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  1 / 16097 MEDLINE  
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PMID:28456841
Autor:Blanco-Gandía MC; Aracil-Fernández A; Montagud-Romero S; Aguilar MA; Manzanares J; Miñarro J; Rodríguez-Arias M
Endereço:Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain.
Título:Changes in gene expression and sensitivity of cocaine reward produced by a continuous fat diet.
Fonte:Psychopharmacology (Berl); 234(15):2337-2352, 2017 Aug.
ISSN:1432-2072
País de publicação:Germany
Idioma:eng
Resumo:RATIONALE: Preclinical studies report that free access to a high-fat diet (HFD) alters the response to psychostimulants. OBJECTIVES: The aim of the present study was to examine how HFD exposure during adolescence modifies cocaine effects. Gene expression of CB1 and mu-opioid receptors (MOr) in the nucleus accumbens (N Acc) and prefrontal cortex (PFC) and ghrelin receptor (GHSR) in the ventral tegmental area (VTA) were assessed. METHODS: Mice were allowed continuous access to fat from PND 29, and the locomotor (10 mg/kg) and reinforcing effects of cocaine (1 and 6 mg/kg) on conditioned place preference (CPP) were evaluated on PND 69. Another group of mice was exposed to a standard diet until the day of post-conditioning, on which free access to the HFD began. RESULTS: HFD induced an increase of MOr gene expression in the N Acc, but decreased CB1 receptor in the N Acc and PFC. After fat withdrawal, the reduction of CB1 receptor in the N Acc was maintained. Gene expression of GHSR in the VTA decreased during the HFD and increased after withdrawal. Following fat discontinuation, mice exhibited increased anxiety, augmented locomotor response to cocaine, and developed CPP for 1 mg/kg cocaine. HFD reduced the number of sessions required to extinguish the preference and decreased sensitivity to drug priming-induced reinstatement. CONCLUSION: Our results suggest that consumption of a HFD during adolescence induces neurobiochemical changes that increased sensitivity to cocaine when fat is withdrawn, acting as an alternative reward.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Receptor, Cannabinoid, CB1); 0 (Receptors, Ghrelin); 0 (Receptors, Opioid, mu); I5Y540LHVR (Cocaine)


  2 / 16097 MEDLINE  
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PMID:29352277
Autor:Villain H; Benkahoul A; Birmes P; Ferry B; Roullet P
Endereço:Centre de Recherches sur la Cognition Animale, Centre de Biologie Intégrative, Université de Toulouse, CNRS, UPS, Toulouse, France.
Título:Influence of early stress on memory reconsolidation: Implications for post-traumatic stress disorder treatment.
Fonte:PLoS One; 13(1):e0191563, 2018.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:Post-traumatic stress disorder (PTSD) is a common consequence of exposure to a life-threatening event. Currently, pharmacological treatments are limited by high rates of relapse, and novel treatment approaches are needed. We have recently demonstrated that propranolol, a ß-adrenergic antagonist, inhibited aversive memory reconsolidation in animals. Following this, in an open-label study 70% of patients with PTSD treated with propranolol during reactivation of traumatic memory exhibited full remission. However, the reason why 30% of these patients did not respond positively to propranolol treatment is still unclear. One of the major candidates as factor of treatment resistance is the patient's early-life traumatic history. To test the role of this factor, mice with pre- or postnatal stress are being tested in fear conditioning and in a new behavioral task, the "city-like", specifically designed as a mouse model of PTSD. After reactivation of the traumatic event, mice received propranolol injection to block the noradrenergic system during memory reconsolidation. Results show that, in the "city-like" test, control mice strongly avoided the shock compartment but also the compartments containing cues associated with the electric shocks. Injection of propranolol after reactivation greatly reduced the memory of the traumatic event, but this effect was not present when mice had received pre- or postnatal stress. Moreover, propranolol produced only a very weak effect in the fear conditioning test, and never changed the corticosterone level whatever the behavioral experiment. Taken together our results suggest that our new behavioural paradigm is well adapted to PTSD study in mice, and that early stress exposure may have an impact on propranolol PTSD treatment outcome. These data are critical to understanding the effect of propranolol treatment, in order to improve the therapeutic protocol currently used in humans.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Adrenergic beta-Antagonists); 9Y8NXQ24VQ (Propranolol); W980KJ009P (Corticosterone)


