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  • 1.
    Azadi, Maryam
    et al.
    Tarbiat Modares Univ, Iran.
    Moazen, Parisa
    Tarbiat Modares Univ, Iran.
    Wiskerke, Joost
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Semnanian, Saeed
    Tarbiat Modares Univ, Iran.
    Azizi, Hossein
    Tarbiat Modares Univ, Iran.
    Preconception paternal morphine exposure leads to an impulsive phenotype in male rat progeny2021In: Psychopharmacology, ISSN 0033-3158, E-ISSN 1432-2072, Vol. 238, p. 3435-3446Article in journal (Refereed)
    Abstract [en]

    Rationale Identifying the long-term neurocognitive implications of opioid addiction may further our understanding of the compulsive nature of this brain disorder. The aim of this study was to examine the effects of paternal adolescent opiate exposure on cognitive performance (visual attention, impulsivity, and compulsivity) in the next generation. Methods Male Wistar rats received escalating doses of morphine (2.5-25 mg/kg, s.c.) or saline for 10 days during adolescence (P30-39). In adulthood (P70-80), these rats were allowed to mate with drug-naive females. Male offspring from morphine- and saline-exposed sires, once in adulthood, were trained and tested in the 5-choice serial reaction time test (5-CSRTT) to evaluate their cognitive abilities under baseline, drug-free conditions as well as following acute (1, 3, 5 mg/kg morphine) and subchronic morphine (5 mg/kg morphine for 5 days) treatment. Behavioral effects of the opioid receptor antagonist naloxone were also assessed. Results Morphine-sired offspring exhibited delayed learning when the shortest stimulus duration (1 s) was introduced, i.e., when cognitive load was highest. These subjects also exhibited a reduced ability to exert inhibitory control, as reflected by increased premature and perseverative responding under drug-free baseline conditions in comparison to saline-sired rats. These impairments could not be reversed by administration of naloxone. Moreover, impulsive behavior was further enhanced in morphine-sired rats following acute and subchronic morphine treatment. Conclusion Paternal opiate exposure during adolescence was found to primarily impair inhibitory control in male progeny. These results further our understanding of the long-term costs and risk of opioid abuse, extending across generations.

  • 2.
    Barchiesi, Riccardo
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Chanthongdee, Kanat
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Mahidol Univ, Thailand.
    Petrella, Michele
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Xu, Li
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Söderholm, Simon
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Domi, Esi
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Augier, Gaëlle
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Coppola, Andrea
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Wiskerke, Joost
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Szczot, Ilona
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Domi, Ana
    Univ Gothenburg, Sweden.
    Adermark, Louise
    Univ Gothenburg, Sweden.
    Augier, Eric
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Cantù, Claudio
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Molecular Medicine and Virology. Linköping University, Faculty of Medicine and Health Sciences.
    Heilig, Markus
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Psykiatricentrum, Psykiatriska kliniken i Linköping.
    Barbier, Estelle
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    An epigenetic mechanism for over-consolidation of fear memories2022In: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 27, no 12, p. 4893-4904Article in journal (Refereed)
    Abstract [en]

    Excessive fear is a hallmark of anxiety disorders, a major cause of disease burden worldwide. Substantial evidence supports a role of prefrontal cortex-amygdala circuits in the regulation of fear and anxiety, but the molecular mechanisms that regulate their activity remain poorly understood. Here, we show that downregulation of the histone methyltransferase PRDM2 in the dorsomedial prefrontal cortex enhances fear expression by modulating fear memory consolidation. We further show that Prdm2 knock-down (KD) in neurons that project from the dorsomedial prefrontal cortex to the basolateral amygdala (dmPFC-BLA) promotes increased fear expression. Prdm2 KD in the dmPFC-BLA circuit also resulted in increased expression of genes involved in synaptogenesis, suggesting that Prdm2 KD modulates consolidation of conditioned fear by modifying synaptic strength at dmPFC-BLA projection targets. Consistent with an enhanced synaptic efficacy, we found that dmPFC Prdm2 KD increased glutamatergic release probability in the BLA and increased the activity of BLA neurons in response to fear-associated cues. Together, our findings provide a new molecular mechanism for excessive fear responses, wherein PRDM2 modulates the dmPFC -BLA circuit through specific transcriptomic changes.

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  • 3.
    Domi, Esi
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Univ Camerino, Italy.
    Xu, Li
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Toivainen Eloff, Sanne
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Wiskerke, Joost
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Coppola, Andrea
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Holm, Lovisa
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Augier, Eric
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Petrella, Michele
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Heilig, Markus
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Psykiatricentrum, Psykiatriska kliniken i Linköping. Linköping University, Center for Medical Image Science and Visualization (CMIV).
    Activation of GABA(B) receptors in central amygdala attenuates activity of PKC delta plus neurons and suppresses punishment-resistant alcohol self-administration in rats2023In: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 48, p. 1386-1395Article in journal (Refereed)
    Abstract [en]

