Selective down-regulation of [125I]Y0-α-conotoxin MII binding in rat mesostriatal dopamine pathway following continuous infusion of nicotine

Mugnaini, Manolo; Garzotti, Marco; Sartori, Ilaria; Pilla, Maria; Repeto, Paolo; Heidbreder, Christian; Tessari, Michela

doi:10.1016/j.neuroscience.2005.09.008

Cited by 61 publications

(62 citation statements)

References 19 publications

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“…It increased the density of D3 receptors in Pro-cognitive effect of nicotine and hyperdopaminergia S Weiss et al WT mice, as already reported in rats (Le Foll et al, 2003), but had no effect on D3 density in DAT KO mice. In both WT and DAT KO mice, oral chronic nicotine treatment increased b2* nAChRs in line with previous results in control mice (for reviews, see Buisson and Bertrand, 2002;Gentry and Lukas, 2002) and decreased a6* nAChRs, as reported previously with autoradiographic labelings in control mouse or rat brain (Lai et al, 2005;Mugnaini et al, 2006), but in contrast with other data from labelings on particulate fractions of rat cerebral areas (Parker et al, 2004). Finally, such a treatment induced opposite variations of a7 nAChRs, which decreased in WT and increased in DAT KO mice.…”

Section: Modulation Of Daergic and Nicotinic Receptor Densities By Chsupporting

confidence: 90%

Nicotine Improves Cognitive Deficits of Dopamine Transporter Knockout Mice without Long-Term Tolerance

Weiss

Nosten‐Bertrand

McIntosh

et al. 2007

Neuropsychopharmacol

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Various studies suggest a dysfunction of nicotinic neurotransmission in schizophrenia and establish that patients suffering from schizophrenia and attention deficit hyperactivity disorder (ADHD) have a high tobacco consumption, potentially for the purpose of selfmedication. Owing to its neuroprotective and procognitive effects, transdermal nicotine was proposed to be an effective treatment of some neurodegenerative and psychiatric diseases. Mice deficient in the dopamine transporter (DAT KO) exhibit a phenotype reminiscent of schizophrenia and ADHD, including hyperdopaminergia, hyperactivity, paradoxical calming by methylphenidate and cognitive deficits, some of which being improved by antipsychotic agents. We recently demonstrated that nicotinic receptor content and function were profoundly modified in DAT KO mice. In this study, we assessed the effects of a chronic nicotine treatment in the drinking water on the nicotine-induced locomotion, anxiety status and learning performance. Chronically nicotine-treated DAT KO mice were always hypersensitive to the hypolocomotor effect of nicotine without tolerance and did not exhibit the anxiogenic effect of nicotine treatment observed in WT mice. Very interestingly, both acute and chronic nicotine treatments greatly improved their deficits in the cued and spatial learning, without eliciting tolerance. We speculate that the procognitive effects of nicotine in DAT KO mice are related to the upregulation of a7 nicotinic receptors in the hippocampus, amygdala, and prelimbic cortex, all areas involved in cognition. Data from our studies on DAT KO mice shed light on the nicotine self-medication in psychiatric patients and suggest that nicotinic agonists could favorably lead to additional therapy of psychiatric diseases.

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Section: Modulation Of Daergic and Nicotinic Receptor Densities By Chsupporting

confidence: 90%

Nicotine Improves Cognitive Deficits of Dopamine Transporter Knockout Mice without Long-Term Tolerance

Weiss

Nosten‐Bertrand

McIntosh

et al. 2007

Neuropsychopharmacol

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“…1C). This finding tallies well with the evidence of very high levels of CntxMII binding in the medial terminal nucleus of the accessory optic tract (MT) (Mugnaini et al, 2006). 6OHDA-induced DA neuron degeneration markedly decreased ␣4, ␤2, and ␤3 subunit levels and caused an almost complete loss of ␣2, ␣5, and ␣6 subunits (Fig.…”

