清水 栄司

BACKGROUND: The Obsessive-Compulsive Inventory (OCI) was designed to evaluate the severity of obsessive-compulsive symptoms in both clinical and non-clinical samples. The aim of the study was to develop a Japanese version of this scale (OCI-J) and validate it in both non-clinical and clinical Japanese samples. FINDINGS: In Study 1, the OCI-J, the Maudsley Obsessional Compulsive Inventory (MOCI), and measures of anxiety and depression were administered to 150 undergraduate students (non-clinical sample) in order to investigate the internal consistency and convergent validity of the OCI-J. Furthermore, 118 non-clinical participants completed the OCI-J after a 2-week interval to determine the test-retest reliability. In Study 2, OCD participants (n = 35), anxiety control participants with panic disorder (n = 22), and healthy control participants (n = 37) completed the OCI-J in order to test its clinical discrimination ability.Correlational analysis indicated moderate to high correlations between the subscales and total scores of the OCI-J and MOCI. In addition, the OCI-J and its subscales demonstrated satisfactory test-retest reliabilities. Finally, the OCI-J showed good clinical discrimination for patients with OCD from healthy and anxiety controls. CONCLUSIONS: The OCI-J is a valid and reliable instrument for measuring OCD symptoms in both clinical and non-clinical samples of Japanese.

Background: The psychological impact of dual-disasters (earthquakes and a nuclear accident), on affected communities is unknown. This study investigated the impact of a dual-disaster (earthquakes and radioactive contamination) on the prevalence of psychological distress in a landlocked city within the Tohoku area, Japan. Methods. A cross-sectional mail-in survey with a random sample of inhabitants from Ichinoseki city was conducted eleven months after the disasters, and data from 902 respondents were analyzed by logistic regression models, with multiple imputation methodology. The K6 was used to determine psychological distress. Results: The estimated prevalence of psychological distress was 48.0 percent. House damage due to earthquakes and anxiety about radioactive contamination were significantly associated with psychological distress (p &lt 0.05), while an interactive effect between house damage and anxiety about radioactive contamination was not significant. Being female, middle-to-low educational status and unemployed were additional risk factors for psychological distress. Conclusions: This dual-disaster was associated with a moderate prevalence of psychological distress in the area. The impact of the earthquake and radioactive contamination appeared additive. © 2014Niitsu et al. licensee BioMed Central Ltd.

Objective: Dopamine supersensitivity psychosis (DSP) is considered to be one cause of treatment-resistant schizophrenia (TRS). The authors investigated the efficacy of risperidone long-acting injections (RLAI) in patients with TRS and DSP. Method: This is a multicenter, prospective, 12-month follow-up, observational study that included unstable and severe TRS patients with and without DSP. 115 patients with TRS were recruited and divided into two groups according to the presence or absence of DSP which was judged on the basis of the clinical courses and neurological examinations. RLAI was administered adjunctively once every 2 weeks along with oral antipsychotics. We observed changes in scores for the Brief Psychiatric Rating Scales (BPRS), Clinical Global Impression-Severity of Illness (CGI-S), Global Assessment of Functioning Scale (GAF), and Extrapyramidal Symptom Rating Scale (ESRS) during the study. Of the assessed 94 patients, 61 and 33 were categorized into the DSP and NonDSP groups, respectively. Results: While baseline BPRS total scores, CGI-S scores and GAF scores did not differ, the ESRS score was significantly higher in the DSP group compared with the NonDSP group. Treatment significantly reduced BPRS total scores and CGI-S scores, and increased GAF scores in both groups, but the magnitudes of change were significantly greater in the DSP group relative to the NonDSP group. ESRS scores were also reduced in the DSP group. Responder rates (>= 20% reduction in BPRS total score) were 62.3% in the DSP group and 21.2% in the NonDSP group. Conclusions: It is suggested that DSP contributes to the etiology of TRS. Atypical antipsychotic drugs in long-acting forms, such as RLAI, can provide beneficial effects for patients with DSP. Clinical trials registration: UMIN (UMIN000008487). (C) 2014 The Authors. Published by Elsevier B.V.

