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Stroke. 1999 Mar;30(3):651-5.
Nicotine increases plasminogen activator inhibitor-1 production by human brain endothelial cells via protein kinase C-associated pathway.

Zidovetzki R, Chen P, Fisher M, Hofman FM, Faraci FM.

Departments of Biology and Neuroscience, University of California, Riverside, CA, USA.

BACKGROUND AND PURPOSE: Smoking both increases stroke risk and reduces the risk of thrombolysis-associated intracerebral hemorrhage. Plasminogen activator inhibitor-1 (PAI-1) is a major regulator of fibrinolysis; elevation of PAI-1 is associated with an increased risk of thrombotic disorders. We studied the effect of nicotine, an important constituent of cigarette smoke, on PAI-1 production by human brain endothelial cells. METHODS: Adult human central nervous system endothelial cells (CNS-EC) were used for tissue culture experiments. We analyzed culture supernatant for PAI-1 protein and measured PAI-1 mRNA (by Northern blot analysis) and protein kinase C (PK-C) activity. RESULTS: Nicotine at 100 nmol/L increased PAI-1 protein production and mRNA expression by CNS-EC. After 72 hours of exposure to nicotine, the concentration of secreted PAI-1 in the cell supernatant was increased 1.90+/-0.2 fold compared with untreated cells. PAI-1 mRNA also increased approximately twofold. Inhibition of PK-C completely abolished this effect. Nicotine had no effect on the concentration of tissue plasminogen activator. CONCLUSIONS: Nicotine increases brain endothelial cell PAI-1 mRNA expression and protein production via PK-C-dependent pathway. These findings provide new insights into why smoking may be associated with predisposition to thrombosis and inversely associated with intracerebral hemorrhage after therapeutic tissue plasminogen activator therapy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066866&dopt=Abstract

Alcohol. 1999 Feb;17(2):139-47.
Operant ethanol self-administration after nicotine treatment and withdrawal.

Nadal R, Samson HH.

Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA. rnadac.uab.es

The effects of chronic intermittent administration of nicotine (NIC) and withdrawal on operant ethanol (EtOH) self-administration were tested in Long-Evans rats (n = 8). EtOH self-administration (10% v/v, Fixed Ratio 4 reinforcement schedule) was induced by the sucrose-substitution procedure. Then the animals were divided into two groups of four rats matched on EtOH self-administration and the locomotor activity following an injection of NIC (0.35 mg/kg, SC) or saline was measured. The groups then received 9 days of injection of either NIC (0.35 mg/kg) or saline and then motor activity was retested using the initial NIC dose. This was followed by 17 days of NIC injections (0.6 mg/kg) or saline injections. A final locomotor test using the higher NIC dose was then conducted. The initial acute administration of NIC had no effect on motor activity compared to saline (measured by the number of horizontal movements). However, after the repeated treatment, the group of animals injected chronically and acutely with NIC showed motor activation in comparison with the animals injected chronically with saline and injected acutely with NIC only on the days of activity testing. At the end of the chronic NIC treatment, operant EtOH self-administration was not changed. However, 6 days after the NIC injections were concluded, a change in the pattern of responding for EtOH was observed in the NIC group, showing a decrease in the mean rate of responding during the first half of the operant self-administration session. When both groups were again tested for locomotor activity at the end of the operant self-administration experiment, the increased motor activity in the NIC group was still observed. The results suggest that alterations in the nicotinic system may affect EtOH self-administration, but this appears to be only modulatory, even with a significant change in locomotor response to NIC following chronic NIC administration.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10064382&dopt=Abstract

Mol Pharmacol. 1999 Mar;55(3):432-43.
Regulation of alpha4beta2 nicotinic receptor desensitization by calcium and protein kinase C.

Fenster CP, Beckman ML, Parker JC, Sheffield EB, Whitworth TL, Quick MW, Lester RA.

Department of Neurobiology, University of Alabama at Birmingham,USA.

Neuronal nicotinic acetylcholine receptor (nAChR) desensitization is hypothesized to be a trigger for long-term changes in receptor number and function observed after chronic administration of nicotine at levels similar to those found in persons who use tobacco. Factors that regulate desensitization could potentially influence the outcome of long-lasting exposure to nicotine. The roles of Ca2+ and protein kinase C (PKC) on desensitization of alpha4beta2 nAChRs expressed in Xenopus laevis oocytes were investigated. Nicotine-induced (300 nM; 30 min) desensitization of alpha4beta2 receptors in the presence of Ca2+ developed in a biphasic manner with fast and slow exponential time constants of tauf = 1.4 min (65% relative amplitude) and taus = 17 min, respectively. Recovery from desensitization was reasonably well described by a single exponential with taurec = 43 min. Recovery was largely eliminated after replacement of external Ca2+ with Ba2+ and slowed by calphostin C (taurec = 48 min), an inhibitor of PKC. Conversely, the rate of recovery was enhanced by phorbol-12-myristate-13-acetate (taurec = 14 min), a PKC activator, or by cyclosporin A (with taurec = 8 min), a phosphatase inhibitor. alpha4beta2 receptors containing a mutant alpha4 subunit that lacks a consensus PKC phosphorylation site exhibited little recovery from desensitization. Based on a two-desensitized-state cyclical model, it is proposed that after prolonged nicotine treatment, alpha4beta2 nAChRs accumulate in a "deep" desensitized state, from which recovery is very slow. We suggest that PKC-dependent phosphorylation of alpha4 subunits changes the rates governing the transitions from "deep" to "shallow" desensitized conformations and effectively increases the overall rate of recovery from desensitization. Long-lasting dephosphorylation may underlie the "permanent" inactivation of alpha4beta2 receptors observed after chronic nicotine treatment.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10051526&dopt=Abstract

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