  3 / 16097 MEDLINE  
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PMID:28456768
Autor:Skorzewska A; Wislowska-Stanek A; Lehner M; Turzynska D; Sobolewska A; Krzascik P; Plaznik A
Endereço:Department of Neurochemistry, Institute of Psychiatry and Neurology, Warsaw, Poland. skorzews@ipin.edu.pl.
Título:Corticotropin releasing factor receptor 1 antagonist differentially inhibits freezing behavior and changes gamma-aminobutyric acidergic activity in the amygdala in low- and high-anxiety rats.
Fonte:J Physiol Pharmacol; 68(1):35-46, 2017 Feb.
ISSN:1899-1505
País de publicação:Poland
Idioma:eng
Resumo:The aim of this study was to examine the effects of non-peptide corticotropin-releasing factor receptor 1 (CRF ) antagonist (antalarmin) administration on rat conditioned fear responses and gamma-aminobutyric acid (GABA)-ergic brain activity (GAD67 expression and GABA concentration) in low-anxiety (LR) and high-anxiety (HR) rats. The animals were divided into the LR and HR groups based on the duration of their conditioned freezing response in the first contextual fear test. After 28 days, the animals were re-subjected to the contextual fear training and test. The rats received an antalarmin injection (10 mg/kg or 20 mg/kg) 80 min before the second exposure to the aversive context. Antalarmin significantly attenuated the conditioned fear response only in the HR rats. The behavioral effect of a lower dose (10 mg/kg) of antalarmin was accompanied by increased GAD67 expression in the prelimbic cortex (PL) and central nucleus of the amygdala (CeA) and an increased GABA concentration in the amygdala. These studies showed that HR rats were more susceptible to the anxiolytic effects of CRF antagonist administration, which were associated with increased GABAergic activity in the medial prefrontal cortex and amygdala. The current data may provide insights into the neurobiological mechanism operating within the mesolimbic CRF-GABA neurotransmitter systems, which may be responsible for individual differences in stress-related diseases. This knowledge can be applied to further elucidate the pathophysiology of anxiety and trauma/stress-related disorders.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (CRF receptor type 1); 0 (Pyrimidines); 0 (Pyrroles); 0 (Receptors, Corticotropin-Releasing Hormone); 0 (antalarmin); 56-12-2 (gamma-Aminobutyric Acid); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1)


  4 / 16097 MEDLINE  
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PMID:27773594
Autor:Pelrine E; Pasik SD; Bayat L; Goldschmiedt D; Bauer EP
Endereço:Biology Department, Barnard College, New York, NY 10027, United States.
Título:5-HT2C receptors in the BNST are necessary for the enhancement of fear learning by selective serotonin reuptake inhibitors.
Fonte:Neurobiol Learn Mem; 136:189-195, 2016 Dec.
ISSN:1095-9564
País de publicação:United States
Idioma:eng
Resumo:Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed to treat anxiety and depression, yet they paradoxically increase anxiety during initial treatment. Acute administration of these drugs prior to learning can also enhance Pavlovian cued fear conditioning. This potentiation has been previously reported to depend upon the bed nucleus of the stria terminalis (BNST). Here, using temporary inactivation, we confirmed that the BNST is not necessary for the acquisition of cued or contextual fear memory. Systemic administration of the SSRI citalopram prior to fear conditioning led to an upregulation of the immediate early gene Arc (activity-regulated cytoskeleton-associated protein) in the oval nucleus of the BNST, and a majority of these neurons expressed the 5-HT2C receptor. Finally, local infusions of a 5-HT2C receptor antagonist directly into the oval nucleus of the BNST prevented the fear memory-enhancing effects of citalopram. These findings highlight the ability of the BNST circuitry to be recruited into gating fear and anxiety-like behaviors.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Receptor, Serotonin, 5-HT2C); 0 (Serotonin 5-HT2 Receptor Antagonists); 0 (Serotonin Uptake Inhibitors); 0DHU5B8D6V (Citalopram)