A meta-analysis study reported serum brain-derived neurotrophic factor (BDNF) levels as a potential biomarker for schizophrenia. However, at the time, commercially available human ELISA kits were unable to distinguish between pro-BDNF (precursor BDNF) and mature BDNF, because of limited antibody specificity. Here, we used new ELISA kits, to examine serum levels of mature BDNF and matrix metalloproteinase-9 (MMP-9), which converts pro-BDNF to mature BDNF in schizophrenia. Sixty-three patients with chronic schizophrenia and 52 age- and sex-matched healthy controls were enrolled. Patients were evaluated using the Brief Psychiatry Rating Scale, the Scale for the Assessment of Negative Symptoms (SANS) and neuropsychological tests. Neither serum mature BDNF nor MMP-9 levels differed between patients and controls. In male subgroups, serum MMP-9 levels of smoking patients were higher than those of non-smoking patients, but this was not observed in male controls or the female subgroup. In patients, serum mature BDNF levels were associated with SANS total scores and the Information subtest scores of the Wechsler Adult Intelligence Scale Revised (WAIS-R), while serum MMP-9 levels were associated with smoking and category fluency scores. These findings suggest that neither mature BDNF nor MMP-9 is a suitable biomarker for schizophrenia, although further studies using large samples are needed. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

日本不安障害学会では，日本精神神経学会精神科用語検討委員会（日本精神神経学会，日本うつ病学会，日本精神科診断学会と連携した，精神科病名検討連絡会）からの依頼を受け，不安障害病名検討ワーキング・グループを組織し，DSM-5のドラフトから，不安障害に関連したカテゴリーの翻訳病名（案）を作成いたしました。<br/>ご存知のように，厚生労働省は，地域医療の基本方針となる医療計画に盛り込むべき疾病として指定してきた，がん，脳卒中，急性心筋梗塞，糖尿病の四大疾病に，新たに精神疾患を加えて「五大疾病」とする方針を決め，多くの都道府県で2013年度以降の医療計画に反映される予定です。<br/>精神疾患に関しては，「統合失調症」や「認知症」のように，common diseasesとして，人口に膾炙するような，馴染みやすい新病名への変更が行われてきております。うつ病も，「大うつ病性障害」という病名ではなく，「うつ病」という言葉で，社会に広く認知されております。<br/>そこで，DSM-5への変更を機に，従来の「不安障害」という旧病名を，「不安症」という新名称に変更したいと考えております。従来診断名である，「不安神経症」から，「神経」をとって，「不安症」となって短縮されているので，一般に馴染みやすいと考えます。ただし，日本精神神経学会での移行期間を考え，カッコ書きで，旧病名を併記する病名変更「不安症（不安障害）」とすることを検討しております。<br/>そのほかにもDSM-5になって変更追加された病名もあるため，翻訳病名（案）（PDFファイル）を作成しました。翻訳病名（案）については，今後も，日本精神神経学会精神科用語検討委員会の中での話し合いが進められていく予定です。どうぞよろしくお願い申し上げます。

Background and objectives: Mental contamination is the experience of feelings of dirtiness without direct physical contact with a contaminant. Imagining a non-consensual kiss from an immoral man (Dirty Kiss task) can evoke feelings of mental contamination in non-clinical female participants. We investigated whether feelings of mental contamination evoked by the Dirty Kiss task are reduced by washing behaviours. Methods: Forty-eight female participants were split into two groups: washing (n=24; asked to wash their hands and mouth after the Dirty Kiss task) and non-washing (n=24; asked to wait without engaging in any behaviour after the Dirty Kiss task). Indices of mental contamination were administered before, immediately after, 5 min after, and 20 min after the task. Results: Mental contamination scores did not significantly differ between the groups at any point. However, in both groups, scores immediately after the Dirty Kiss task were significantly higher than those 5 or 20 min later. Limitations: The long-term effects of washing behaviour on mental contamination were not clarified. Conclusions: Mental contamination can be reduced by washing behaviour, although no more effectively than waiting without washing. (C) 2013 Elsevier Ltd. All rights reserved.

