Effects of α4/β2- and α7-nicotine acetylcholine receptor agonists on prepulse inhibition of the acoustic startle response in rats and mice

Schreiber, Rudy; Dalmus, M.; Vry, Jean De

doi:10.1007/s00213-001-0927-8

Cited by 78 publications

(70 citation statements)

References 25 publications

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“…It is not clear which nAChRs subtypes are responsible for this effect. In rodents, a4b2 subunit of nAChRs, but not a7, appears to regulate acoustic PPI (Schreiber et al, 2002). However, there is strong evidence suggesting that a7 nAChR (for a recent review see Martin and Freedman, 2007) and to a lesser extent a4b2 nAChR (Breese et al, 2000;Durany et al, 2000;Marutle et al, 2001;Faraone et al, 2004;De Luca et al, 2006) are involved in the pathology of schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

“…However, other studies have shown no effect, or even the opposite effect (Decker et al, 1997;Faraday et al, 1999;Mirza et al, 2000;Schreiber et al, 2002). Several studies in healthy humans have generally affirmed the nicotinic enhancement of PPI (Kumari et al, 1996;Della Casa et al, 1998;Duncan et al, 2001), but the opposite effect has also been reported in studies using cigarettes with high nicotine content (Hutchison et al, 2000).…”

Section: Introductionmentioning

confidence: 98%

“…Animal studies have shown that nicotine enhances acoustic PPI in some rodent strains (Acri, 1994;Curzon et al, 1994;Acri et al, 1995;Faraday et al, 1999;Schreiber et al, 2002;Spielewoy and Markou, 2004); an effect thought to be mediated by nicotinic acetylcholine receptors (nAChRs) (Schreiber et al, 2002;Suemaru et al, 2004). However, other studies have shown no effect, or even the opposite effect (Decker et al, 1997;Faraday et al, 1999;Mirza et al, 2000;Schreiber et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Hong

Wonodi

Lewis

et al. 2007

Neuropsychopharmacol

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Acoustic prepulse inhibition (PPI) is considered an important biomarker in animal studies of psychosis and a number of psychiatric conditions. Nicotine has been shown to improve acoustic PPI in some animal strains and in humans. However, there is little data on effects of nicotine on acoustic PPI in schizophrenia patients using a double-blind, placebo-controlled study design. The primary aim of the current study was to test the effect of nicotine nasal spray on acoustic PPI in schizophrenia patients. The secondary aim was to test nicotine effect on prepulse facilitation (PPF). The study included 18 schizophrenia patient smokers and 12 healthy control smokers, tested in a double-blind, placebo-controlled, crossover, randomized design immediately after nicotine or saline placebo nasal sprays. PPI was tested using 120 ms prepulse-pulse interval. PPF was tested using 4500 ms prepulse-pulse interval. The results showed a significant main effect of drug on PPI in that nicotine improved PPI compared to placebo (p ¼ 0.008) with no drug by diagnosis interaction (p ¼ 0.90). Improvement in PPI in response to nicotine was significantly correlated with the baseline severity of clinical symptoms (r ¼ 0.59, p ¼ 0.02) in patients. There was no significant drug or drug by diagnosis interaction for the 4500 ms prepulse-pulse interval condition. However, nicotine improved inhibition in a subgroup of subjects exhibiting PPF (p ¼ 0.002). In conclusion, the findings confirmed that nicotine transiently improves acoustic PPI in schizophrenia patients. Additionally, schizophrenia patients with more clinical symptoms may have benefited more from nicotinic effect on PPI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Hong

Wonodi

Lewis

et al. 2007

Neuropsychopharmacol

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“…AR-R 17779, an AstraZeneca product, is an acetylcholine analogue with full agonist properties at the α7 nicotinic cholinergic receptor. This compound does not enhance the inhibition of startle in DBA/2 mice [123,124,125] or improve accuracy and speed of response on a five-choice serial reaction time [126,127]. ABT-418, has some agonist properties at the α7 nicotinic cholinergic receptors, but is a less potent agonist than nicotine [128] and restores deficient auditory gating in DBA/2 mice as well as rats with fimbria-fornix lesions, but similar to nicotine, fails to produce continued improvement with a second dose [54].…”

Section: Dmxba As a Prototype Drugmentioning

confidence: 99%

“…In rodent studies, nicotine improves PPI in a model of deficient schizophrenia-like PPI [99]. Administration of DMXBA also improves deficient PPI [100].…”

Section: Dmxba As a Prototype Drugmentioning

confidence: 99%

Treating schizophrenia symptoms with an α7 nicotinic agonist, from mice to men

Olincy

Stevens

2007

Biochemical Pharmacology

125

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Current antipsychotic treatments fail to fully address the range of symptoms of schizophrenia, particularly with respect to social and occupational dysfunctions. Recent work has highlighted the role of nicotinic in both cognitive and attentional deficits as well as deficient processing of repetitive sensory information. The predilection for schizophrenia patients to be extremely heavy cigarette smokers may be related to their attempt to compensate for a reduction in hippocampal α7 nicotinic cholinergic receptors by delivering exogenous ligand to the remaining receptors. Studies in rodent models of both learning and memory deficits and deficits in sensory inhibition have confirmed a role for α7 subtype of the nicotinic cholinergic receptors in these processes. Rodent studies also demonstrated the efficacy of a selective partial α7 nicotinic agonist, DMXBA, to improve these deficits. Subsequent human clinical trials demonstrated improved sensory inhibition in 12 schizophrenia patients and showed improvement in several subtests of the RBANS learning and memory assessment instrument. These data suggest that therapeutic agents selected for α7 nicotinic activity may have utility in treating certain symptoms of schizophrenia. KeywordsSchizophrenia; nicotinic receptors; DMXBA; P50 auditory evoked potential; cognitive deficits; nicotine Although the positive symptoms such as hallucinations and delusions of schizophrenia are partially treated with the available antipsychotic medications, social and occupational dysfunction remains a major issue in treating this disorder. Cognitive deficits have been identified as more closely related to ability to adequately function [1]. In the search for new and more effective therapeutic agents for schizophrenia, recent attention has turned the nicotinic cholinergic receptors system. α7 and P50 Auditory GatingPeople with schizophrenia, in addition to the cardinal symptoms of hallucinations and delusions, suffer from the inability to focus attention. This may stem from being overwhelmed

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Startle Reflex and Psychophysiology

Meehan¹,

Miranda²

2013

The Wiley‐Blackwell Handbook of Addiction Psychopharmacology

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Effects of α4/β2- and α7-nicotine acetylcholine receptor agonists on prepulse inhibition of the acoustic startle response in rats and mice

Cited by 78 publications

References 25 publications

Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Treating schizophrenia symptoms with an α7 nicotinic agonist, from mice to men

Startle Reflex and Psychophysiology

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