Characterization of clozapine-induced changes in synaptic plasticity in the hippocampal–mPFC pathway of anesthetized rats

Matsumoto, Machiko; Shikanai, Hiroki; Togashi, Hiroko; Izumi, Tohru; Kitta, Takeya; Hirata, Riki; Yamaguchi, Taku; Yoshioka, Mitsuhiro

doi:10.1016/j.brainres.2007.12.010

Cited by 27 publications

(20 citation statements)

References 34 publications

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“…In contrast to the eight studies reported above, two found no effect of the typical antipsychotic haloperidol on LTP (Gemperle et al 2003; Matsumoto et al 2008) and one found that chronic haloperidol enhanced LTP in the absence of magnesium (Centonze et al 2004). In the first of these, rat prelimbic cortex slices were bathed in 0.2 µM haloperidol, causing a reduction in EPSP slope prior to tetanization but no impairment in LTP (Gemperle et al 2003).…”

Section: Antipsychotics and Ltpcontrasting

confidence: 61%

“…In the second study, the intraperitonneal injections of 1 mg/kg haloperidol did not impair LTP in the hippocampus of rabbits (Matsumoto et al 2008). Another research group performing a similar experiment showed a different effect, reporting impaired LTP (Itsuki Jibiki et al 1993).…”

Section: Antipsychotics and Ltpmentioning

confidence: 92%

“…Twelve studies (Abe et al 2009a, 2009b; Centonze et al 2004; Dunwiddie et al 1982; Finn et al 1980; Frey et al 1990; Gemperle et al 2003; Itsuki Jibiki et al 1993; Matsumoto et al 2008; Mody et al 1984; Xu and Yao 2010; Xu et al 2009) have investigated the effects of typical antipsychotics on LTP. Eleven of these studies were performed in wild type animals and under physiologic conditions, and one in slices from the brain of mutant mice lacking the dopamine transporter protein.…”

Section: Antipsychotics and Ltpmentioning

confidence: 99%

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Effects of antipsychotic D2 antagonists on long-term potentiation in animals and implications for human studies

Price

Salavati

Graff‐Guerrero

et al. 2014

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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In people with schizophrenia, cognitive abilities - including memory - are strongly associated with functional outcome. Long-term potentiation (LTP) is a form of neuroplasticity that is believed to be the physiological basis for memory. It has been postulated that antipsychotic medication can impair long-term potentiation and cognition by altering dopaminergic transmission. Thus, a systematic review was performed in order to assess the relationship between antipsychotics and D2 antagonists on long-term potentiation. The majority of studies on LTP and antipsychotics have found that acute administration of antipsychotics was associated with impairments in LTP in wild type animals. In contrast, chronic administration and acute antipsychotics in animal models of schizophrenia were not. Typical and atypical antipsychotics and other D2 antagonists behaved similarly, with the exception of clozapine and olanzapine. Clozapine caused potentiation independent of tetanization, while olanzapine facilitated tetanus-induced potentiation. These studies are limited in their ability to model the effects of antipsychotics in patients with schizophrenia as they were largely performed in wild type animals as opposed to humans with schizophrenia, and assessed after acute rather than chronic treatment. Further studies using patients with schizophrenia receiving chronic antipsychotic treatment are needed to better understand the effects of these medications in this population.

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Section: Antipsychotics and Ltpcontrasting

confidence: 61%

Section: Antipsychotics and Ltpmentioning

confidence: 92%

Section: Antipsychotics and Ltpmentioning

confidence: 99%

See 1 more Smart Citation

Effects of antipsychotic D2 antagonists on long-term potentiation in animals and implications for human studies

Price

Salavati

Graff‐Guerrero

et al. 2014

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…APDs block D2 receptors that are located anteriorly in hippocampus and in highest concentrations in DG, CA1 and subiculum. Additionally, APDs have been shown to alter LTP in hippocampal subfields, through D1 dopamine receptor actions [35, 36], modulating activity dependent plasticity [21]. Activity within the perforant pathway is modulated by dopamine, affecting the integration of perforant pathway and schafer collateral transmission into CA1 [37].…”

Section: Discussionmentioning

confidence: 99%

Learning and Generalization in Schizophrenia: Effects of Disease and Antipsychotic Drug Treatment