Brain metabolite concentrations change dynamically throughout development, especially during early childhood. The purpose of this study was to investigate the brain metabolite concentrations of neonates (postconceptional age (PCA): 30 to 43 weeks) using single-voxel magnetic resonance spectroscopy (MRS) and to discuss the relationships between the changes in the concentrations of such metabolites and brain development during the neonatal period. A total of 83 neonatal subjects were included using the following criteria: the neonates had to be free of radiological abnormalities, organic illness, and neurological symptoms; the MR spectra had to have signal-to-noise ratios &gt;= 4; and the estimated metabolite concentrations had to display Cramer-Rao lower bounds of &lt;= 30%. MRS data (echo time/repetition time, 30/5000 ms; 3T) were acquired from the basal ganglia (BG), centrum semiovale (CS), and the cerebellum. The concentrations of five metabolites were measured: creatine, choline, N-acetylaspartate, myo-inositol, and glutamate/glutamine complex (Glx). One hundred and eighty-four MR spectra were obtained (83 BG, 77 CS, and 24 cerebellum spectra). Creatine, N-acetylaspartate, and Glx displayed increases in their concentrations with PCA. Choline was not correlated with PCA in any region. As for myo-inositol, its concentration decreased with PCA in the BG, whereas it increased with PCA in the cerebellum. Quantitative brain metabolite concentrations and their changes during the neonatal period were assessed. Although the observed changes were partly similar to those detected in previous reports, our results are with more subjects (n = 83), and higher magnetic field (3T). The metabolite concentrations examined in this study and their changes are clinically useful indices of neonatal brain development.

Cognitive behaviour therapy (CBT) is widely regarded as an effective treatment for social anxiety disorder (SAD) in Europe and North America. The theoretical orientations underlying CBT models and treatment interventions developed in Western cultures were typically constrained by Western conceptualizations of SAD. This case study reports on the use of CBT for Japanese SAD, demonstrating the successful implementation of cognitive techniques grounded in the Clark &amp Wells model. The patient was a Japanese female with excessively high standards for workplace social performance. Therapy mainly comprised case formulation, behavioural experiments, and opinion surveying based on the Clark &amp Wells model. These techniques allowed the patient to reduce the strength of maladaptive cognitions and lower her excessively high standards for social performance. CBT treatment using the Clark &amp Wells model was effective and suitable for Japanese SAD, at least in the present case. We also discuss the cross-cultural differences of SAD and adaptation of CBT.

Perinatal exposure to bisphenol A (BPA), an endocrine-disrupting chemical, affects the central nervous system, including effects on emotional responses and neurotransmitter release. In this study, we investigated the effects of BPA (250 ng/kg/day, from gestational day 10 to postnatal day 20) on fear memory and serotonin (5-HT) metabolites in the brain using contextual fear conditioning (FC) and high-performance liquid chromatography (HPLC), respectively, in adult and juvenile mice of both sexes. Furthermore, we studied the effects of BPA on the gene expression of 5-HT metabolite-related enzymes and 5-HT receptors using quantitative real-time RT PCR in the brains of juvenile females. BPA enhanced fear memory and increased serotonin metabolite (5-HIAA) levels and 5-HIAA/5-HT in the hippocampus, the striatum, the midbrain, the pons, and the medulla oblongata of juvenile female mice. In contrast, alterations in those areas were much smaller in adult females and in both juvenile and adult males. Furthermore, BPA induced increases in the expression levels of Tph2, Slc6a4, and Maoa mRNA in the hippocampus of juvenile females, indicating that BPA induces hyper 5-HT turnover in the hippocampus. Our results suggest that perinatal exposure to a low dose of BPA enhances fear memory and the 5-HTergic system in juvenile mice. (C) 2013 Elsevier Inc. All rights reserved.

Background: Trainings of the kneeling position, such as standing exercise on the knees and kneeling gait, have been anecdotally used in physical therapy to improve postural control of patients with various pathological conditions. However, clinical evidence is lacking and the movement characteristics of these kneeling trainings have not been well explored. The purpose of this study is to clarify the movement characteristics of the kneeling gait compared with the normal gait. Methods: Twenty healthy volunteers (10 men and 10 women) aged 22-34 years were recruited. Participants were required to perform the kneeling gait and the normal gait at a self-selected comfortable speed on the treadmill. Surface electromyograms (EMG) and center of mass (COM) displacements were measured during each task. Results: The EMGs of the gait-related proximal muscles during the kneeling gait were greater than during the normal gait, even at a comfortable speed. The COM displacement to the lateral direction was longer during the kneeling gait than it was during the normal gait. Furthermore, mechanical energy efficiency during the kneeling gait was less than that during the normal gait. Conclusion: The results suggest that the kneeling gait is an effective exercise to strengthen the gait-related proximal muscles. The increased muscle activities during the kneeling gait were probably due to the compensatory movements of the trunk and the pelvis. © 2012 Elsevier B.V.

