Review of Clinical Correlates of P50 Sensory Gating Abnormalities in Patients with Schizophrenia

Potter, David; Summerfelt, Ann; Gold, James M.; Boyer, Robert

doi:10.1093/schbul/sbj050

Cited by 243 publications

(162 citation statements)

References 58 publications

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“…P50 inhibition also improved. More detailed information on this area is available in several recent reviews (Levin, 2002;Martin et al, 2004;Potter et al, 2006).…”

Section: Alpha7nachr and Information Processingmentioning

confidence: 99%

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Conejero-Goldberg

Davies

Ulloa

2008

Neuroscience & Biobehavioral Reviews

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Alzheimer's disease (AD) is the leading cause of dementia affecting over 25 million people worldwide. Classical studies focused on the description and characterization of the pathological hallmarks found in AD patients including the neurofibrillary tangles and the amyloid plaques. Current strategies focus on the etiology of these hallmarks and the different mechanisms contributing to neurodegeneration. Among them, recent studies reveal the close interplay between the immunological and the neurodegenerative processes. This article examines the implications of the alpha7 nicotinic acetylcholine receptor (alpha7nAChR) as a critical link between inflammation and neurodegeneration in AD. Alpha7nAChRs are not only expressed in neurons but also in Glia cells where they can modulate the immunological responses contributing to AD. Successful therapeutic strategies against AD should consider the connections between inflammation and neurodegeneration. Among them, alpha7nAChR may represent a pharmacological target to control these two mechanisms during the pathogenesis of neurodegenerative and behavioral disorders.

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“…P50 inhibition also improved. More detailed information on this area is available in several recent reviews (Levin, 2002;Martin et al, 2004;Potter et al, 2006).…”

Section: Alpha7nachr and Information Processingmentioning

confidence: 99%

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Conejero-Goldberg

Davies

Ulloa

2008

Neuroscience & Biobehavioral Reviews

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“…Three studies investigated differential psychopharmacological effects with measures of central inhibition or gating: prepulse inhibition (PPI) of the acoustic startle response and suppression of the P50 event-related potential in a condition-test paradigm (P50 gating) (Csomor et al 2008;Knott et al 2010;Vollenweider et al 2006). Both gating processes provide the individual with the ability to negotiate a sensory-laden environment by blocking out excess or trivial stimuli so that an individual can focus attention on the most salient aspects of the stimulusladen environment (Braff et al 2001;Potter et al 2006). Vollenweider et al (2006) demonstrated that the antipsychotic clozapine significantly increased PPI levels in low PPI performers but showed no effect in high PPI performers.…”

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confidence: 99%

Nicotine differentially modulates antisaccade performance in healthy male non-smoking volunteers stratified for low and high accuracy

et al. 2011

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RATIONALE: Nicotinergic agents are currently examined as possible pro-cognitive drugs for a variety of clinical conditions marked by cognitive deficits, such as attention deficit hyperactivity disorder (ADHD) or schizophrenia. The response to acute nicotine is heterogeneous across subjects and samples; however, only a few reliable predictors of response have been identified. OBJECTIVES: We tested the hypothesis that baseline performance level in cognitive control may be a predictor of the cognitive effects of nicotine. METHODS: We tested 28 healthy Caucasian, male, non-smoking volunteers with the antisaccade task, an oculomotor measure of cognitive control. Participants were given a 7-mg nicotine patch in a double-blind, placebo-controlled, counterbalanced, within-subjects design. Subjects were stratified into high and low performers based on their antisaccade error rate in the placebo condition (median split). RESULTS: Nicotine tended to reduce response time variability of prosaccade latency (p = 0.06). There was no main effect of nicotine on antisaccade error rate (p = 0.31). However, nicotine significantly reduced antisaccade error rate in the low-accuracy probands while leaving performance of the high-accuracy probands unaffected (interaction, p < 0.05). Furthermore, we found a nicotine-induced reduction of response time variability of antisaccade latency at one target location in the low-performing group (interaction, p < 0.05). CONCLUSIONS: The present results demonstrate the importance of baseline performance differences for the effectiveness of pharmacological enhancement of cognitive control. More generally, the results suggest that stimulation of the nicotinic acetylcholine receptor system might be an effective way of improving cognition in people with poor cognitive performance, such as patients with ADHD or schizophrenia. AbstractRationale: Nicotinergic agents are currently being examined as possible pro-cognitive drugs for a variety of clinical conditions marked by cognitive deficits, such as attention deficit hyperactivity disorder (ADHD) or schizophrenia. The response to acute nicotine is heterogeneous across subjects and samples; however, only few reliable predictors of response have been identified. Objectives:We tested the hypothesis that baseline performance level in cognitive control may be a predictor of the cognitive effects of nicotine. Methods: We tested 28 healthy Caucasian, male, non-smoking volunteers with the antisaccade task, an oculomotor measure of cognitive control.Participants were given a 7-mg nicotine patch in a double-blind, placebo-controlled, counterbalanced, within-subjects design. Subjects were stratified into high and low performers based on their antisaccade error rate in the placebo condition (median-split). Results: Nicotine tended to reduce response time variability of prosaccade latency (p=0.06). There was no main effect of nicotine on antisaccade error rate (p=0.31). However, nicotine significantly reduced antisaccade error rate in the low accuracy proban...