Shohamy

Mihalakos

Chin

et al. 2010

Biological Psychiatry

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Background Schizophrenia involves alterations in hippocampal function. The implications of these alterations for memory function in the illness remain poorly understood. Furthermore, it remains unknown how memory is impacted by drug treatments for schizophrenia. The goal of this study was to delineate specific memory processes that are disrupted in schizophrenia and explore how they are affected by medication. We specifically focus on memory generalization - the ability to flexibly generalize memories in novel situations. Methods Individuals with schizophrenia (n=56) and healthy controls (n=20) were tested on a computerized memory generalization paradigm. Participants first engage in trial-by-error associative learning. They are then asked to generalize what they learned by responding to novel stimulus combinations. Individuals with schizophrenia were tested on or off anti-psychotic medication, using a between-subject design that eliminates concerns about learning-set effects. Results Individuals with schizophrenia were selectively impaired in their ability to generalize knowledge, despite having intact learning and memory accuracy. This impairment was found only in individuals tested off medication. Individuals tested on medication generalized almost as well as healthy controls. This between-group difference was selective to memory generalization. Conclusion These findings suggest that individuals with schizophrenia have a selective alteration in the ability to flexibly generalize past experience towards novel learning environments. This alteration is unaccompanied by global memory defect. Additionally, the results indicate a robust generalization difference based on medication status. These results suggest that hippocampal abnormalities in schizophrenia may be alleviated with anti-psychotic medication, with important implications for understanding adaptive memory-guided behavior.

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“…Â 30 mm, Eicom) with electrochemical detection (ECD-300, Eicom), as described previously (Yoshioka et al, 1995;Matsumoto et al, 2005Matsumoto et al, , 2008. The mobile phase, which consisted of 2.1 mM sodium 1-decansulfonate, 0.1 mM EDTA2Na/0.1 M phosphate buffer (pH 6.0), and 1% (v/v) methanol, was pumped at a rate of 1 ml/min.…”

Section: Serotonin and Dopamine Analysismentioning

confidence: 99%

The Serotonergic Projection from the Median Raphe Nucleus to the Ventral Hippocampus is Involved in the Retrieval of Fear Memory Through the Corticotropin-Releasing Factor Type 2 Receptor

Ohmura

Izumi

Yamaguchi

et al. 2010

Neuropsychopharmacol

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Several different studies have separately established that serotonin, corticotropin-releasing factor (CRF) receptors, and the hippocampus are involved in fear memory retrieval. The main aim of this study is to connect these separate studies. To assess the levels of anxiety/fear, we used the contextual fear-conditioning test and the elevated plus maze test as memory-dependent and memory-independent tasks, respectively. We injected CRF receptor antagonists or vehicle into the median raphe nucleus (MRN) 10 min before behavioral tests. As a result, 1000 ng of astressin 2B (CRF 2 receptor antagonist), but not 250 ng of antalarmin (CRF 1 receptor antagonist), significantly suppressed the expression rate of freezing behavior in the contextual fear-conditioning test. However, in the elevated plus maze test, there was no difference between astressin 2B-injected rats and saline-injected rats in the time spent in open arms. Neither the amount of exploratory behavior nor the moving distance in the EPM of astressin 2B-injected rats differed from that of vehicle-injected rats. Moreover, when we assessed the extracellular serotonin release in the ventral hippocampus in freely moving rats through in vivo microdialysis, it was shown that the blockade of the CRF 2 receptor in the MRN suppressed serotonin release in the ventral hippocampus during fear memory retrieval. These results indicated that endogenous CRF and/or related ligands that were released in the MRN could activate the CRF 2 receptor and stimulate serotonin release in the ventral hippocampus, thereby inducing fear memory retrieval.

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Characterization of clozapine-induced changes in synaptic plasticity in the hippocampal–mPFC pathway of anesthetized rats

Cited by 27 publications

References 34 publications

Effects of antipsychotic D2 antagonists on long-term potentiation in animals and implications for human studies

Effects of antipsychotic D2 antagonists on long-term potentiation in animals and implications for human studies

Learning and Generalization in Schizophrenia: Effects of Disease and Antipsychotic Drug Treatment

The Serotonergic Projection from the Median Raphe Nucleus to the Ventral Hippocampus is Involved in the Retrieval of Fear Memory Through the Corticotropin-Releasing Factor Type 2 Receptor

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