Objective: The aim of this study is to clarify the symptomatology of the eating disorders examining the prefrontal function and activity associated with self-regulation among participants with or without eating disorders. Methods: Ten patients with anorexia nervosa, fourteen with bulimia nervosa, and fourteen healthy control participants performed two cognitive tasks assessing self-regulatory functions, an auditorily distracted word fluency task and a rock-paper-scissors task under the measurements on prefrontal oxyhemoglobin concentration with near infrared spectroscopy. The psychiatric symptoms of patient groups were assessed with several questionnaires. Results: Patients with bulimia nervosa showed decreased performances and prefrontal hyper activation patterns. Prefrontal activities showed a moderate negative correlation with task performances not in the patient groups but only in the healthy participants. The prefrontal activities of the patient groups showed positive correlations with some symptom scale aspects. Conclusions: The decreased cognitive abilities and characteristic prefrontal activation patterns associated with self-regulatory functions were shown in patients with bulimia nervosa, which correlated with their symptoms. These findings suggest inefficient prefrontal self-regulatory function of bulimia nervosa that associate with its symptoms.

BACKGROUND: Cognitive behavior therapy (CBT) is regarded as an effective treatment for social anxiety disorder (SAD) in Europe and North America. Individual CBT might be acceptable and effective for patients with SAD even in non-Western cultures; therefore, we conducted a feasibility study of individual CBT for SAD in Japanese clinical settings. We also examined the baseline predictors of outcomes associated with receiving CBT. METHODS: This single-arm trial employed a 14-week individual CBT intervention. The primary outcome was the self-rated Liebowitz Social Anxiety Scale, with secondary measurements of other social anxiety and depressive severity. Assessments were conducted at baseline, after a waiting period before CBT, during CBT, and after CBT. RESULTS: Of the 19 subjects screened, 15 were eligible for the study and completed the outcome measures at all assessment points. Receiving CBT led to significant improvements in primary and secondary SAD severity (ps < .001). The mean total score on the Liebowitz Social Anxiety Scale improved from 91.8 to 51.7 (before CBT to after CBT), and the within-group effect size at the end-point assessment was large (Cohen's d = 1.71). After CBT, 73% of participants were judged to be treatment responders, and 40% met the criteria for remission. We found no significant baseline predictors of those outcomes. CONCLUSION: Despite several limitations, our treatment-which comprises a 14-week, individual CBT program-seems feasible and may achieve favorable treatment outcomes for SAD in Japanese clinical settings. Further controlled trials are required in order to address the limitations of this study. TRIAL REGISTRATION: UMIN-CTR UMIN000005897.

40代女。主診断は強迫性障害(OCD)で、併存疾患にうつ病があった。認知行動療法(CBT)を週1回、50分のペースで行った。併用した薬物療法は継続して行った。セッションの初期では、不快な雑念や行動を軽減するための対処法としてMP法を用いた行動活性化を実施した。中期では危機の理論と心配の理論の比較を行い、脅威的解釈に介入を行った。後期では、曝露反応妨害法(ERP)が実施された。症例の症状はセッションを経るごとに軽減された。ERPでは「題名が思い出せない音楽をセッション内で聴いてもらい、その題名を調べないで次のセッションまで過ごす」という課題を実施し、難なく遂行することができた。

Deficit syndrome, which is characterized by primary and enduring negative symptoms, is a homogeneous subtype within schizophrenia. Negative symptoms in schizophrenia are currently considered to be closely linked with frontal lobe impairment. However, the etiology in the frontal lobe of people with deficit syndrome is not fully understood. We measured regional cerebral blood flow (rCBF) with single photon emission computed tomography (SPECT) in 33 patients with deficit syndrome, 40 patients with nondeficit syndrome, and 45 healthy controls, and we compared groups using the voxel-wise method. Schizophrenia combined group, the deficit syndrome and the nondeficit syndrome presented hypoperfusion in mainly the medial and lateral prefrontal cortices. The deficit syndrome group showed a significant decrease in rCBF in the right orbitofrontal cortex (OFC) compared to the nondeficit group. These results demonstrated that at-rest hypofrontality was a common feature within the disease group and suggested that the OFC might play an important role in the development of severe negative symptoms in people with deficit syndrome. (C) 2012 Elsevier B. V. All rights reserved.

