Nicotine for the treatment of Tourette's syndrome

Sanberg, Paul R.; Silver, Archie A.; Shytle, R. Douglas; Philipp, M K; Cahill, David W.; Fogelson, Harold; McConville, Brian J.

doi:10.1016/s0163-7258(96)00199-4

Cited by 94 publications

(49 citation statements)

References 39 publications

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Section: Discussionmentioning

confidence: 99%

“…It may be that any amelioration of such side effects by nicotine persists, even after withdrawal of nicotine itself. There is precedent for such an effect with nicotine augmentation of haloperidol treatment for Tourette's Syndrome (Sanberg et al 1997).The threshold for nicotine effects on extrapyramidal syndromes may also be different for various movement disorders. We found an acute effect of nicotine withdrawal ameliorating dyskinetic movements.…”

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confidence: 99%

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Nicotine Withdrawal and Psychiatric Symptoms in Cigarette Smokers with Schizophrenia

Dalack

1999

Neuropsychopharmacology

115

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It is well known that the prevalence of smoking among those with schizophrenia is two to three times higher than that in the general population and considerably higher than that among those with other psychiatric illnesses de Leon et al. 1995). Crosssectional studies have suggested that smoking may be a marker of more severe schizophrenic illness and may affect treatment by modulating side effects of antipsychotic medication (Sandyk and Kay 1991;Goff et al. 1992). For example, neuroleptic-induced parkinsonism (NIP) is often found to be less prevalent among schizophrenics who smoke (Decina et al. 1990), whereas, the rate of tardive dyskinesia had been variably reported to be higher or lower (Yassa et al. 1987;Menza et al. 1991). The suggested effects of smoking on NIP may be accounted for by the faster metabolic clearance of neuroleptics attributable to hepatic microsomal enzyme upregulation caused by the products of tobacco combustion (Benowitz 1988), although some studies sug- et al. 1985;Jann et al. 1986). A number of explanations for the extensive cooccurrence of smoking with schizophrenia have been forwarded (Freedman et al. 1997;Glassman 1993). Some have focused on the ameliorating effects of nicotine on attentional abnormalities found in schizophrenia (Freedman et al. 1997;Adler et al. 1993), whereas, others have posited that the effects of nicotine on reward reinforcement and negative symptoms of schizophrenia are important (Glassman 1993;Nisell et al. 1995). Systematic studies of the effects of nicotine withdrawal have not been reported.The available cessation data suggest that smoking cessation rates among smokers with schizophrenia are quite low (Covey et al. 1994;Addington et al. 1997;Ziedonis and George 1997). In part, this may relate to lower motivation to quit (Ziedonis and George 1997). We have reported cases that suggested that attempts to cut down or quit smoking led to an exacerbation of psychiatric symptoms and a return to smoking (Dalack and Meador-Woodruff 1996).The very high prevalence of smoking among those with schizophrenia, coupled with our clinical impression that smoking abstinence may to lead to an exacerbation of psychiatric symptoms, led us to consider whether smoking in schizophrenia might be an attempt to self-medicate symptoms of the illness or side effects of treatment. Accordingly, we used an experimental paradigm that most closely paralleled our clinical observations. We conducted a randomized, double-blind, placebo-controlled crossover study to examine the effect of acute nicotine withdrawal on psychiatric symptoms and medication side effects in smokers with schizophrenia. Our goal was to examine the following hypotheses.1. Acute nicotine withdrawal will exacerbate psychiatric symptoms in heavy smokers with schizophrenia. 2. Treatment of acute withdrawal by transdermal nicotine patch will mitigate both the increase in withdrawal symptoms and psychiatric symptoms. 3. Neuroleptic-induced parkinsonism will worsen during acute nicotine withdrawal; tardive dyskinesia will not ch...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Nicotine Withdrawal and Psychiatric Symptoms in Cigarette Smokers with Schizophrenia

Dalack

1999

Neuropsychopharmacology

115

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“…Nicotinic receptors are implicated in many important f unctions of the mammalian neocortex, including memory formation (Granon et al, 1995) and neuronal regulation of regional cerebral blood flow (Gitelman and Prohovnik, 1992;Uchida et al, 1997), as well as cortical pathologies such as Alzheimer's disease (Whitehouse et al, 1988;Newhouse et al, 1997), epilepsy (Steinlein et al, 1995, and Tourette's syndrome (Sanberg et al, 1997(Sanberg et al, , 1998. The cellular basis for the effects of nicotinic receptor stimulation is currently unknown but lies within its effects on the complex interactions between the excitatory glutamatergic pyramidal neurons and the inhibitory interneurons.…”

