ArticleBritish journal of pharmacology2005
Desensitization of neuronal nicotinic receptors of human neuroblastoma SH-SY5Y cells during short or long exposure to nicotine.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- The Effect of the Anticonvulsant Topiramate on Acetylcholine-Induced Calcium Signals is Linked to Sirt-1 Activity.The European journal of neuroscience · 2026Article
- Drug Discovery Targeting Nicotinic Acetylcholine Receptors for Hearing Loss.International journal of molecular sciences · 2026Review
- Nicotine induces morphological and functional changes in astrocytes via nicotinic receptor activity.Glia · 2021Article
- Considerations for the Use of SH-SY5Y Neuroblastoma Cells in Neurobiology.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The Influence of Nicotine on Lung Tumor Growth, Cancer Chemotherapy, and Chemotherapy-Induced Peripheral Neuropathy.The Journal of pharmacology and experimental therapeutics · 2018Review
- Nicotinic receptor activation contrasts pathophysiological bursting and neurodegeneration evoked by glutamate uptake block on rat hypoglossal motoneurons.The Journal of physiology · 2016Article
- From the Cover: Prenatal Nicotinic Exposure Attenuates Respiratory Chemoreflexes Associated With Downregulation of Tyrosine Hydroxylase and Neurokinin 1 Receptor in Rat Pup Carotid Body.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Considerations for the use of SH-SY5Y neuroblastoma cells in neurobiology.Methods in molecular biology (Clifton, N.J.) · 2013Article
- A single administration of low-dose varenicline saturates α4β2* nicotinic acetylcholine receptors in the human brain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Increased nicotinic receptor desensitization in hypoglossal motor neurons following chronic developmental nicotine exposure.Journal of neurophysiology · 2012Article
- Alpha 7 nicotinic acetylcholine receptor expression and activity during neuronal differentiation of PC12 pheochromocytoma cells.Journal of molecular neuroscience : MN · 2010Article
- Cholinergic receptor pathways involved in apoptosis, cell proliferation and neuronal differentiation.Cell communication and signaling : CCS · 2009Article
- Cholinergic interneurons control the excitatory input to the striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal nicotinic ACh receptors (nAChRs) readily desensitize in the presence of an agonist. However, when the agonist is applied for minutes, hours or days, it is unclear how extensive desensitization is, how long it persists after agonist removal and whether nAChRs consequently change their pharmacological properties. These issues were explored with electrophysiological studies of native receptors of voltage-clamped human neuroblastoma SH-SY5Y cells. Puffer pulses of nicotine (1 mM)-evoked inward currents partly antagonized by methyllycaconitine (MLA; 10 nM) or alpha-conotoxin MII (MII; 10 nM), suggesting contribution by alpha7 and alpha3 subunit containing receptors, respectively. Nicotine-evoked currents desensitized with 150 ms time constant and fully recovered after a few s washout. Although the current induced by 10 min application of nicotine (10 microM) decayed to baseline indicating complete desensitization, puffer applications of maximally effective doses of nicotine still generated small responses (22% of control). Similar responses to puffer-applied nicotine were observed when nicotine was chronically incubated for 8 or 48 h. On nicotine washout, cells recovered their response amplitude within 5 min and then increased it (about 50% of untreated controls) after 30 min without altering response kinetics or sensitivity to MLA and MII. The present results suggest that native nAChRs of SH-SY5Y cells preserved a degree of responsiveness during chronic application of nicotine, and that they rapidly recovered on washout to generate larger responses without changes in kinetics or pharmacology. These data indicate strong compensatory mechanisms to retain nicotinic receptor function during long-term exposure to nicotine.
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