内科系学会社会保険連合（略称：内保連）は，加盟する118の内科系学会から構成され，提示される学術的根拠に基づき， 社会保険医療の在り方を提言し，その診療報酬の適正化を促進することを目的とした組織です。日本不安障害学会は，平成25（2013）年5月，内保連への加盟が承認されました。また，不安障害の認知行動療法の医療保険点数化を目指し，内保連に，以下のような平成26年度診療報酬改定提案書を提出いたしました。6月には，内保連の精神科関連委員会，心身医学関連委員会のヒアリングを受けまして，8月には厚生労働省からのヒアリングが予定されております。日本総合病院精神医学会からも，趣旨にご賛同いただき，共同提案としていただきました。また，日本トラウマティックストレス学会にもご支援をお願いいたしております。平成26年度改定をめざし，不安障害の認知行動療法の医療保険点数化を推進していきたいと思いますので，会員の先生方におかれましては，ご支援のほど，どうぞよろしくお願い申し上げます。

INTRODUCTION: Pharmacotherapy and cognitive behavioural therapy (CBT) are consistently effective as first-line treatments for social anxiety disorders (SADs). Nevertheless, pharmacotherapy is often the first choice in clinical practice. In many countries, the first line of pharmacotherapy involves the administration of a selective serotonin reuptake inhibitor (SSRI). Although a significant proportion of patients with SAD fail to respond to the initial SSRI administration, there is no standard approach to the management of SSRI-resistant SAD. This paper describes the study protocol for a randomised controlled trial to evaluate the clinical effectiveness of CBT as a next-step strategy, concomitant with conventional treatment, for patients with SSRI-resistant SAD. METHODS AND ANALYSIS: This Prospective Randomized Open Blinded End-point study is designed with two parallel groups, with dynamic allocation at the individual level. The interventions for the two groups are conventional treatment, alone, and CBT combined with conventional treatment, for 16 weeks. The primary end-point of SAD severity will be assessed by an independent assessor using the Liebowitz Social Anxiety Scale, and secondary end-points include severity of other social anxieties, depressive severity and functional impairment. All measures will be assessed at weeks 0 (baseline), 8 (halfway point) and 16 (postintervention) and the outcomes will be analysed based on the intent-to-treat. Statistical analyses are planned for the study design stage so that field materials can be appropriately designed. ETHICS AND DISSEMINATION: This study will be conducted at the academic outpatient clinic of Chiba University Hospital. Ethics approval was granted by the Institutional Review Board of Chiba University Hospital. All participants will be required to provide written informed consent. The trial will be implemented and reported in accordance with the recommendations of CONSORT. CLINICAL TRIAL REGISTRATION NUMBER: UMIN000007552.

Bisphenol A (BPA), an endocrine-disrupting chemical, is widely present in the environment. It has been reported that perinatal exposure to low doses of BPA that are less than the tolerable daily intake level (50 mu g/kg/day) affects anxiety-like behavior and dopamine levels in the brain. Although the dopaminergic system in the brain is considered to be related to anxiety, no study has reported the effects of low-dose BPA exposure on the dopaminergic system in the brain and on anxiety-like behavior using the same methods of BPA exposure. To investigate the relationship between alterations in anxiety-like behavior and changes in the dopaminergic system in the brain induced by BPA, we examined the effects of BPA on anxiety-like behavior using an open field test in juvenile and adult mice and measured DA and DOPAC levels and the DOPAC/DA ratio in the dorsal hippocampus (HIP), amygdala (AMY), and medulla oblongata (MED) using high-performance liquid chromatography (HPLC) in adult mice. In males, BPA decreased the time spent in the center area of the open field in both juveniles and adults. In addition, BPA increased DA levels in the dorsal HIP and MED and decreased the DOPAC/DA ratio in the dorsal HIP, AMY, and MED in adults. The activity of monoamine oxidase (MAO)-B, the enzyme that metabolizes DA into DOPAC, was reduced in the MED. In females, those changes were not observed. These results suggest that an increase in anxiety-like behavior induced by perinatal exposure to BPA may be related to decreases in DA metabolites in the brain, and there are sex differences in those BPA effects. (C) 2012 Elsevier Inc. All rights reserved.

