ArticleSynapse (New York, N.Y.)2019
Nicotine excites VIP interneurons to disinhibit pyramidal neurons in auditory cortex.
Article in Synapse (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- Chronic nicotine reverses age-related decline of interneuron markers in mouse auditory cortex.Frontiers in aging neuroscience · 2026Article
- Nicotinic Modulation of Fast-Spiking Neurons in Rat Somatosensory Cortex across Development.eNeuro · 2025Article
- Delayed integration of somatostatin interneurons into visual circuits.Nature communications · 2025Article
- Article
- A disinhibitory microcircuit in the temporal association cortex for fear retrieval to pure tones.Scientific reports · 2025Article
- Expression of Neuronal Nicotinic Acetylcholine Receptor and Early Oxidative DNA Damage in Aging Rat Brain-The Effects of Memantine.International journal of molecular sciences · 2025Article
- Vasoactive intestinal peptide-expressing interneurons modulate the effect of behavioral state on cortical activity.Frontiers in cellular neuroscience · 2024Article
- VIP interneurons regulate cortical size tuning and visual perception.Cell reports · 2023Article
- Increased pyramidal and VIP neuronal excitability in rat primary auditory cortex directly correlates with tinnitus behaviour.The Journal of physiology · 2023Article
- Cognitive impairment in schizophrenia: aetiology, pathophysiology, and treatment.Molecular psychiatry · 2023Review
- VIP interneurons regulate cortical size tuning and visual perception.bioRxiv : the preprint server for biology · 2023Article
- A sleep-active basalocortical pathway crucial for generation and maintenance of chronic pain.Nature neuroscience · 2023Article
- Article
- Local and long-range GABAergic circuits in hippocampal area CA1 and their link to Alzheimer's disease.Frontiers in neural circuits · 2023Review
- Desensitizing nicotinic agents normalize tinnitus-related inhibitory dysfunction in the auditory cortex and ameliorate behavioral evidence of tinnitus.Frontiers in neuroscience · 2023Article
- ACh signaling modulates activity of the GABAergic signaling network in the basolateral amygdala and behavior in stress-relevant paradigms.Molecular psychiatry · 2022Article
- Highly unstable heterogeneous representations in VIP interneurons of the anterior cingulate cortex.Molecular psychiatry · 2022Article
- Article
- Cell-Type Specific Neuromodulation of Excitatory and Inhibitory NeuronsFrontiers in neural circuits · 2022Article
- Nicotine Enhances Amplitude and Consistency of Timing of Responses to Acoustic Trains in A1.Frontiers in neural circuits · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Nicotine activates nicotinic acetylcholine receptors and improves cognitive and sensory function, in part by its actions in cortical regions. Physiological studies show that nicotine amplifies stimulus-evoked responses in sensory cortex, potentially contributing to enhancement of sensory processing. However, the role of specific cell types and circuits in the nicotinic modulation of sensory cortex remains unclear. Here, we performed whole-cell recordings from pyramidal (Pyr) neurons and inhibitory interneurons expressing parvalbumin (PV), somatostatin (SOM), and vasoactive intestinal peptide (VIP) in mouse auditory cortex, in vitro. Bath application of nicotine strongly depolarized and excited VIP neurons, weakly depolarized Pyr neurons, and had no effect on the membrane potential of SOM or PV neurons. The use of receptor antagonists showed that nicotine's effects on VIP and Pyr neurons were direct and indirect, respectively. Nicotine also enhanced the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) in Pyr, VIP, and SOM, but not PV, cells. Using Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), we show that chemogenetic inhibition of VIP neurons prevents nicotine's effects on Pyr neurons. Since VIP cells preferentially contact other inhibitory interneurons, we suggest that nicotine drives VIP cell firing to disinhibit Pyr cell somata, potentially making Pyr cells more responsive to auditory stimuli. In parallel, activation of VIP cells also directly inhibits Pyr neurons, likely altering integration of other synaptic inputs. These cellular and synaptic mechanisms likely contribute to nicotine's beneficial effects on cognitive and sensory function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.