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Involvement of dopamine D2 and glutamate NMDA receptors in the antidepressant-like effect of amantadine in mice
Inara Fernanda MisiutaRaupp-BarcaroaIsabella Carolineda Silva DiasaErikaMeyerbJeane Cristina FonsecaVieiraaGiovanada Silva PereiraaArthur RibeiroPetkowiczaR?bia Maria Weffortde OliveirabRobertoAndreatinia
doi : 10.1016/j.bbr.2021.113443
Volume 413, 10 September 2021, 113443
The present study investigated the pharmacological mechanisms of the antidepressant-like effects of amantadine in mice and their influence on hippocampal neurogenesis. To improve the translational validity of preclinical results, reproducibility across laboratories and replication in other animal models and species are crucial. Single amantadine administration at doses of 50 and 75 mg/kg resulted in antidepressant-like effects in mice in the tail suspension test (TST), reflected by an increase in immobility time. The effects of amantadine were seen at doses that did not alter locomotor activity. The tyrosine hydroxylase inhibitor ?-methyl-?-tyrosine did not influence the anti-immobility effect of amantadine in the TST. Pretreatment with the ?1 adrenergic receptor antagonist prazosin, ? adrenergic receptor antagonist propranolol, ?2 adrenergic receptor antagonist yohimbine, and ?2 adrenergic receptor agonist clonidine did not alter the antidepressant-like effect of amantadine. However, amantadine’s effect was blocked by the dopamine D2 receptor antagonist haloperidol and glutamate receptor agonist N-methyl-D-aspartate (NMDA). Repeated amantadine administration (50 mg/kg) also exerted an antidepressant-like effect, paralleled by an increase in hippocampal neurogenesis. The present results demonstrate that the antidepressant-like effects of amantadine may be mediated by its actions on D2 and NMDA receptors and likely involve hippocampal neurogenesis.
TREK-1 potassium channels participate in acute and long-lasting nociceptive hypersensitivity induced by formalin in rats
GuadalupeGarc?aVladimir A.Mart?nez-RojasJanetMurbarti?n
doi : 10.1016/j.bbr.2021.113446
Volume 413, 10 September 2021, 113446
TREK-1 channels are expressed in small nociceptive dorsal root ganglion (DRG) neurons where they participate in acute inflammatory and neuropathic pain. However, the role of TREK-1 in persistent pain is not well understood. The aim of this study was to investigate the local peripheral and spinal participation of TREK-1 in formalin-induced acute and long-lasting nociceptive hypersensitivity. Local peripheral or intrathecal pre-treatment with spadin, selective blocker of TREK-1, increased acute flinching behavior and secondary mechanical allodynia and hyperalgesia behavior observed 6 days after formalin injection. Local peripheral or intrathecal pre-treatment with BL-1249, selective opener of TREK-1, decreased long-lasting secondary mechanical allodynia and hyperalgesia induced by formalin. Pre-treatment with BL-1249 prevented the pro-nociceptive effect of spadin on acute nociception and long-lasting mechanical allodynia and hyperalgesia in rats. Pre-treatment with two recombinant channels that produce a high TREK-1 current, S300A and S333A (non-phosphorylated state of TREK-1), reduced formalin-induced acute pain and long-lasting mechanical allodynia and hyperalgesia. Besides, post-treatment with S300A, S333A or BL-1249 reversed long-lasting mechanical allodynia and hyperalgesia induced by formalin. Formalin increased TREK-1 expression at 1 and 6 days in DRG and dorsal spinal cord in rats, whereas that it increased c-fos expression at the DRG. Intrathecal repeated transfection of rats with S300A and S333A or injection with BL-1249 reduced formalin-induced enhanced c-fos expression. Data suggest that TREK-1 activity at peripheral and spinal sites reduces neuronal excitability in the process of acute and long-lasting nociception induced by formalin in rats.
