The Cholinergic Rapid Eye Movement Sleep Induction Test With RS-86

Berger, Thomas; Riemann, Dieter; Höchli, D.; Spiegel, René

doi:10.1001/archpsyc.1989.01810050035006

Cited by 123 publications

(32 citation statements)

References 32 publications

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“…1990). Similar results have been found for other muscarinic cholinergic agonists, such as orally administered RS-86 (Berger, Riemann, Hochli, & Spiegel, 1989).…”

Section: Prophylactic Use Of Drugs In Sleep Deprivation Researchsupporting

confidence: 88%

Use of Stimulants to Ameliorate the Effects of Sleep Loss During Sustained Performance

Babkoff¹,

Krueger²

1992

Military Psychology

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“…1990). Similar results have been found for other muscarinic cholinergic agonists, such as orally administered RS-86 (Berger, Riemann, Hochli, & Spiegel, 1989).…”

Section: Prophylactic Use Of Drugs In Sleep Deprivation Researchsupporting

confidence: 88%

Use of Stimulants to Ameliorate the Effects of Sleep Loss During Sustained Performance

Babkoff¹,

Krueger²

1992

Military Psychology

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“…There have been several studies on the effects of cholinergic/anticholinergic challenge on polysomnographic measures in other psychiatric disorders (Berger et al 1989;Poland et al 1997), but this strategy had not been employed in schizophrenia. In an exploratory study (Tandon et al 1991b), we compared the effects of biperiden on sleep measures in 12 schizophrenic patients and 10 normal controls.…”

Section: Effects Of Biperiden On Polysomnographic Measures In Schizopmentioning

confidence: 99%

“…Because multiple noncholinergic mechanisms influence both DST response and polysomnographic results, however, these data are suggestive at best and do not lend themselves to any definitive interpretation. In the hope of determining the cholinergic contribution to these abnormalities and providing a more refined index of central cholinergic function than simple baseline parameters, we turned our attention to studying the effects of cholinergic/anticholinergic modulation using polysomnography (Sitaram and Gillin 1980;Gillin and Sitaram 1984).There have been several studies on the effects of cholinergic/anticholinergic challenge on polysomnographic measures in other psychiatric disorders (Berger et al 1989;Poland et al 1997), but this strategy had not been employed in schizophrenia. In an exploratory study (Tandon et al 1991b), we compared the effects of biperiden on sleep measures in 12 schizophrenic patients and 10 normal controls.…”

mentioning

confidence: 99%

The Cholinergic System in Schizophrenia Reconsidered: Anticholinergic Modulation of Sleep and Symptom Profiles

Tandon

Taylor

DeQuardo

et al. 1999

Neuropsychopharmacology

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Receptors, Cholinergic; Receptors, muscarinic; Parasympathetic nervous system; Sleep, REM; Symptoms, positive; Symptoms, negative The dopamine (DA) hypothesis has dominated biochemical and pharmacological research on schizophrenia for about two decades. Although pharmacological data implicate increased DA activity in the pathogenesis of positive symptoms of schizophrenia, there is minimal association with negative symptoms (Crow 1980;Andreasen and Olsen 1982;Angrist et al. 1980). The poorly elucidated pathogenesis of negative symptoms and the unique properties of the atypical antipsychotic clozapine (Jibson and Tandon 1998) have encouraged a reappraisal of the role of the DA system in schizophrenia. Newer approaches to evaluating neurochemical abnormalities in schizophrenia include consideration of other neurotransmitter systems. Models of DA-serotonin (Meltzer 1989), DA-glutamate (Carlsson and Carlsson 1990), DA-acetylcholine (Tandon and Greden 1989), and DA-norepinephrine (van Kammen et al. 1990) interactions have been proposed. Although these models still accord DA a significant role in schizophrenia pathophysiology, they suggest that altered balance between DA and one (or more) of these other neurotransmitter systems may be the principal neurochemical abnormality related to the production of schizophrenic symptoms. Some of the earliest pharmacological treatments for schizophrenia included cholinergic agents (Cohen et al. 1944;Collard et al. 1946;Pfeiffer and Jenney 1957), and in the 1970s, several investigators suggested that cholinergic activity may be reduced in schizophrenia (Friedhoff and Alpert 1973;Janowsky et al. 1973;Davis et al. 1975;Singh and Kay 1979). There was no direct evidence of altered cholinergic functioning in schizophrenic patients, however, and pharmacological trials with cholinergic agents were generally ineffective (Rowntree et al. 1950;Gerlach et al. 1977;Davis and Berger 1978). With few exceptions (Johnstone et al. 1983;Singh et al. 1987), cholinergic mechanisms were increasingly considered irrelevant to the pathophysiology of schizophrenia and discussed predominantly with reference to the treatment of undesirable extrapyramidal side effects of neuroleptics (Richelson 1984). Indirect evidence from several lines of research, however, suggests that the cholinergic system may differentially influence positive and negative symptoms in schizophrenia (Tandon and Greden 1989).We and others have been conducting various studies to evaluate the role of the cholinergic system in schizophrenia, based on a primary hypothesis that DA-acetylcholine (ACh) interactions are of central importance in the production of positive and negative symptoms of schizophrenia (Tandon and Greden 1989;Tandon and Greden 1991). Based on available data and on observations of the course of positive and negative symptoms during the acute phase of the illness (Donlon and Blacker 1973;Docherty et al. 1978;Tandon et al. 1990a), we posited a role for disruption in DA-ACh balance in the expression of positive and negat...