Section: Nachr Subunits Expressed In Da Neurons Of Ventral Midbrainsupporting

confidence: 87%

Nicotinic Acetylcholine Receptors in the Mesolimbic Pathway: Primary Role of Ventral Tegmental Area α6β2* Receptors in Mediating Systemic Nicotine Effects on Dopamine Release, Locomotion, and Reinforcement

Gotti¹,

Guiducci²,

Tedesco³

et al. 2010

J. Neurosci.

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208

236

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␣6* nicotinic acetylcholine receptors (nAChRs) are highly and selectively expressed by mesostriatal dopamine (DA) neurons. These neurons are thought to mediate several behavioral effects of nicotine, including locomotion, habit learning, and reinforcement. Yet the functional role of ␣6* nAChRs in midbrain DA neurons is mostly unknown. The aim of this study was to determine the composition and in vivo functional role of ␣6* nAChR in mesolimbic DA neurons of male rats. Immunoprecipitation and immunopurification techniques coupled with cell-specific lesions showed that the composition of ␣6* nAChR in the mesostriatal system is heterogeneous, with (non-␣4)␣6␤2* being predominant in the mesolimbic pathway and ␣4␣6␤2* in the nigrostriatal pathway. We verified whether ␣6* receptors mediate the systemic effects of nicotine on the mesolimbic DA pathway by perfusing the selective antagonists ␣-conotoxin MII (CntxMII) (␣3/␣6␤2* selective) or ␣-conotoxin PIA (CntxPIA) (␣6␤2* selective) into ventral tegmental area (VTA). The intra-VTA perfusion of CntxMII or CntxPIA markedly decreased systemic nicotine-elicited DA release in the nucleus accumbens and habituated locomotion; the intra-VTA perfusion of CntxMII also decreased the rate of nicotine infusion in the maintenance phase of nicotine, but not of food, self-administration. Overall, the results of these experiments show that the ␣6␤2* nAChRs expressed in the VTA are necessary for the effects of systemic nicotine on DA neuron activity and DA-dependent behaviors such as locomotion and reinforcement, and suggest that ␣6␤2*-selective compounds capable of crossing the blood-brain barrier may affect the addictive properties of nicotine and therefore be useful in the treatment of tobacco dependence.

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“…Rodent studies have shown that intravenous nicotine self-administration leads to an increase in the number of α6* receptors in rats [114], but a decrease in the number of striatal α6* receptors in rodents chronically treated with nicotine by means of minipumps [115,116] or receiving it in drinking water [117]. These apparently discrepant results may be due to the different modalities of nicotine administration leading to differences in nicotine concentration in the brain and/or the kinetics or duration of receptor exposure, which may differently affect α6* nAChRs.…”

Section: Regulation Of Native Subtypes By Chronic Nicotine Exposurementioning

confidence: 99%

Structural and functional diversity of native brain neuronal nicotinic receptors

Gotti

Clementi

Fornari

et al. 2009

Biochemical Pharmacology

415

430

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 Although some of the neural circuits involved in the acute and chronic effects of nicotine have been identified, much less is known about which native nAChR subtypes are involved in specific physiological functions and pathophysiological conditions.We briefly review some recent findings concerning the structure and function of native nAChRs, focusing on the subtypes identified in the meso-striatal and habenulo-interpeduncular pathways, two systems involved in nicotine reinforcement and withdrawal. We also discuss recent findings concerning the effect of chronic nicotine on the expression of native subtypes.

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Selective down-regulation of [125I]Y0-α-conotoxin MII binding in rat mesostriatal dopamine pathway following continuous infusion of nicotine

Cited by 61 publications

References 19 publications

Nicotine Improves Cognitive Deficits of Dopamine Transporter Knockout Mice without Long-Term Tolerance

Nicotine Improves Cognitive Deficits of Dopamine Transporter Knockout Mice without Long-Term Tolerance

Nicotinic Acetylcholine Receptors in the Mesolimbic Pathway: Primary Role of Ventral Tegmental Area α6β2* Receptors in Mediating Systemic Nicotine Effects on Dopamine Release, Locomotion, and Reinforcement

Structural and functional diversity of native brain neuronal nicotinic receptors

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