|1.||Shytle, R D: 9 articles (07/2002 - 01/2000)|
|2.||Sanberg, P R: 9 articles (07/2002 - 01/2000)|
|3.||George, Tony P: 7 articles (12/2009 - 04/2005)|
|4.||Vessicchio, Jennifer C: 5 articles (03/2007 - 04/2005)|
|5.||Sacco, Kristi A: 5 articles (03/2007 - 04/2005)|
|6.||Silver, A A: 5 articles (07/2002 - 01/2000)|
|7.||Termine, Angelo: 4 articles (10/2006 - 04/2005)|
|8.||Newman, M B: 4 articles (01/2002 - 04/2001)|
|9.||Cooke, John P: 3 articles (05/2010 - 09/2003)|
|10.||Zarrindast, Mohammad-Reza: 3 articles (07/2008 - 05/2002)|
05/01/1995 - "Intraperitoneal (20 mg/kg) or i.c.v. (60 micrograms/mouse) injection of mecamylamine further strengthened the tremor. "
03/08/1958 - "Psychosis and tremor due to mecamylamine."
08/01/2001 - "After chronic nicotine administration for 7 days, the nicotinic antagonist mecamylamine (1.0 mg/kg, s.c.) precipitated withdrawal with the appearance of somatic signs (teeth chattering and shakes/tremors) and a significant increase in extracellular ACh to 125% of baseline, while extracellular DA decreased to 65%. "
05/01/1997 - "Mecamylamine (0.5 mg/kg, i.p), administered before the nicotine injection on each day, abolished the tail-tremor. "
06/01/1975 - "Both tremor and antidiuresis correlate fairly well with brain nicotine levels whereas mecamylamine-nicotine antagonism is less clearly reflected in brain nicotine levels."
|2.||Alcoholism (Alcohol Abuse)
02/01/2012 - "This ability of mecamylamine might be a potential advantage in the treatment of alcoholism."
10/09/1998 - "Thus, mecamylamine or other antagonists specifically aimed at ventral tegmental nicotinic acetylcholine receptors could represent a new pharmacological treatment principle against alcohol abuse, the efficacy of which should be explored in high-scale alcohol consumers or alcoholics."
01/01/2009 - "These results provide further support that mecamylamine is effective in reducing alcohol consumption and preference, and nicotinic-receptor-based drugs could further be explored as potential treatments for alcoholism."
|3.||Tobacco Use Disorder (Nicotine Dependence)
02/01/2007 - "Mecamylamine produced a significant increase in overt signs of withdrawal in the 23-hour access animals comparable to that observed in previous studies of nicotine dependence. "
02/01/2008 - "As bPiDDB has properties different from the prototypical nAChR antagonist mecamylamine, further development may lead to novel nAChR antagonists for the treatment of tobacco dependence."
02/01/2007 - "Nicotine dependence was assessed by examining physical signs of withdrawal following an injection of the nicotinic antagonist mecamylamine (1.5 mg/kg, i.p.). "
03/01/1984 - "Mecamylamine (MCL) has been shown to extinguish nicotine dependence in rats and monkeys. "
03/01/1984 - "Clinical evaluation of mecamylamine for withdrawal from nicotine dependence."
|4.||Tourette Syndrome (Tourette's Syndrome)
09/01/2001 - "The safety and efficacy of mecamylamine as a monotherapy in children and adolescents with Tourette's disorder (TD) was investigated in an 8-week multicenter, double-blind, placebo-controlled study. "
09/01/2001 - "Multicenter, double-blind, placebo-controlled study of mecamylamine monotherapy for Tourette's disorder."
04/01/2001 - "4. These findings may have important therapeutic implications since clinical observations have shown that low doses of mecamylamine reduce tension and anxiety in patients with Tourette syndrome."
01/01/2000 - "Mecamylamine in Tourette's syndrome: a two-year retrospective case study."
08/29/1998 - "Treatment of Tourette's syndrome with mecamylamine."
06/18/1986 - "Since: spontaneous activity of Renshaw cells is related to the respiratory drive; persists after C7 spinal transection and after mecamylamine poisoning of the axonal recurrent pathway; and might appear before sustained phrenic activity, the assumption of a central respiratory drive impinging on the Renshaw cells has to be retained."
01/01/1988 - "Many lines of evidence support the importance of direct interactions with various sites on the AChR: 1) morphological and toxicological studies with (+) physostigmine showed that anti-ChE activity is not essential to protect animals against toxicity by irreversible ChE inhibitors; 2) (-)physostigmine is far more effective against OP poisoning; 3) open channel blockers such as mecamylamine with no significant anti-ChE activity enhance the protective action of (-)physostigmine; 4) neostigmine, pyridostigmine, (-)physostigmine and (+)physostigmine showed qualitatively and quantitatively distinct toxicity and damage to endplate morphology and function. "
01/01/1988 - "2. In prophylaxis and during the very early phase of OP poisoning, carbamates, especially (-)physostigmine combined with mecamylamine and atropine, could protect almost 100% of the animals exposed to multiple lethal doses of OPs. "
01/01/1986 - "Prophylactic Action of Hexamethonium, Trimethaphan, and Mecamylamine against Diisopropyl Fluorophosphate Poisoning in Mice. "
01/01/1986 - "Prophylactic action of hexamethonium, trimethaphan, and mecamylamine against diisopropyl fluorophosphate poisoning in mice."
|2.||Nicotinic Receptors (Nicotinic Acetylcholine Receptor)
|4.||Neostigmine (Neostigmine Bromide)
|6.||Pyridostigmine Bromide (Pyridostigmine)
|8.||Morphine (MS Contin)
|9.||Acetylcholine (Acetylcholine Chloride)
|2.||Self Administration (Administration, Self)
|4.||Drug Therapy (Chemotherapy)