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Up-regulation of L-type voltage-dependent calcium channels after long term exposure to nicotine in cerebral cortical neurons.
J Biol Chem. 2002 Mar 08; 277(10):7979-88.JB

Abstract

Effects of long term (72-h) exposure to low concentration (0.1 mum) of nicotine on various types of voltage-dependent Ca(2+) channels (VDCCs) and neuronal nicotinic acetylcholine receptors (nnAChRs) were examined using primary cultures of mouse cerebral cortical neurons. High potassium (30 mm KCl)-stimulated (45)Ca(2+) influx into the neurons increased with increasing the duration of nicotine exposure and its concentrations. The maximal increase of the KCl-stimulated (45)Ca(2+) influx was found 24 h after the initiation of exposure and thereafter maintained up to 72 h. This enhancement of KCl-induced (45)Ca(2+) influx after 72-h exposure to 0.1 mum nicotine was completely abolished by concomitant exposure with mecamylamine, an inhibitor for nnAChRs. Only the component of the KCl-induced (45)Ca(2+) influx observed after long term exposure to nicotine, which was sensitive to nifedipine, an inhibitor of L-type VDCCs, was facilitated, while the (45)Ca(2+) influx through P/Q- and N-type VDCCs showed no changes. Moreover, enhanced immunoreactivity against antibody for the alpha(1C) subunit of L-type VDCCs was recognized, whereas no changes in immunoreactivities against antibodies for alpha(1A) and alpha(1B) subunits of other types of VDCCs were noted. In addition, a Western blot analysis showed an increase of immunoreactivities against antibodies for alpha(1D) and alpha(2)/delta(1), and expression of mRNA for L-type VDCC subunit, alpha(1F), was also enhanced, although beta(4) mRNA expression was not changed. Whole cell patch clamp analysis revealed that the increase of the amplitude of Ba(2+) currents was also recognized in the neurons exposed to nicotine, and nicardipine reduced this increased amplitude to the level of the amplitude detected in nontreated neurons with nicardipine. The up-regulation of alpha(4) and beta(2) subunits, but not the alpha(3) subunit of nnAChRs, was also noted after the nicotine exposure when examining by the Western blot analysis. Taken together, these results indicate that the long term exposure of the neurons to a low concentration of nicotine induces both increased (45)Ca(2+) influx through up-regulated L-type VDCCs and nnAChR up-regulation.

Authors+Show Affiliations

Department of Pharmacology, Kawasaki Medical School, Matsushima, Kurashiki 701-0192, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11756415

Citation

Katsura, Masashi, et al. "Up-regulation of L-type Voltage-dependent Calcium Channels After Long Term Exposure to Nicotine in Cerebral Cortical Neurons." The Journal of Biological Chemistry, vol. 277, no. 10, 2002, pp. 7979-88.
Katsura M, Mohri Y, Shuto K, et al. Up-regulation of L-type voltage-dependent calcium channels after long term exposure to nicotine in cerebral cortical neurons. J Biol Chem. 2002;277(10):7979-88.
Katsura, M., Mohri, Y., Shuto, K., Hai-Du, Y., Amano, T., Tsujimura, A., Sasa, M., & Ohkuma, S. (2002). Up-regulation of L-type voltage-dependent calcium channels after long term exposure to nicotine in cerebral cortical neurons. The Journal of Biological Chemistry, 277(10), 7979-88.
Katsura M, et al. Up-regulation of L-type Voltage-dependent Calcium Channels After Long Term Exposure to Nicotine in Cerebral Cortical Neurons. J Biol Chem. 2002 Mar 8;277(10):7979-88. PubMed PMID: 11756415.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Up-regulation of L-type voltage-dependent calcium channels after long term exposure to nicotine in cerebral cortical neurons. AU - Katsura,Masashi, AU - Mohri,Yutaka, AU - Shuto,Keijiro, AU - Hai-Du,Yan, AU - Amano,Taku, AU - Tsujimura,Atsushi, AU - Sasa,Masashi, AU - Ohkuma,Seitaro, Y1 - 2001/12/27/ PY - 2002/1/5/pubmed PY - 2002/4/16/medline PY - 2002/1/5/entrez SP - 7979 EP - 88 JF - The Journal of biological chemistry JO - J Biol Chem VL - 277 IS - 10 N2 - Effects of long term (72-h) exposure to low concentration (0.1 mum) of nicotine on various types of voltage-dependent Ca(2+) channels (VDCCs) and neuronal nicotinic acetylcholine receptors (nnAChRs) were examined using primary cultures of mouse cerebral cortical neurons. High potassium (30 mm KCl)-stimulated (45)Ca(2+) influx into the neurons increased with increasing the duration of nicotine exposure and its concentrations. The maximal increase of the KCl-stimulated (45)Ca(2+) influx was found 24 h after the initiation of exposure and thereafter maintained up to 72 h. This enhancement of KCl-induced (45)Ca(2+) influx after 72-h exposure to 0.1 mum nicotine was completely abolished by concomitant exposure with mecamylamine, an inhibitor for nnAChRs. Only the component of the KCl-induced (45)Ca(2+) influx observed after long term exposure to nicotine, which was sensitive to nifedipine, an inhibitor of L-type VDCCs, was facilitated, while the (45)Ca(2+) influx through P/Q- and N-type VDCCs showed no changes. Moreover, enhanced immunoreactivity against antibody for the alpha(1C) subunit of L-type VDCCs was recognized, whereas no changes in immunoreactivities against antibodies for alpha(1A) and alpha(1B) subunits of other types of VDCCs were noted. In addition, a Western blot analysis showed an increase of immunoreactivities against antibodies for alpha(1D) and alpha(2)/delta(1), and expression of mRNA for L-type VDCC subunit, alpha(1F), was also enhanced, although beta(4) mRNA expression was not changed. Whole cell patch clamp analysis revealed that the increase of the amplitude of Ba(2+) currents was also recognized in the neurons exposed to nicotine, and nicardipine reduced this increased amplitude to the level of the amplitude detected in nontreated neurons with nicardipine. The up-regulation of alpha(4) and beta(2) subunits, but not the alpha(3) subunit of nnAChRs, was also noted after the nicotine exposure when examining by the Western blot analysis. Taken together, these results indicate that the long term exposure of the neurons to a low concentration of nicotine induces both increased (45)Ca(2+) influx through up-regulated L-type VDCCs and nnAChR up-regulation. SN - 0021-9258 UR - https://www.unboundmedicine.com/medline/citation/11756415/Up_regulation_of_L_type_voltage_dependent_calcium_channels_after_long_term_exposure_to_nicotine_in_cerebral_cortical_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0021-9258(19)36391-4 DB - PRIME DP - Unbound Medicine ER -