Section: Abstract: Single-cell Pcr; Neuropeptides; Calcium-binding Pmentioning

confidence: 99%

Selective Excitation of Subtypes of Neocortical Interneurons by Nicotinic Receptors

et al. 1999

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The cellular mechanisms by which neuronal nicotinic cholinergic receptors influence many aspects of physiology and pathology in the neocortex remain primarily unknown. Whole-cell recordings and single-cell reverse transcription (RT)-PCR were combined to analyze the effect of nicotinic receptor agonists on different types of neurons in acute slices of rat neocortex. Nicotinic receptor agonists had no effect on pyramidal neurons and on most types of interneurons, including parvalbuminexpressing fast spiking interneurons and somatostatinexpressing interneurons, but selectively excited a subpopulation of interneurons coexpressing the neuropeptides vasoactive intestinal peptide (VIP) and cholecystokinin. This excitation persisted in the presence of glutamate, GABA, and muscarinic receptor antagonists and in the presence of tetrodotoxin and low extracellular calcium, suggesting that the depolarization was mediated through the direct activation of postsynaptic nicotinic receptors. The responses were blocked by the nicotinic receptor antagonists dihydro-␤-erythroidine and mecamylamine and persisted in the presence of the ␣7 selective nicotinic receptor antagonist methyllycaconitine, suggesting that the involved nicotinic receptors lacked the ␣7 subunit. Single-cell RT-PCR analysis indicated that the majority of the interneurons that responded to nicotinic stimulation coexpressed the ␣4, ␣5, and ␤2 nicotinic receptor subunits. Therefore, these results provide a role for non-␣7 nicotinic receptors in the selective excitation of a subpopulation of neocortical interneurons. Because the neocortical interneurons expressing VIP have been proposed previously to regulate regional cortical blood flow and metabolism, these results also provide a cellular basis for the neuronal regulation of cortical blood flow mediated by acetylcholine. Key words: single-cell PCR; neuropeptides; calcium-binding proteins; methyllycaconitine; dihydro-␤-erythroidine; acetylcholine; mecamylamineNicotinic receptors are implicated in many important f unctions of the mammalian neocortex, including memory formation (Granon et al., 1995) and neuronal regulation of regional cerebral blood flow (Gitelman and Prohovnik, 1992;Uchida et al., 1997), as well as cortical pathologies such as Alzheimer's disease (Whitehouse et al., 1988;Newhouse et al., 1997), epilepsy (Steinlein et al., 1995, and Tourette's syndrome (Sanberg et al., 1997(Sanberg et al., , 1998. The cellular basis for the effects of nicotinic receptor stimulation is currently unknown but lies within its effects on the complex interactions between the excitatory glutamatergic pyramidal neurons and the inhibitory interneurons.A variety of different neuronal nicotinic receptor subunits have been cloned and named ␣2-␣9 and ␤2-␤4 (Elgoyhen et al., 1994;Le Novere and Changeux, 1995). C lassically, two broad subfamilies of nicotinic receptors have been characterized in neurons according to their sensitivity to ␣-bungarotoxin. Subunits ␣7 and ␣8 form a family of ␣-bungarotoxin-sensitive channels (Couturier...

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“…Moreover, it has been suggested that nicotine can lock the brain into an attentional processing mode whereby there are fewer lapses in attention and therefore less omissions (Mancuso et al, 1999). These observations may underlie the ability of nicotine to enhance attention and improve the symptomatology of various human diseases including schizophrenia (Yang et al, 2002), Alzheimer's disease (White and Levin, 1999), attention deficit hyperactivity disorder (Shytle et al, 2002), Parkinson's disease (O'Neill et al, 2002), and Tourette's syndrome (Sanberg et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Nicotine Improves Sustained Attention in Mice: Evidence for Involvement of the α7 Nicotinic Acetylcholine Receptor

Young

Finlayson

Spratt

et al. 2004

Neuropsychopharmacol

209

174

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In humans, nicotine has been shown to improve attention in both normal and impaired individuals. Observations in rats reflect some, but not all aspects of the nicotine-induced improvements in humans. To date these findings have not been replicated in mice. To examine the effect of nicotine on sustained attention in mice, we have established a version of the 5-choice serial reaction-time (5-CSR) task with graded levels of difficulty, based upon spatial displacement and a variable intertrial interval. Using this paradigm, microgram doses of nicotine produced a consistent reduction in the level of omissions and an improvement in proportion correct in normal mice. This improvement in sustained attention was made irrespectively of whether mice had previously received nicotine. In an attempt to elucidate which nicotinic acetylcholine receptor (nAChR) subtype(s) mediate this effect, we examined the performance of a7 nAChR knockout (KO) mice in the 5-CSR task. a7 nAChR KO mice not only acquired the task more slowly than their wild-type littermates, but on attaining asymptotic performance, they exhibited a higher level of omissions. In conclusion, by increasing the level of task difficulty, the performance of mice was maintained at sufficiently low levels to allow a demonstrable improvement in performance upon nicotine administration. Furthermore, as a7 KO mice are clearly impaired in the acquisition and asymptotic performance of this task, the a7 nAChR may be involved in mediating these effects of nicotine.

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Nicotine for the treatment of Tourette's syndrome

Cited by 94 publications

References 39 publications

Nicotine Withdrawal and Psychiatric Symptoms in Cigarette Smokers with Schizophrenia

Nicotine Withdrawal and Psychiatric Symptoms in Cigarette Smokers with Schizophrenia

Selective Excitation of Subtypes of Neocortical Interneurons by Nicotinic Receptors

Nicotine Improves Sustained Attention in Mice: Evidence for Involvement of the α7 Nicotinic Acetylcholine Receptor

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