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“…Increasing cholinergic activity using physostigmine (an anticholinesterase inhibitor) provides a challenge uniquely capable of exacerbating depressive symptoms in currently depressed patients with MDD and inducing depressive symptoms in currently manic patients with BD. [4][5][6][7][8][9] The cholinergic system also is implicated in depression by evidence showing that polysomnographic responses to muscarinic receptor agonists [10][11][12] and neuroendocrine and pupillary responses to cholinomimetics [13][14][15][16] are exaggerated in depressed patients and that some muscarinic receptor gene polymorphisms are associated with an elevated incidence of depression. 17,18 Elevated cholinergic function thus was hypothesized to participate in the pathogenesis of mood disorders.…”

mentioning

confidence: 99%

Antidepressant Efficacy of the Antimuscarinic Drug Scopolamine

Furey¹,

Drevets²

2006

Arch Gen Psychiatry

390

292

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Context-The need for improved therapeutic agents that more quickly and effectively treat depression is critical. In a pilot study we evaluated the role of the cholinergic system in cognitive symptoms of depression and unexpectedly observed rapid reductions in depression severity following the administration of the antimuscarinic drug scopolamine hydrobromide (4 μg/kg intravenously) compared with placebo (P=.002). Subsequently a clinical trial was designed to assess more specifically the antidepressant efficacy of scopolamine.Objective-To evaluate scopolamine as a potential antidepressant agent.Design-Two studies were conducted: a double-blind, placebo-controlled, dose-finding study followed by a double-blind, placebo-controlled, crossover clinical trial. Setting-The National Institute of Mental Health.Patients-Currently depressed outpatients aged 18 to 50 years meeting DSM-IV criteria for recurrent major depressive disorder or bipolar disorder. Of 39 eligible patients, 19 were randomized and 18 completed the trial.Interventions-Multiple sessions including intravenous infusions of placebo or scopolamine hydrobromide (4 μg/kg). Individuals were randomized to a placebo/ scopolamine or scopolamine/ placebo sequence (series of 3 placebo sessions and series of 3 scopolamine sessions). Sessions occurred 3 to 5 days apart.Main Outcome Measures-Psychiatric evaluations using the Montgomery-Asberg Depression Rating Scale and the Hamilton Anxiety Rating Scale were performed to assess antidepressant and antianxiety responses to scopolamine.Results-The placebo/scopolamine group showed no significant change during placebo infusion vs baseline; reductions in depression and anxiety rating scale scores (P<.001 for both) were observed after the administration of scopolamine compared with placebo. The scopolamine/ placebo group also showed reductions in depression and anxiety rating scale scores (P<.001 for both) after the administration of scopolamine, relative to baseline, and these effects persisted as they received placebo. In both groups, improvement was significant at the first evaluation after scopolamine administration (P≤.002).Conclusion-Rapid, robust antidepressant responses to the antimuscarinic scopolamine occurred in currently depressed patients who predominantly had poor prognoses.Correspondence: Maura L. Furey, PhD, Mood and Anxiety Disorders Program, National Institute of Mental Health, National Institutes of Health, 15K North Dr, Bldg 15K, Room 115B, Bethesda, MD 20892 (mfurey@mail.nih.gov). Additional Information: A use-patent application for the use of scopolamine as an antidepressant agent has been filed. NIH Public Access Author ManuscriptArch Gen Psychiatry. Author manuscript; available in PMC 2012 January 3. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptMajor depression is the leading cause of years lived with disability. 1 A range of antidepressant agents is available, but 30% to 40% of patients with major depressive disorder (MDD) do not respond to initial treatment, 2 an...

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The Cholinergic Rapid Eye Movement Sleep Induction Test With RS-86

Cited by 123 publications

References 32 publications

Use of Stimulants to Ameliorate the Effects of Sleep Loss During Sustained Performance

Use of Stimulants to Ameliorate the Effects of Sleep Loss During Sustained Performance

The Cholinergic System in Schizophrenia Reconsidered: Anticholinergic Modulation of Sleep and Symptom Profiles

Antidepressant Efficacy of the Antimuscarinic Drug Scopolamine

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