Chronic Nicotine Administration in the Drinking Water Affects the Striatal Dopamine in Mice

Pietilä, Kirsi; Ahtee, Liisa

doi:10.1016/s0091-3057(00)00235-5

Cited by 41 publications

(36 citation statements)

References 75 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After 8 weeks of nicotine treatment in the drinking water and 24 h withdrawal, WT mice exhibited tolerance to the hypolocomotion induced by a challenge dose of nicotine, as reported previously (Sparks and Pauly, 1999;Pietila and Ahtee, 2000; for reviews, see Malin, 2001;Picciotto and Corrigall, 2002). In contrast, such chronic treatment did not induce tolerance of DAT KO mice to nicotine-induced hypolocomotion.…”

Section: Modulation Of Daergic and Nicotinic Receptor Densities By Chsupporting

confidence: 78%

“…This increased basal hyperactivity was reminiscent of the withdrawal syndrome described previously in mice after such treatment (Pietila and Ahtee, 2000;Gaddnas et al, 2001). In contrast, chronic nicotine treatment had no significant effect on the basal locomotion of DAT KO (Figure 2).…”

Section: Absence Of Tolerance To Nicotine-induced Hypolocomotion In Nsupporting

confidence: 66%

“…The increased basal locomotor activity could be owing to higher reactivity of DAT KO mice to aging or to 8-week experimentation, including weighing, exposure to actimeter cages and/or saccharin treatment. Oral chronic nicotine treatment of WT mice significantly increased their basal locomotor activity by + 15% during treatment (treatment: F 1,186 ¼ 7.91, p ¼ 0.009; Figure 1), probably due to behavioral sensitization and/or to withdrawal syndrome (Pietila and Ahtee, 2000;Gaddnas et al, 2001). The same chronic nicotine treatment slightly decreased, but not significantly, basal locomotor activity of DAT KO mice.…”

Section: Effect Of Chronic Nicotine Treatment On the Basal Locomotor mentioning

confidence: 92%

“…Nicotine was administered for 8 weeks in the drinking water (as only source of fluid), at a concentration of 70 mg/ml (free base), supplemented with 2% saccharin (Pietila and Ahtee, 2000). Control mice received 2% saccharin in their drinking water.…”

Section: Animals and Chronic Treatment By Nicotinementioning

confidence: 99%

“…In the present study, we investigated if acute nicotineinduced effects in DAT KO mice persist after chronic nicotine treatment. We chose to deliver nicotine in the drinking water, a more physiological administration mode (Pekonen et al, 1993;Pietila and Ahtee, 2000). We assessed the effects of chronic nicotine treatment on nicotineinduced locomotion and on the anxiety status of WT and DAT KO mice.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

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

Weiss

Nosten‐Bertrand

McIntosh

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

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.

show abstract

Section: Modulation Of Daergic and Nicotinic Receptor Densities By Chsupporting

confidence: 78%

Section: Absence Of Tolerance To Nicotine-induced Hypolocomotion In Nsupporting

confidence: 66%

Section: Effect Of Chronic Nicotine Treatment On the Basal Locomotor mentioning

confidence: 92%

Section: Animals and Chronic Treatment By Nicotinementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

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

Weiss

Nosten‐Bertrand

McIntosh

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

Antrodia camphorataattenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice

Yang

Korivi

Chen

et al. 2017

Environmental Toxicology

View full text Add to dashboard Cite

Cigarette smoke exposure activates several cellular mechanisms predisposing to atherosclerosis, including oxidative stress, dyslipidemia, and vascular inflammation. Antrodia camphorata, a renowned medicinal mushroom in Taiwan, has been investigated for its antioxidant, anti-inflammatory, and antiatherosclerotic properties in cigarette smoke extracts (CSE)-treated vascular smooth muscle cells (SMCs), and ApoE-deficient mice. Fermented culture broth of Antrodia camphorata (AC, 200-800 µg/mL) possesses effective antioxidant activity against CSE-induced ROS production. Treatment of SMCs (A7r5) with AC (30-120 µg/mL) remarkably ameliorated CSE-induced morphological aberrations and cell death. Suppressed ROS levels by AC corroborate with substantial inhibition of CSE-induced DNA damage in AC-treated A7r5 cells. We found CSE-induced apoptosis through increased Bax/Bcl-2 ratio, was substantially inhibited by AC in A7r5 cells. Notably, upregulated SOD and catalase expressions in AC-treated A7r5 cells perhaps contributed to eradicate the CSE-induced ROS generation, and prevents DNA damage and apoptosis. Besides, AC suppressed AP-1 activity by inhibiting the c-Fos/c-Jun expressions, and NF-κB activation through inhibition of I-κBα degradation against CSE-stimulation. This anti-inflammatory property of AC was accompanied by suppressed CSE-induced VEGF, PDGF, and EGR-1 overexpressions in A7r5 cells. Furthermore, AC protects lung fibroblast (MRC-5) cells from CSE-induced cell death. In vivo data showed that AC oral administration (0.6 mg/d/8-wk) prevents CSE-accelerated atherosclerosis in ApoE-deficient mice. This antiatherosclerotic property was associated with increased serum total antioxidant status, and decreased total cholesterol and triacylglycerol levels. Thus, Antrodia camphorata may be useful for prevention of CSE-induced oxidative stress and diseases. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 2070-2084, 2017.

show abstract

Molecular and Cellular Mechanisms of Action of Nicotine in the CNS

Barik

Wonnacott

Handbook of Experimental Pharmacology

View full text Add to dashboard Cite

Nicotine achieves its psychopharmacological effects by interacting with nicotinic acetylcholine receptors (nAChRs) in the brain. There are numerous subtypes of nAChR that differ in their properties, including their sensitivity to nicotine, permeability to calcium and propensity to desensitise. The nAChRs are differentially localised to different brain regions and are found on presynaptic terminals as well as in somatodendritic regions of neurones. Through their permeability to cations, these ion channel proteins can influence both neuronal excitability and cell signalling mechanisms, and these various responses can contribute to the development or maintenance of dependence. However, many questions and uncertainties remain in our understanding of these events and their relevance to tobacco addiction. In this chapter, we briefly overview the fundamental characteristics of nAChRs that are germane to nicotine's effects and then consider the cellular responses to acute and chronic nicotine, with particular emphasis on dopamine systems because they have been the most widely studied in the context of nicotine dependence. Where appropriate, methodological aspects are critically reviewed.

show abstract

Chronic Nicotine Administration in the Drinking Water Affects the Striatal Dopamine in Mice

Cited by 41 publications

References 75 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

Antrodia camphorataattenuates cigarette smoke-induced ROS production, DNA damage, apoptosis, and inflammation in vascular smooth muscle cells, and atherosclerosis in ApoE-deficient mice

Molecular and Cellular Mechanisms of Action of Nicotine in the CNS

Contact Info

Product

Resources

About