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“…This is said to be indicative of sensory gating: cerebral activity is maintained towards the first stimulus until neurological processing of it has been completed. Potter et al (2006) also describe sensory gating as "…the pre-attentional habituation of responses to repeated exposure to the same sensory stimulus." The fact that both people who suffer from schizophrenia and their first-degree relatives show a lack of pre-pulse inhibition demonstrates a possible liability to this illness.…”

Section: Sensory Gating In Schizophreniamentioning

confidence: 99%

Nicotine and symptoms of schizophrenia: the 2017 picture

Conway¹

2017

MRAJ

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The tendency of people who suffer with schizophrenia to consume large amounts of cigarettes and to extract more nicotine from these cigarettes is well-known. A sizeable body of work investigating this has concluded that smoking in people with schizophrenia improves the dysfunctional sensory gating intrinsic to this disease. This has been recognised at least since the late 1980s. Consequently, the pro-cognitive effect of nicotine is now well-recognised and has led to the investigation of nicotinic receptor modulators as potential treatments for schizophrenia. Particular interest has focused on the treatment of negative symptoms in this illness. While there is a solid theoretical basis for this line of drug development, in practice, later-stage drug trials of compounds such as TC-5619 (bradanicline) in Phase 2 and EVP-6124 (encenicline) in Phase 3 have been disappointing. Numerous intolerable side-effects have been important in limiting the clinical use of such compounds. It is conceivable that the reason for intolerable side-effects might be a consequence of the wide distribution of nicotinic cholinergic receptors: α 7 nicotinic receptors are found in several cerebral areas, in the spleen and in lymphocytes at lymph nodes.Later-stage drug development trials which reveal insurmountable administration problems are perhaps indicative of the great practical distance between theoretical recognition of a potential therapeutic agent and its eventual translational appearance in the armory against an illness. Given that this is the case it may still be worthwhile to look at the simple administration of exogenous nicotine via e-cigarettes or chewing-gum as an adjunctive agent in the treatment of schizophrenia in the interim. More prosaically, the banning of smoking in many hospital premises in the UK has led to a difficulty in the practical management of acutely ill people with schizophrenia in the in-patient setting. In a group of people who are profoundly psychiatrically unwell, and often physically compromised to some degree because of their cigarette consumption, alternative management techniques for the latter must be explored. Use of exogenous nicotine replacement in a less harmful delivery manner than cigarettes in a group of people who have a clear physiological reason for smoking -i.e. to increase their deficient endogenous cerebral nicotine levels -is worthwhile to investigate. Very recent work in exactly this direction has been undertaken. Nursing management of such patients may be greatly improved as a result, as may their on-going engagement with the therapeutic team. Here is an illustration of how theoretical considerations eventually come to have a pragmatic consequence in the day-to-day management of people with severe and enduring mental illnesses like schizophrenia.

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Review of Clinical Correlates of P50 Sensory Gating Abnormalities in Patients with Schizophrenia

Cited by 243 publications

References 58 publications

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Alpha7 nicotinic acetylcholine receptor: A link between inflammation and neurodegeneration

Nicotine differentially modulates antisaccade performance in healthy male non-smoking volunteers stratified for low and high accuracy

Nicotine and symptoms of schizophrenia: the 2017 picture

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