomically defined neuronal circuits.
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http://dx.doi.org/10.1016/j.neuron.2014.07.037 | DOI Listing |
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 PDFPLoS Comput Biol
September 2025
Faculty of Science, Cognitive and Systems Neuroscience Group, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, the Netherlands.
Predictive coding (PC) proposes that our brains work as an inference machine, generating an internal model of the world and minimizing predictions errors (i.e., differences between external sensory evidence and internal prediction signals).
View Article and Find Full Text PDFJ Neurosci
September 2025
Lendület Laboratory of Thalamus Research, HUN-REN Institute of Experimental Medicine; Budapest, Hungary
The paraventricular thalamic nucleus (PVT) integrates subcortical signals related to arousal, stress, addiction, and anxiety with top-down cortical influences. Increases or decreases in PVT activity exert profound, long-lasting effects on behavior related to motivation, addiction and homeostasis. Yet the sources of its subcortical excitatory and inhibitory afferents, their distribution within the PVT, and their integration with layer-specific cortical inputs remain unclear.
View Article and Find Full Text PDFJ Neurochem
September 2025
Department of Biology and Biotechnologies "Charles Darwin", Sapienza University of Rome, Rome, Italy.
Patients with Duchenne muscular dystrophy (DMD) may experience neurobehavioral and cognitive concerns, including psychiatric symptoms, due to the absence of full-length dystrophin (Dp427), frequently accompanied by deficiencies in shorter isoforms. The lack of dystrophin affects neurophysiological processes from the uterine phase, impacting neural circuitry in brain regions such as the prefrontal cortex, hippocampus, and cerebellum. This leads to reduced inhibitory GABAergic transmission and altered hippocampal glutamatergic signaling.
View Article and Find Full Text PDFStudy Objectives: Brief sleep loss alters cognition and the activity and synaptic structures of both principal neurons and interneurons in hippocampus. However, although sleep-dependent coordination of activity between hippocampus and neocortex is essential for memory consolidation, much less is known about how sleep loss affects neocortical input to hippocampus, or excitatory-inhibitory balance within neocortical structures. We aimed to test how the synaptic structures of SST+ interneurons in lateral and medial entorhinal cortex (LEC and MEC), which are the major neocortical input to hippocampus, are affected by brief sleep disruption in the hours following learning.
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