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Dual effects of nicotine on dopamine neurons mediated by different nicotinic receptor subtypes.
Int J Neuropsychopharmacol. 2003 Mar; 6(1):1-11.IJ

Abstract

Burst firing of dopaminergic neurons has been found to represent a particularly effective means of increasing dopamine release in terminal areas as well as activating immediate early genes in dopaminoceptive cells. Spontaneous burst firing is largely controlled by the level of activation of NMDA receptors in the ventral tegmental area (VTA) as a consequence of glutamate released from afferents arising mainly in the prefrontal cortex. Nicotine has been found to effectively increase burst firing of dopaminergic cells. This effect of nicotine may be due to an alpha 7 nicotinic receptor-mediated presynaptic facilitation of glutamate release in the VTA. By the use of in-vivo single-cell recordings and immunohistochemistry we here evaluated the role of alpha 7 nicotinic receptors in nicotine-induced burst firing of dopamine cells in the VTA and the subsequent activation of immediate early genes in dopaminoceptive target areas. Nicotine (0.5 mg/kg s.c.) was found to increase firing rate and burst firing of dopaminergic neurons. In the presence of methyllycaconitine (MLA, 6.0 mg/kg i.p.) nicotine only increased firing rate. Moreover, in the presence of dihydro-beta-erythroidine (DH beta E, 1.0 mg/kg i.p.), an antagonist at non-alpha 7 nicotinic receptors, nicotine produced an increase in burst firing without increasing the firing rate. Nicotine also increased Fos-like immunoreactivity in dopamine target areas, an effect that was antagonized with MLA but not with DH beta E. Our data suggest that nicotine's augmenting effect on burst firing is, indeed, due to stimulation of alpha 7 nicotinic receptors whereas other nicotinic receptors seem to induce an increase in firing frequency.

Authors+Show Affiliations

Department of Physiology and Pharmacology, Section of Neuropsychopharmacology, Karolinska Institutet, 171 77 Stockholm, Sweden.No 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

12899731

Citation

Schilström, Björn, et al. "Dual Effects of Nicotine On Dopamine Neurons Mediated By Different Nicotinic Receptor Subtypes." The International Journal of Neuropsychopharmacology, vol. 6, no. 1, 2003, pp. 1-11.
Schilström B, Rawal N, Mameli-Engvall M, et al. Dual effects of nicotine on dopamine neurons mediated by different nicotinic receptor subtypes. Int J Neuropsychopharmacol. 2003;6(1):1-11.
Schilström, B., Rawal, N., Mameli-Engvall, M., Nomikos, G. G., & Svensson, T. H. (2003). Dual effects of nicotine on dopamine neurons mediated by different nicotinic receptor subtypes. The International Journal of Neuropsychopharmacology, 6(1), 1-11.
Schilström B, et al. Dual Effects of Nicotine On Dopamine Neurons Mediated By Different Nicotinic Receptor Subtypes. Int J Neuropsychopharmacol. 2003;6(1):1-11. PubMed PMID: 12899731.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dual effects of nicotine on dopamine neurons mediated by different nicotinic receptor subtypes. AU - Schilström,Björn, AU - Rawal,Nina, AU - Mameli-Engvall,Monica, AU - Nomikos,George G, AU - Svensson,Torgny H, PY - 2002/10/07/revised PY - 2003/8/6/pubmed PY - 2009/4/7/medline PY - 2003/8/6/entrez SP - 1 EP - 11 JF - The international journal of neuropsychopharmacology JO - Int. J. Neuropsychopharmacol. VL - 6 IS - 1 N2 - Burst firing of dopaminergic neurons has been found to represent a particularly effective means of increasing dopamine release in terminal areas as well as activating immediate early genes in dopaminoceptive cells. Spontaneous burst firing is largely controlled by the level of activation of NMDA receptors in the ventral tegmental area (VTA) as a consequence of glutamate released from afferents arising mainly in the prefrontal cortex. Nicotine has been found to effectively increase burst firing of dopaminergic cells. This effect of nicotine may be due to an alpha 7 nicotinic receptor-mediated presynaptic facilitation of glutamate release in the VTA. By the use of in-vivo single-cell recordings and immunohistochemistry we here evaluated the role of alpha 7 nicotinic receptors in nicotine-induced burst firing of dopamine cells in the VTA and the subsequent activation of immediate early genes in dopaminoceptive target areas. Nicotine (0.5 mg/kg s.c.) was found to increase firing rate and burst firing of dopaminergic neurons. In the presence of methyllycaconitine (MLA, 6.0 mg/kg i.p.) nicotine only increased firing rate. Moreover, in the presence of dihydro-beta-erythroidine (DH beta E, 1.0 mg/kg i.p.), an antagonist at non-alpha 7 nicotinic receptors, nicotine produced an increase in burst firing without increasing the firing rate. Nicotine also increased Fos-like immunoreactivity in dopamine target areas, an effect that was antagonized with MLA but not with DH beta E. Our data suggest that nicotine's augmenting effect on burst firing is, indeed, due to stimulation of alpha 7 nicotinic receptors whereas other nicotinic receptors seem to induce an increase in firing frequency. SN - 1469-5111 UR - https://www.unboundmedicine.com/medline/citation/12899731/Dual_effects_of_nicotine_on_dopamine_neurons_mediated_by_different_nicotinic_receptor_subtypes_ L2 - https://academic.oup.com/ijnp/article-lookup/doi/10.1017/S1461145702003188 DB - PRIME DP - Unbound Medicine ER -