ReviewBiochemical pharmacology2007
Role of endogenous nicotinic signaling in guiding neuronal development.
Review in Biochemical pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed.
- Review
- Interacting withActa pharmaceutica Sinica. B · 2020Article
- Acute sleep deprivation during pregnancy in rats: Rapid elevation of placental and fetal inflammation and kynurenic acid.Neurobiology of stress · 2020Article
- Distribution of α7 Nicotinic Acetylcholine Receptor Subunit mRNA in the Developing Mouse.Frontiers in neuroanatomy · 2019Article
- [β2-nicotinic acetylcholine receptor promotes development of GABANan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- Differential Effects of Nicotine Exposure on the Hippocampus Across Lifespan.Current neuropharmacology · 2018Review
- Neuronal and Extraneuronal Nicotinic Acetylcholine Receptors.Current neuropharmacology · 2018Review
- Perinatal nicotine exposure impairs the maturation of glutamatergic inputs in the auditory brainstem.The Journal of physiology · 2017Article
- A Drosophila model for developmental nicotine exposure.PloS one · 2017Article
- Early postnatal nicotine exposure disrupts the α2* nicotinic acetylcholine receptor-mediated control of oriens-lacunosum moleculare cells during adolescence in rats.Neuropharmacology · 2016Article
- Changes in Nicotinic Neurotransmission during Enteric Nervous System Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Early postnatal nicotine exposure causes hippocampus-dependent memory impairments in adolescent mice: Association with altered nicotinic cholinergic modulation of LTP, but not impaired LTP.Neurobiology of learning and memory · 2015Article
- Research tool: Validation of floxed α7 nicotinic acetylcholine receptor conditional knockout mice using in vitro and in vivo approaches.The Journal of physiology · 2014Article
- Neuronal AChE splice variants and their non-hydrolytic functions: redefining a target of AChE inhibitors?British journal of pharmacology · 2013Review
- Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior.Neuron · 2012Review
- Sticking out of the crowd: the molecular identity and development of cholecystokinin-containing basket cells.The Journal of physiology · 2012Review
- Chronic neonatal nicotine exposure increases excitation in the young adult rat hippocampus in a sex-dependent manner.Brain research · 2012Article
- Prenatal nicotine exposure increases GABA signaling and mucin expression in airway epithelium.American journal of respiratory cell and molecular biology · 2011Article
- Alpha 7 nicotinic acetylcholine receptor expression and activity during neuronal differentiation of PC12 pheochromocytoma cells.Journal of molecular neuroscience : MN · 2010Article
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Spontaneous nicotinic cholinergic activity is widespread in the developing nervous system. One of the major components mediating this activity is the nicotinic acetylcholine receptor with alpha7 subunits (alpha7-nAChR) and high relative calcium permeability. We recently reported that alpha7-nAChRs co-localize in part with GABA(A) receptors during development, and the sites become co-innervated by cholinergic and GABAergic terminals. Patch-clamp recording either from embryonic chick ciliary ganglion neurons or from early postnatal mouse hippocampal interneurons reveals that alpha7-nAChR activation can impose a rapid and reversible decrease in GABA(A) receptor responses. The effect extends to GABAergic synaptic currents, and depends on intracellular calcium, calcium/calmodulin-dependent protein kinase II, and MAP kinase in the postsynaptic cell. Over the longer term, nicotinic activity has a more profound effect: it determines the time during development when GABAergic signaling converts from excitation to inhibition. It does this by changing the pattern of chloride transporters to establish the mature chloride gradient required for inhibitory GABAergic responses. The excitatory phase of GABAergic signaling is critical for proper development and integration of neurons into circuits. By driving the conversion of GABAergic signaling, nicotinic activity not only terminates one set of developmental instructions, but also initiates another by collaborating with GABAergic inhibition to impose new instructions. The results reveal a multi-layered pattern of activity-dependent controls in development and indicate the significance of nicotinic signaling in shaping these events.
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