    Alcohol use despite negative consequences is a core phenomenon of alcohol addiction. We recently used alcohol self-administration that is resistant to footshock punishment as a model of this behavior, and found that activity of PKC delta + GABAergic neurons in the central amygdala (CeA) is a determinant of individual susceptibility for punishment resistance. In the present study, we examined whether activation of GABA(B) receptors in CeA can attenuate the activity of PKC delta + neurons in this region, and whether this will result in suppression of punishment- resistant alcohol self-administration in the minority of rats that show this behavior. Systemic administration of the clinically approved GABA(B) agonist baclofen (1 and 3 mg/kg) dose- dependently reduced punishment-resistant alcohol self-administration. Bilateral microinjections of baclofen into CeA (64 ng in 0.3 mu l/side) reduced the activity of PKC delta + neurons, as measured by Fos expression. This manipulation also selectively suppressed punished alcohol self-administration in punishment-resistant rats. Expression analysis indicated that virtually all CeA PKC delta + neurons express the GABA(B) receptor. Using in vitro electrophysiology, we found that baclofen induced hyperpolarization of CeA neurons, reducing their firing rate in response to depolarizing current injections. Together, our findings provide a potential mechanism that contributes to the clinical efficacy of baclofen in alcohol addiction. Therapeutic use of baclofen itself is limited by problems of tolerance and need for dose escalation. Our findings support a mechanistic rationale for developing novel, improved alcohol addiction medications that target GABA(B) receptors, and that lack these limitations, such as e.g., GABA(B) positive allosteric modulators (PAM:s).

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  • 4.
    Pieslinger, Johan
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Wiskerke, Joost
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences.
    Igelström, Kajsa
    Linköping University, Department of Biomedical and Clinical Sciences, Division of Neurobiology. Linköping University, Faculty of Medicine and Health Sciences.
    Contributions of face processing, social anhedonia and mentalizing to the expression of social autistic-like traits2022In: Frontiers in Behavioral Neuroscience, E-ISSN 1662-5153, Vol. 16, article id 1046097Article in journal (Refereed)
    Abstract [en]

    Quantitative autistic-like traits (QATs) are a constellation of traits that mirror those of clinical autism and are thought to share the same mechanisms as the condition. There is great interest in identifying the genetic and neurobiological basis of QATs, but progress is hindered by the composite nature of these clinically based constructs. Social QATs are defined according to the diagnostic criteria for autism, comprising multiple potential neural mechanisms that may contribute to varying degrees. The objective of this study was to decompose social QATs into more specific constructs, in line with the Research Domain Criteria (RDoC). We chose constructs with trait-like properties and known or suggested significance for autistic social function: 1) social anhedonia, 2) prosopagnosia (face blindness), and 3) mentalizing (attributing mental states to images of eyes). We hypothesized that these constructs may all contribute to observed variance in social QATs. We recruited 148 adults with a broad range of QATs (mean age 37.9 years, range 18–69; 50% female; 5.4% autistic) to an experimental behavioral study conducted online. We estimated social QATs using the social factor of the Comprehensive Autistic Traits Inventory. We used the Oxford Face Matching Task and the Reading the Mind in the Eyes Test to measure face matching ability and mentalizing, respectively. Social anhedonia traits were measured with the Anticipatory and Consummatory Interpersonal Pleasure Scale, and prosopagnosic traits with the 20-item Prosopagnosia Index. A combination of frequentist and Bayesian statistics was used to test the social constructs as predictors of social QATs. We found that social anhedonic traits, prosopagnosic traits, and face matching performance were likely predictors of social QATs, whereas mentalizing showed limited contribution. The findings support prosopagnosic and anhedonic traits, but not mentalizing deficits, as dimensional predictors of individual differences in social function across the autistic spectrum. Further, the study strongly suggest that social reward systems and face processing networks play significant and independent roles in autistic-like social function.

  • 5.
    Wiskerke, Joost
    et al.
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Brain Health Institute, Rutgers University/Rutgers Biomedical and Health Sciences, 683 Hoes Lane, Piscataway, NJ, United States.
    Stern, Heléne
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Princeton Neuroscience Institute and Department of Psychology, Princeton University, Washington Road, Princeton, NJ, United States.
    Igelström, Kajsa
    Linköping University, Department of Biomedical and Clinical Sciences, Center for Social and Affective Neuroscience. Linköping University, Faculty of Medicine and Health Sciences. Princeton Neuroscience Institute and Department of Psychology, Princeton University, Washington Road, Princeton, NJ, United States.
    Camouflaging of repetitive movements in autistic female and transgender adults2018Manuscript (preprint) (Other academic)
    Abstract [en]

    Repetitive movements (RMs), colloquially called “stimming” among adult autistic people and “motor stereotypies” among scientists, are common in autism. These behaviors fall under the domain of restricted and repetitive behaviors in the current edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). RMs can be socially disruptive or cause self-harm, but can also be experienced as cognitively or emotionally helpful and even enjoyable. Overt RMs are less common in females than in males, which could contribute to clinical difficulties in detecting their autism. In the social domain, autistic people with intact intelligence can often mask their social difficulties through various compensation strategies, and females appear especially skilled at it. Subjective report from verbally able adults may be useful as a first step in detecting potential camouflaging of RMs, and to provide a foundation for further studies. We founded an Internet-based outreach platform that became particularly successful in reaching female and transgender individuals. We recruited 342 individuals to an anonymous online questionnaire, collected data about self-reported RMs and probed for potential camouflaging. The cohort comprised 56% formally diagnosed participants and 44% who self-identified as autistic, and 17% of all participants reported non-cisgender identity. Thus, in addition to diagnosed women, we reached two populations that would normally be excluded from autism studies: transgender and undiagnosed participants. We found high rates of RMs in both diagnosed and self-identifying participants, and a striking prevalence of camouflaging. We suggest that camouflaging of RMs may contribute to underdiagnosis of autism, at least in females and transgender people, and that further studies on this topic are exceptionally important.

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