Midkine (MK) is strongly expressed during the midgestation period of embryogenesis, while its expression is nearly undetectable in the normal adult brain. However, recent evidences suggest that MK may play various roles in the pathological phenomena of the adult brain. MK binds strongly to Abeta peptides and neutralizes its cytotoxic activity. The findings about elevated MK levels in brain and serum of patients with Alzheimer disease (AD) suggest that MK may be induced to counteract Abeta-related pathophysiology in AD. On the other hand, MK was found to promote the survival of mouse mesencephalic (mainly dopaminergic) neurons in culture. Midkine-deficient (Mdk(-/-)) mice transiently exhibited a delay in postnatal hippocampal development with a working memory deficit and increased anxiety only at the age of 4 weeks. Adult Mdk(-/-) mice exhibited a hypodopaminergic state in the striatum, the prepulse inhibition deficits, and social interaction impairments. These findings suggested that midkine may contribute to the pathophysiology of dopamine-related disorders including schizophrenia and Parkinson's disease.

Panic disorder (PD) is a moderately heritable anxiety disorder whose pathogenesis is not well understood. Due to the lack of power in previous association studies, genes that are truly associated with PD might not be detected. In this study, we conducted a genome-wide association study (GWAS) in two independent data sets using the Affymetrix Mapping 500K Array or Genome-Wide Human SNP Array 6.0. We obtained imputed genotypes for each GWAS and performed a meta-analysis of two GWAS data sets (718 cases and 1717 controls). For follow-up, 12 single-nucleotide polymorphisms (SNPs) were tested in 329 cases and 861 controls. Gene ontology enrichment and candidate gene analyses were conducted using the GWAS or meta-analysis results. We also applied the polygenic score analysis to our two GWAS samples to test the hypothesis of polygenic components contributing to PD. Although genome-wide significant SNPs were not detected in either of the GWAS nor the meta-analysis, suggestive associations were observed in several loci such as BDKRB2 (P = 1.3 x 10(-5), odds ratio = 1.31). Among previous candidate genes, supportive evidence for association of NPY5R with PD was obtained (gene-wise corrected P = 6.4 x 10(-4)). Polygenic scores calculated from weakly associated SNPs (P&lt;0.3 and 0.4) in the discovery sample were significantly associated with PD status in the target sample in both directions (sample I to sample II and vice versa) (P&lt;0.05). Our findings suggest that large sets of common variants of small effects collectively account for risk of PD.

強迫性障害(OCD)患者(20代女性)に曝露反応療法(ERP)を行ったところ、手洗い時間は減少したが、うつ症状が増悪し、ERPの実践が困難な状況に陥った。スーパーバイザーの指導の下、信念を特定する介入によって、うつ症状が改善し、ERPの継続が可能となり改善に至った症例について報告した。症状評価尺度の数値の変化から患者に馴化が十分に生じていないことを把握し、信念を明らかにする介入ができたことで、患者はOCDと信念の関係、およびERPを実践する意義をより良く理解したと思われる。そのことで治療意欲が回復し、ERPに積極的に取り組むことが可能となり、改善に至ったと思われた。

Recently, Monfils et al. [9] and Clem and Huganir [3] have shown that an isolated retrieval trial before the extinction sessions (retrieval-extinction) in mice and rats prevented the renewal and spontaneous recovery of the original fear memory by inhibiting reconsolidation in a hippocampus-independent manner. In contrast, Chan et al. [2], using the same paradigm, reported that retrieval extinction in rats augmented the renewal and reinstatement of extinguished fear. However, it remains unclear whether or not retrieval extinction in a hippocampus-independent paradigm erases the original fear memory by inhibiting reconsolidation. We therefore conducted three experiments to investigate whether or not retrieval extinction erases the original fear memory by inhibiting reconsolidation in mice. Our major findings were as follows. (1) Retrieval-extinction in mice did not suppress spontaneous recovery and fear renewal in a hippocampus-independent paradigm. (2) Fear renewal was observed when retrieval-strong extinction in a hippocampus-independent paradigm was performed. (3) Retrieval extinction in a hippocampus-dependent paradigm did not erase the original fear memory. These results suggested that fear extinction after retrieval in mice does not inhibit reconsolidation of previously consolidated fear memory in either a hippocampus-independent or -dependent paradigm. (C) 2012 Elsevier Ireland Ltd. All rights reserved.