ArticleNeurochemical research2008
Chronic nicotine alters nicotinic receptor-induced presynaptic Ca2+ responses in isolated nerve terminals.
Article in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 5 citations in OpenAlex.
- Targeting glutamate homeostasis for potential treatment of nicotine dependence.Brain research bulletin · 2016Review
- Impact of sustained exposure to β-amyloid on calcium homeostasis and neuronal integrity in model nerve cell system expressing α4β2 nicotinic acetylcholine receptors.The Journal of biological chemistry · 2013Article
- Defining pre-synaptic nicotinic receptors regulated by beta amyloid in mouse cortex and hippocampus with receptor null mutants.Journal of neurochemistry · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Brain nicotinic receptors display pronounced permeability for Ca2+ and localize to presynaptic nerve terminals, in addition to postsynaptic sites. Chronic exposure to nicotine has been shown to alter brain nicotinic receptor expression, but the functional consequences for presynaptic Ca2+ have not been directly examined. Here, we used confocal imaging to assess Ca2+ responses in individual nerve terminals from cortices of mice treated up to 14 days with nicotine as compared to vehicle-treated controls. Chronic nicotine treatment led to substantially enhanced amplitudes of presynaptic Ca2+ responses to acute application of nicotine at concentrations of 50 nM (2-fold) and 500 nM (1.7-fold), but not 50 microM. In addition, increased expression of high-affinity nicotinic receptors on isolated terminals was observed following chronic treatment, as determined immunocytochemically and pharmacologically. These findings suggest that chronic exposure to nicotine may lead to enhanced sensitivity to nicotine at select presynaptic sites in brain via up-regulation of high-affinity nicotinic receptors.
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Registered trials
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.