Phencyclidine-Induced Cognitive Deficits in Mice Are Improved by Subsequent Subchronic Administration of the Novel Selective α7 Nicotinic Receptor Agonist SSR180711

Hashimoto, Kenji; Ishima, Tamaki; Fujita, Yūkō; Matsuo, Masaaki; Kobashi, Tatsuhiro; Takahagi, Makoto; Tsukada, Hideo; Iyo, Masaomi

doi:10.1016/j.biopsych.2007.04.034

Cited by 104 publications

(82 citation statements)

References 43 publications

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“…We show that SSR180711 was able to alleviate abnormally persistent LI produced by acute MK801 and neonatal NOS blockade; these models are believed to model cognitive aspects of schizophrenia and the activity here was consistent with previous findings with a7-nAChR agonists (Arendash et al, 1995;Hashimoto et al, 2008;Levin et al, 1999;Meyer et al, 1998;Olincy and Stevens, 2007;Pichat et al, 2007;Timmermann et al, 2007;Wishka et al, 2006). Rather unexpectedly SSR180711 potentiated LI in normal rats and reversed amphetamine-induced LI disruption, two models considered predictive of activity against positive symptoms of schizophrenia (Gray et al, 1991;Kilts, 2001;Lipska, 2004;Lipska and Weinberger, 2000;Moser et al, 2000;Powell and Miyakawa, 2006;Smith et al, 2007;Weiner, 1990Weiner, , 2003 .…”

Section: Discussionsupporting

confidence: 78%

“…Reversal of MK801-induced persistent LI by SSR180711 is consistent with previous findings that this agent reversed cognitive deficits induced by the administration of the NMDA antagonists MK801 and phencyclidine (PCP), in mice and rats (Hashimoto et al, 2008;Pichat et al, 2007). It is also in line with the efficacy of other nicotinic agonists in antagonizing the behavioral effects of NMDA blockade (Mastropaolo et al, 2004;Rezvani and Levin, 2003;Tizabi et al, 1998), although nicotine failed to reverse PCP-induced deficit in prepulse inhibition (PPI), a model of impaired sensorimotor gating in schizophrenia (Suemaru et al, 2004), and augmented MK801-induced impairment of PPI (Levin et al, 2005).…”

Section: Reversal Of Abnormally Persistent Li: Putative Efficacy For supporting

confidence: 78%

“…MK801-induced attentional perseveration is reversed by atypical APDs and glycinergic NMDA-enhancers but not typical APDs (Black et al, 2008;GaislerSalomon et al, 2008;Gaisler-Salomon and Weiner, 2003;Lipina et al, 2005), consistent with the differential efficacy of these treatments for negative/cognitive symptoms (Harvey et al, 2005;Heresco-Levy et al, 2005). As SSR180711 was shown to reverse NMDA blockade-induced cognitive deficits (impaired novelty discrimination and object recognition as well as memory deficits in the Morris water maze; Hashimoto et al, 2008;Pichat et al, 2007) here we expected that it would reverse MK801-induced persistent LI.…”

Section: Introductionmentioning

confidence: 62%

“…a7 agonists have been shown to improve performance in various cognitive tasks in rodents, including one-way active avoidance, 8 or 17-arm radial maze, Morris water maze, object recognition and social recognition (Arendash et al, 1995;Hashimoto et al, 2008;Kem, 2000;Levin et al, 1999;Pichat et al, 2007;Timmermann et al, 2007;Van Kampen et al, 2004;Wishka et al, 2006). The dual effect of SSR180711 exerted on disrupted and persistent LI is particularly remarkable in that in terms of effects on performance, the drug influenced the pre-exposed MK801 and neonatal L-NoArg groups in opposite direction from that of the pre-exposed amphetamine group, namely, improved conditioning in the former and impaired conditioning in the latter.…”

Section: Ssr180711-behavioral and Psychological Profilementioning

confidence: 99%

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Pro-Cognitive and Antipsychotic Efficacy of the α7 Nicotinic Partial Agonist SSR180711 in Pharmacological and Neurodevelopmental Latent Inhibition Models of Schizophrenia

