
Neuron, Journal Year: 2019, Volume and Issue: 102(5), P. 960 - 975.e6
Published: April 23, 2019
Language: Английский
Neuron, Journal Year: 2019, Volume and Issue: 102(5), P. 960 - 975.e6
Published: April 23, 2019
Language: Английский
Nature Neuroscience, Journal Year: 2020, Volume and Issue: 24(1), P. 129 - 139
Published: Dec. 7, 2020
Language: Английский
Citations
126Journal of Neuroscience, Journal Year: 2017, Volume and Issue: 37(45), P. 10826 - 10834
Published: Nov. 8, 2017
A substantial portion of our sensory experience happens during active behaviors such as walking around or paying attention. How do systems work behaviors? Neural processing in can be shaped by behavior multiple ways ranging from a modulation responsiveness sharpening tuning to dynamic change response properties functional connectivity. Here, we review recent findings on the different systems: insect vision, rodent thalamus, and cortices. We discuss circuit-level mechanisms that might lead these modulations their potential role function. Finally, highlight open questions future perspectives this exciting new field.
Language: Английский
Citations
96eLife, Journal Year: 2019, Volume and Issue: 8
Published: July 8, 2019
Dravet Syndrome (DS) is a severe neurodevelopmental disorder caused by pathogenic loss of function variants in the gene SCN1A which encodes voltage gated sodium (Na+) channel subunit Nav1.1. GABAergic interneurons expressing parvalbumin (PV-INs) and somatostatin (SST-INs) exhibit impaired excitability DS (Scn1a+/-) mice. However, third major class - those vasoactive intestinal peptide (VIP-IN) -is unknown. We recorded VIP-INs brain slices from Scn1a+/-mice wild-type littermate controls found prominent impairment irregular spiking (IS), but not continuous adapting (CA) VIP-INs, Scn1a+/- Application Nav1.1-specific toxin Hm1a rescued observed deficits. The IS vs. CA firing pattern determined expression KCNQ channels; switched to tonic with both pharmacologic blockade M-current muscarinic acetylcholine receptor activation. These results show that express Nav1.1 are dysfunctional DS, may contribute pathogenesis.
Language: Английский
Citations
94Neuron, Journal Year: 2019, Volume and Issue: 102(6), P. 1223 - 1234.e4
Published: April 30, 2019
Language: Английский
Citations
91Neuron, Journal Year: 2018, Volume and Issue: 99(1), P. 98 - 116.e7
Published: June 21, 2018
Language: Английский
Citations
89Cell Reports, Journal Year: 2021, Volume and Issue: 34(8), P. 108774 - 108774
Published: Feb. 1, 2021
Extensive hierarchical yet highly reciprocal interactions among cortical areas are fundamental for information processing. However, connectivity rules governing the specificity of such corticocortical connections, and top-down feedback projections in particular, poorly understood. We analyze synaptic strength from functionally relevant brain to diverse neuronal types primary somatosensory cortex (S1). Long-range different preferentially engage specific sets GABAergic neurons S1. Projections other cortices strongly recruit parvalbumin (PV)-positive lead PV neuron-mediated feedforward inhibition pyramidal In contrast, inputs whisker-related motor biased vasoactive intestinal peptide (VIP)-positive potentially result VIP disinhibition. Regardless input areas, somatostatin-positive receive relatively weak long-range inputs. Computational analyses suggest that a characteristic combination IN S1 represents area.
Language: Английский
Citations
67Trends in Neurosciences, Journal Year: 2021, Volume and Issue: 44(8), P. 643 - 657
Published: May 15, 2021
Language: Английский
Citations
58eLife, Journal Year: 2022, Volume and Issue: 11
Published: Nov. 23, 2022
Neocortex is classically divided into distinct areas, each specializing in different function, but all could benefit from reinforcement feedback to inform and update local processing. Yet it remains elusive how global signals like reward punishment are represented cortical computations. Previously, we identified a neuron type, vasoactive intestinal polypeptide (VIP)-expressing interneurons, auditory cortex that recruited by behavioral reinforcers mediates disinhibitory control inhibiting other inhibitory neurons. As the same circuit present virtually throughout cortex, wondered whether VIP neurons likewise cortex. We monitored neural activity dozens of regions using three-dimensional random access two-photon microscopy fiber photometry while mice learned an discrimination task. found during initial learning produce rapid, cortex-wide activation most interneurons. This recruitment mode showed variations temporal dynamics individual across areas. Neither weak sensory tuning interneurons visual nor their arousal state modulation was fully predictive reinforcer responses. suggest response supports cell-type-specific mechanism which organism-level information about regulates processing plasticity.
Language: Английский
Citations
41Cell Reports, Journal Year: 2023, Volume and Issue: 42(6), P. 112628 - 112628
Published: June 1, 2023
Dravet syndrome (DS) is a severe neurodevelopmental disorder caused by loss-of-function variants in SCN1A, which encodes the voltage-gated sodium channel subunit Nav1.1. We recently showed that neocortical vasoactive intestinal peptide interneurons (VIP-INs) express Nav1.1 and are hypoexcitable DS (Scn1a+/−) mice. Here, we investigate VIP-IN function at circuit behavioral level performing vivo 2-photon calcium imaging awake wild-type (WT) Scn1a+/− pyramidal neuron activation during transition from quiet wakefulness to active running diminished mice, optogenetic of VIP-INs restores activity WT levels locomotion. selective Scn1a deletion reproduces core autism-spectrum-disorder-related behaviors addition cellular- circuit-level deficits function, but without epilepsy, sudden death, or avoidance seen global model. Hence, impaired vivo, may underlie non-seizure cognitive comorbidities DS.
Language: Английский
Citations
25Cell Reports, Journal Year: 2024, Volume and Issue: 43(2), P. 113718 - 113718
Published: Jan. 30, 2024
How mechanical allodynia following nerve injury is encoded in patterns of neural activity the spinal cord dorsal horn (DH) remains incompletely understood. We address this mice using spared model neuropathic pain and vivo electrophysiological recordings. Surprisingly, despite dramatic behavioral over-reactivity to stimuli injury, an overall increase sensitivity or reactivity DH neurons not observed. do, however, observe a marked decrease correlated firing patterns, including synchrony stimulus-evoked firing, across DH. Alterations temporal are recapitulated by silencing parvalbumin+ (PV+) interneurons, previously implicated allodynia, as allodynic pain-like behaviors. These findings reveal decorrelated network activity, driven alterations PV+ prominent feature suggest restoration proper potential therapeutic strategy treat chronic pain.
Language: Английский
Citations
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