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Brain Res. 2002 Oct 25;953(1-2):53-62.
Neuropathy-specific analgesic action of intrathecal nicotinic agonists and its spinal GABA-mediated mechanism.

Rashid MH, Ueda H.

Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan.

The effect of the nicotinic acetylcholine receptor (nAChR) agonists at the spinal level has not been well studied in neuropathic states. In the present report, we demonstrate the efficacy of intrathecal nicotinic agonists in partial sciatic nerve injury-induced neuropathy model mice. Intrathecal (i.t.) administration of (-)nicotine and (+)epibatidine, at doses without undesirable effects, had no antinociceptive action in sham-operated mice. However, they completely reversed the thermal and mechanical hyperalgesia in partial sciatic nerve-injured mice. This neuropathy-specific analgesic action of i.t. (-)nicotine and (+)epibatidine is attributed to different subtypes of nAChRs at the spinal level. After antagonism experiments with mecamylamine, dihydro-beta-erythroidine and methyllycaconitine, it was observed that (-)nicotine-induced analgesia was mediated through the alpha4beta2 subtype of nAChR while the (+)epibatidine-induced one was mediated through non-alpha4beta2 subtype of nAChR. Moreover, i.t. pretreatment with NMDA receptor antagonist did not block nicotinic analgesia. Similar to nicotinic agonists, gamma-aminobutyric acid receptor (GABA(A)) agonist muscimol (i.t.) produced neuropathy-specific analgesic action giving analgesia only in nerve-injured mice. The GABA(A) antagonists bicuculline and picrotoxin significantly blocked the analgesic effects of muscimol as well as that of (-)nicotine and (+)epibatidine. On the other hand, i.t. injection of nicotinic antagonist mecamylamine and GABA(A) antagonist picrotoxin in sham-operated mice induced a thermal hyperalgesia without any effects in nerve-injured animals suggesting the presence of a tonic inhibitory tone on nociceptive transmission through the spinal cholinergic-GABAergic system. These results also suggest that the neuropathy-specific analgesic action of intrathecal nicotinic agonists was due to stimulation of this cholinergic-GABAergic system whose inhibitory tone had been reduced due to injury.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12384238&dopt=Abstract

Pesqui Odontol Bras. 2002 Jul-Sep;16(3):234-8.
[Effect of nicotine on the viability and morphology of fibroblasts: in vitro study]

[Article in Portuguese]

Martinez AE, Silverio KG, Rossa C Jr.

Departamento de Diagnostico e Cirurgia, Faculdade de Odontologia de Araraquara, Universidade Estadual Paulista.

The aim of this study was to evaluate, in vitro, the effect of nicotine on the viability and morphology of fibroblasts from a continuous lineage. Two experimental groups were prepared, with different drug dosages (0 - control, 10 microgram 100 microgram, 0.5 mg, 1 mg) and conditioning time (1 and 24 hours). Twelve-well microplates were utilized. Each well received 2 ml of fresh culture medium and 1 ml of a solution containing 1 x 10(5) cells/ml. Nicotine was then added to the wells, at the tested concentrations. After the incubation period, cell viability was assessed by means of 0.4% trypan blue staining. Cell viability and morphology were assessed in an inverted microscope, by a single examiner, who was blind as to the experimental groups. The experiment was repeated 5 times. Regarding morphology, in the 1-hour conditioned group there was statistically significant difference between the control group and the group with the greatest dose of nicotine. These differences were also observed between the control group and all nicotine groups after 24 hours. The results of the Kruskal-Wallis test revealed that more unviable cells were found in the groups exposed to nicotine, in comparison with the control group, both after 1 and 24 hours of conditioning (p < 0.05). Moreover, with increasing doses of nicotine there was a directly proportional increase in the number of unviable cells, both after 1 and 24 hours of exposure (p = 0.0053 and p = 0.00001, respectively). The conclusion of this study is that nicotine can alter, in vitro, the viability and morphology of fibroblasts in a manner proportional to the dose and time of exposure.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12386685&dopt=Abstract

Am J Physiol Heart Circ Physiol. 2003 Feb;284(2):H528-34. Epub 2002 Oct 10.
Impairment of nitric oxide synthase-dependent dilatation of cerebral arterioles during infusion of nicotine.

Fang Q, Sun H, Mayhan WG.

Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha 68198-4575, USA.

The effects of nicotine on nitric oxide synthase (NOS)-dependent reactivity of cerebral arterioles remain uncertain. Our first goal was to examine whether infusion of nicotine alters NOS-dependent reactivity of cerebral arterioles. Our second goal was to examine the mechanisms that may account for the effects of nicotine on cerebral arterioles. We measured the diameter of pial arterioles to NOS-dependent (ADP and acetylcholine) and NOS-independent (nitroglycerin) agonists before and after the infusion of nicotine (2 microg x kg(-1) x min(-1) iv for 30 min, followed by a maintenance dose of 0.35 microg x kg(-1) x min(-1)). ADP- and acetylcholine-induced vasodilatation was impaired after the infusion of nicotine. In contrast, nicotine did not alter vasodilatation to nitroglycerin. Next, we examined whether the impaired responses of pial arterioles during infusion of nicotine may be related to oxygen radicals. We found that application of superoxide dismutase or tetrahydrobiopterin during infusion of nicotine could prevent impaired NOS-dependent vasodilatation. Thus acute exposure of cerebral vessels to nicotine specifically impairs NOS-dependent dilatation via the production of oxygen radicals possibly related to an alteration in the utilization of tetrahydrobiopterin.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12388280&dopt=Abstract

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as hair loss. The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

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