  5 / 16097 MEDLINE  
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PMID:29054591
Autor:Allen MT; Myers CE; Williams D; Servatius RJ
Endereço:School of Psychological Sciences, University of Northern Colorado, Greeley, CO, USA; Rutgers Biomedical Health Sciences, Stress and Motivated Behavior Institute, Rutgers University, Newark, NJ, United States. Electronic address: michael.allen@unco.edu.
Título:US alone trials presented during acquisition do not disrupt classical eyeblink conditioning: Empirical and computational findings.
Fonte:Behav Brain Res; 338:101-108, 2018 Feb 15.
ISSN:1872-7549
País de publicação:Netherlands
Idioma:eng
Resumo:Studies of partial reinforcement in eyeblink conditioning have typically shown slower learning of a CS-US association when paired CS-US trials are interleaved with CS-alone trials. However, recent work has shown that CS-US learning is not slowed by interleaved US-alone trials. This discrepancy is surprising since both partial reinforcement protocols reduce the total number of paired CS-US trials. Previously, Kimble et al. (1955) reported that inserting a block of US-alone trials during CS-US training did not disrupt eyeblink acquisition. Here, we sought to replicate and extend these findings by comparing interleaved vs. blocked US-alone trials during CS-US paired training. Ninety-seven undergraduates volunteered for this experiment for research credit. Participants received 60 acquisition trials, consisting of either 100% CS-US paired trials, 50% US-alone trials intermixed with CS-US paired trials, or a block of 20 US-alone trials inserted between blocks of 20 CS-US trials. We also utilized a previously published computational model of hippocampal and cerebellar learning to test the effects of these US-alone protocols. Both empirical and computational results supported the finding that US-alone trials, either intermixed or inserted as a block of trials, do not disrupt acquisition of conditioned eyeblinks. Possible neural substrates of these US-alone effects are discussed.
Tipo de publicação: JOURNAL ARTICLE


  6 / 16097 MEDLINE  
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PMID:28466092
Autor:Montagud-Romero S; Nuñez C; Blanco-Gandia MC; Martínez-Laorden E; Aguilar MA; Navarro-Zaragoza J; Almela P; Milanés MV; Laorden ML; Miñarro J; Rodríguez-Arias M
Endereço:Department of Psychobiology, Facultad de Psicología, Universitat de Valencia, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain.
Título:Repeated social defeat and the rewarding effects of cocaine in adult and adolescent mice: dopamine transcription factors, proBDNF signaling pathways, and the TrkB receptor in the mesolimbic system.
Fonte:Psychopharmacology (Berl); 234(13):2063-2075, 2017 Jul.
ISSN:1432-2072
País de publicação:Germany
Idioma:eng
Resumo:RATIONALE: Repeated social defeat (RSD) increases the rewarding effects of cocaine in adolescent and adult rodents. OBJECTIVE: The aim of the present study was to compare the long-term effects of RSD on the conditioned rewarding effects of cocaine and levels of the transcription factors Pitx3 and Nurr1 in the ventral tegmental area (VTA), the dopamine transporter (DAT), the D2 dopamine receptor (D2DR) and precursor of brain-derived neurotrophic factor (proBDNF) signaling pathways, and the tropomyosin-related kinase B (TrkB) receptor in the nucleus accumbens (NAc) in adult and adolescent mice. METHODS: Male adolescent and young adult OF1 mice were exposed to four episodes of social defeat and were conditioned 3 weeks later with 1 mg/kg of cocaine. In a second set of mice, the expressions of the abovementioned dopaminergic and proBDNF and TrkB receptor were measured in VTA and NAc, respectively. RESULTS: Adolescent mice experienced social defeats less intensely than their adult counterparts and produced lower levels of corticosterone. However, both adult and adolescent defeated mice developed conditioned place preference for the compartment associated with this low dose of cocaine. Furthermore, only adolescent defeated mice displayed diminished levels of the transcription factors Pitx3 in the VTA, without changes in the expression of DAT and D2DR in the NAc. In addition, stressed adult mice showed a decreased expression of proBDNF and the TrkB receptor, while stressed adolescent mice exhibited increased expression of latter without changes in the former. CONCLUSION: Our findings suggest that dopaminergic pathways and proBDNF signaling and TrkB receptors play different roles in social defeat-stressed mice exposed to cocaine.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Brain-Derived Neurotrophic Factor); 0 (DRD2 protein, human); 0 (Membrane Glycoproteins); 0 (Protein Precursors); 0 (Receptors, Dopamine D2); 0 (Transcription Factors); 0 (brain-derived neurotrophic factor precursor); EC 2.7.10.1 (Receptor, trkB); EC 2.7.10.1 (tropomyosin-related kinase-B, human); I5Y540LHVR (Cocaine); VTD58H1Z2X (Dopamine); W980KJ009P (Corticosterone)