Barak

Arad

Levie

et al. 2009

Neuropsychopharmacol

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Schizophrenia symptoms can be segregated into positive, negative and cognitive, which exhibit differential sensitivity to drug treatments. Accumulating evidence points to efficacy of a7 nicotinic receptor (nAChR) agonists for cognitive deficits in schizophrenia but their activity against positive symptoms is thought to be minimal. The present study examined potential pro-cognitive and antipsychotic activity of the novel selective a7 nAChR partial agonist SSR180711 using the latent inhibition (LI) model. LI is the reduced efficacy of a previously nonreinforced stimulus to gain behavioral control when paired with reinforcement, compared with a novel stimulus. Here, no-drug controls displayed LI if non-reinforced pre-exposure to a tone was followed by weak but not strong conditioning (2 vs 5 tone-shock pairings). MK801 (0.05 mg/kg, i.p.) -treated rats as well as rats neonatally treated with nitric oxide synthase inhibitor L-NoArg (10 mg/kg, s.c.) on postnatal days 4-5, persisted in displaying LI with strong conditioning, whereas amphetamine (1 mg/kg) -treated rats failed to show LI with weak conditioning. SSR180711 (0.3, 1, 3 mg/kg, i.p.) was able to alleviate abnormally persistent LI produced by acute MK801 and neonatal L-NoArg; these models are believed to model cognitive aspects of schizophrenia and activity here was consistent with previous findings with a7-nAChR agonists. In addition, unexpectedly, SSR180711 (1, 3 mg/kg, i.p.) potentiated LI with strong conditioning in nodrug controls and reversed amphetamine-induced LI disruption, two effects considered predictive of activity against positive symptoms of schizophrenia. These findings suggest that SSR180711 may be beneficial not only for the treatment of cognitive symptoms in schizophrenia, as reported multiple times previously, but also positive symptoms.

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Section: Discussionsupporting

confidence: 78%

Section: Reversal Of Abnormally Persistent Li: Putative Efficacy For supporting

confidence: 78%

Section: Introductionmentioning

confidence: 62%

Section: Ssr180711-behavioral and Psychological Profilementioning

confidence: 99%

See 2 more Smart Citations

Pro-Cognitive and Antipsychotic Efficacy of the α7 Nicotinic Partial Agonist SSR180711 in Pharmacological and Neurodevelopmental Latent Inhibition Models of Schizophrenia

Barak

Arad

Levie

et al. 2009

Neuropsychopharmacol

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“…Indicating complex alterations of the cholinergic system, rodent schizophrenia models revealed reduced a 7 -nAChreceptor (nAChR) expression levels and an increased release of acetylcholine (Hashimoto et al, 2008a;Nelson et al, 2002). Accordingly, postmortem studies and pharmacological challenges have reported further evidence of decreased expression levels of a 7 -nAChR in patients with schizophrenia (D'Souza and Markou, 2012;Martin-Ruiz et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Smoking Restores Impaired LTD-Like Plasticity in Schizophrenia: a Transcranial Direct Current Stimulation Study

Strube

Bunse

Nitsche

et al. 2014

Neuropsychopharmacol

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Impaired neuroplastic responses following noninvasive brain stimulation have been reported repeatedly in schizophrenia patients. These findings have been associated with deficits in GABAergic, glutamatergic, and cholinergic neurotransmission. Although various neurophysiological studies have indicated a relationship between nicotine and neuroplasticity in healthy individuals, the present study is the first investigation into the impact of nicotine on LTD-like plasticity in patients with schizophrenia. Cortical excitability and cortical plasticity were explored in 30 schizophrenia patients (17 smoker, 13 nonsmoker) and 45 healthy controls (13 smoker, 32 nonsmoker) by using single-pulse transcranial magnetic stimulation (TMS) before and following cathodal transcranial direct current stimulation (tDCS) applied to the left primary motor cortex. Our analysis revealed abolished LTD-like plasticity in nonsmoking schizophrenia patients. However, these plasticity deficits were not present in smoking schizophrenia patients. In healthy controls, significant MEP reductions following cathodal tDCS were observed in nonsmoking individuals, but only trend-level reductions in smokers. In smoking schizophrenia patients, the severity of negative symptoms correlated positively with reduced neuroplasticity, whereas nonsmoking patients displayed the opposite effect. Taken together, the data of our study support the notion of an association between chronic smoking and the restitution of impaired LTD-like plasticity in schizophrenia patients. Although replication and further research are needed to better understand this relationship, our findings indicate that nicotine intake might stabilize the impaired inhibition-facilitation balance in the schizophrenic brain through a complex interaction between cortical plasticity, and GABAergic and cholinergic neurotransmission, and might explain the reduced prevalence of negative symptoms in this population.

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α7 Nicotinic Acetylcholine Receptors in the Treatment of Schizophrenia

Hajós¹,

Rogers²

2012

Targets and Emerging Therapies for Schizophrenia

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Phencyclidine-Induced Cognitive Deficits in Mice Are Improved by Subsequent Subchronic Administration of the Novel Selective α7 Nicotinic Receptor Agonist SSR180711

Cited by 104 publications

References 43 publications

Pro-Cognitive and Antipsychotic Efficacy of the α7 Nicotinic Partial Agonist SSR180711 in Pharmacological and Neurodevelopmental Latent Inhibition Models of Schizophrenia

Pro-Cognitive and Antipsychotic Efficacy of the α7 Nicotinic Partial Agonist SSR180711 in Pharmacological and Neurodevelopmental Latent Inhibition Models of Schizophrenia

Smoking Restores Impaired LTD-Like Plasticity in Schizophrenia: a Transcranial Direct Current Stimulation Study

α7 Nicotinic Acetylcholine Receptors in the Treatment of Schizophrenia

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