  7 / 16097 MEDLINE  
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PMID:27779622
Autor:Milligan-Saville JS; Graham BM
Endereço:School of Psychology, The University of New South Wales Australia, Sydney, NSW, Australia.
Título:Mothers do it differently: reproductive experience alters fear extinction in female rats and women.
Fonte:Transl Psychiatry; 6(10):e928, 2016 10 25.
ISSN:2158-3188
País de publicação:United States
Idioma:eng
Resumo:Fear extinction is the laboratory basis of exposure therapy for anxiety disorders. Recent findings have revealed that estradiol is necessary to the consolidation of extinction memories in females. These findings are based on studies conducted using virgin rats and young women whose reproductive history is unknown. We hypothesized that motherhood, which results in extensive endocrinological, neurobiological and behavioral changes, may lead to alterations in fear extinction in females. We used a cross-species translational approach to investigate the impact of reproductive experience on fear extinction and fear relapse in female rats (n=116) and women (n=64). Although freezing during extinction recall was associated with estrous cycle phase during extinction training in virgin rats, this association was mitigated in age-matched reproductively experienced rats, even when fear extinction occurred 3 months after pups had been weaned, and even though reproductively experienced rats exhibited attenuated serum estradiol levels. In addition, although serum estradiol levels predicted extinction recall in human women with no prior reproductive experience, no such association was found in women with children. Finally, although virgin rats displayed both renewal and reinstatement after fear extinction, these common relapse phenomena were absent in rats with reproductive experience. Together, these findings suggest that reproductive experience alters the endocrine and behavioral features of fear extinction in females long after the hormonal surges of pregnancy and lactation have diminished. These results highlight the need to incorporate both hormonal and reproductive status as important factors in current models of fear extinction in females.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:4TI98Z838E (Estradiol)


  8 / 16097 MEDLINE  
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PMID:28747623
Autor:Monosov IE
Endereço:Departments of Neuroscience and Biomedical Engineering, Washington University in St. Louis, St. Louis, MO, 63110, USA. ilya.monosov@gmail.com.
Título:Anterior cingulate is a source of valence-specific information about value and uncertainty.
Fonte:Nat Commun; 8(1):134, 2017 07 26.
ISSN:2041-1723
País de publicação:England
Idioma:eng
Resumo:Anterior cingulate cortex (ACC) is thought to control a wide range of reward, punishment, and uncertainty-related behaviors. However, how it does so is unclear. Here, in a Pavlovian procedure in which monkeys displayed a diverse repertoire of reward-related, punishment-related, and uncertainty-related behaviors, we show that many ACC-neurons represent expected value and uncertainty in a valence-specific manner, signaling value or uncertainty predictions about either rewards or punishments. Other ACC-neurons signal prediction information about rewards and punishments by displaying excitation to both (rather than excitation to one and inhibition to the other). This diversity in valence representations may support the role of ACC in many behavioral states that are either enhanced by reward and punishment (e.g., vigilance) or specific to either reward or punishment (e.g., approach and avoidance). Also, this first demonstration of punishment-uncertainty signals in the brain suggests that ACC could be a target for the treatment of uncertainty-related disorders of mood.Rewards or punishments elicit diverse behavioral responses; however, the neural circuits underlying such flexibility are unclear. Here Monosov shows that this diversity could be supported by neurons in the anterior cingulate that represent expected value and uncertainty in a valence-specific manner.
Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.


  9 / 16097 MEDLINE  
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PMID:29023466
Autor:Lommen MJJ; Duta M; Vanbrabant K; de Jong R; Juechems K; Ehlers A
Endereço:Department of Experimental Psychology, University of Oxford, Oxford, United Kingdom.
Título:Training discrimination diminishes maladaptive avoidance of innocuous stimuli in a fear conditioning paradigm.
Fonte:PLoS One; 12(10):e0184485, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:Anxiety disorders are the most common mental disorder worldwide. Although anxiety disorders differ in the nature of feared objects or situations, they share a common mechanism by which fear generalizes to related but innocuous objects, eliciting avoidance of objects and situations that pose no objective risk. This overgeneralization appears to be a crucial mechanism in the persistence of anxiety psychopathology. In this study we test whether an intervention that promotes discrimination learning reduces generalization of fear, in particular, harm expectancy and avoidance compared to an irrelevant (control) training. Healthy participants (N = 80) were randomly allocated to a training condition. Using a fear conditioning paradigm, participants first learned visual danger and safety signals (set 1). Baseline level of stimulus generalization was tested with ambiguous stimuli on a spectrum between the danger and safety signals. There were no differences between the training groups. Participants then received the stimulus discrimination training or a control training. After training, participants learned a new set of danger and safety signals (set 2), and the level of harm expectancy generalization and behavioural avoidance of ambiguous stimuli was tested. Although the training groups did not differ in fear generalization on a cognitive level (harm expectancy), the results showed a different pattern of avoidance of ambiguous stimuli, with the discrimination training group showing less avoidance of stimuli that resembled the safety signals. These results support the potential of interventions that promote discrimination learning in the treatment of anxiety disorders.
Tipo de publicação: JOURNAL ARTICLE


  10 / 16097 MEDLINE  
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PMID:28957678
Autor:Lee SC; Amir A; Haufler D; Pare D
Endereço:Center for Molecular and Behavioral Neuroscience, 197 University Avenue, Rutgers University-Newark, Newark, NJ 07102, USA.
Título:Differential Recruitment of Competing Valence-Related Amygdala Networks during Anxiety.
Fonte:Neuron; 96(1):81-88.e5, 2017 Sep 27.
ISSN:1097-4199
País de publicação:United States
Idioma:eng
Resumo:The basolateral amygdala (BL) is involved in fear and anxiety, but it is currently unclear how the same network supports these two states. To address this question, we trained rats on appetitive and aversive conditioning in different contexts. Distinct groups of BL neurons displayed increased activity during appetitive (CS-R) versus aversive (CS-S) conditioned stimuli (R cells and S cells, respectively), and they were typically inhibited by the other CS. When the CS-S was presented in the safe context, rats entered a long-lasting, anxiety-like state characterized by increased inter-CS freezing and impaired reward seeking. During this state, a subset of BL cells ("state cells") showed sustained shifts in baseline activity whose time course matched that of the behavioral changes. Many state cells with increased firing rates were S cells, whereas R cells only included state cells with reduced firing rates. Thus, anxiety involves persistent activity changes that are differentially expressed by subsets of valence-specific BL neurons.
Tipo de publicação: JOURNAL ARTICLE



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