The effects of emotional stimuli and oxytocin on inhibition ability and response execution in macaque monkeys
MarziehMowlavi VardanjaniabSadeghGhasemianabVahidSheibaniabFarshadA. Mansouric
doi : 10.1016/j.bbr.2021.113409
Volume 413, 10 September 2021, 113409
Social and emotional content of environmental stimuli influence executive control of behavior. There has been a great variability in the behavioral effects of emotional stimuli in humans. These variabilities might arise from other contextual factors, such as specific task demands or natural hormones, which potentially interact with emotional stimuli in modulating executive functions. This study aimed at examining the effects of social-emotional visual stimuli and a natural hormone (oxytocin) on inhibition ability and response execution of macaque monkeys. In a crossover design, monkeys received inhaled oxytocin or its vehicle before performing a stop-signal task in which they must respond rapidly to a visual go-cue in Go trials but inhibit the initiated response following the onset of a stop-cue in Stop trials. The social-emotional content (negative, positive or neutral) of the go-cue was changed trial-by-trial. We found that monkeys’ inhibition ability was significantly influenced by the social-emotional content of stimuli and appeared as an enhanced inhibition ability when monkeys were exposed to negative stimuli. However, response execution was not influenced by the emotional content of stimuli in the current or preceding trials. The same dose of oxytocin, which modulated working memory in monkeys, had no significant effect on the inhibition ability, but significantly decreased monkeys’ response time regardless of the stimulus valence. Our findings indicate that emotional stimuli, valence dependently, influence monkeys’ inhibition ability but not their response execution and suggest that oxytocin might attenuate reorientation of cognitive resources to the task irrelevant emotional information.
Inactivation of posterior but not anterior dorsomedial caudate-putamen impedes learning with self-administered nicotine stimulus in male rats
Christopher L.RobisonaTheodoreKazanaRikki L.A.MillerbNicoleCovaaSergiosCharntikova
doi : 10.1016/j.bbr.2021.113438
Volume 413, 10 September 2021, 113438
The rodent caudate-putamen is a large heterogeneous neural structure with distinct anatomical connections that differ in their control of learning processes. Previous research suggests that the anterior and posterior dorsomedial caudate-putamen (a- and p-dmCPu) differentially regulate associative learning with a non-contingent nicotine stimulus. The current study used bilateral NMDA-induced excitotoxic lesions to the a-dmCPu and p-dmCPu to determine the functional involvement of a-dmCPu and p-dmCPu in appetitive learning with contingent nicotine stimulus. Rats with a-dmCPu, p-dmCPu, or sham lesions were trained to lever-press for intravenous nicotine (0.03 mg/kg/inf) followed by access to sucrose 30 s later. After 1, 3, 9, and 20 nicotine-sucrose training sessions, appetitive learning in the form of a goal-tracking response was assessed using a non-contingent nicotine-alone test. All rats acquired nicotine self-administration and learned to retrieve sucrose from a receptacle at equal rates. However, rats with lesions to p-dmCPu demonstrated blunted learning of the nicotine-sucrose association. Our primary findings show that rats with lesions to p-dmCPu had a blunted goal-tracking response to a non-contingent nicotine administration after 20 consecutive days of nicotine-sucrose pairing. Our findings extend previous reports to a contingent model of nicotine self-administration and show that p-dmCPu is involved in associative learning with nicotine stimulus using a paradigm where rats voluntarily self-administer nicotine infusions that are paired with access to sucrose—a paradigm that closely resembles learning processes observed in humans.
Disturbance of the reciprocal-interaction between the OXTergic and DAergic systems in the CNS causes atypical social behavior in syntaxin 1A knockout mice
TomonoriFujiwaraabTakefumiKofujibcKimioAkagawab
doi : 10.1016/j.bbr.2021.113447
Volume 413, 10 September 2021, 113447
Several studies have shown that oxytocin (OXT) modulates social behavior. Similarly, monoamines such as dopamine (DA) play a role in regulating social behavior. Previous studies have demonstrated that the soluble N-ethylmaleimide-sensitive fusion attachment protein receptor (SNARE) protein syntaxin 1A (STX1A) regulates the secretion of OXT and monoamines, and that STX1A gene knockout (STX1A KO) mice exhibit atypical social behavior, such as deficient social recognition, due to reduced OXT release. In this study, we analyzed the neural mechanism regulating social behavior by OXT and/or DA using STX1A KO mice as a model animal. We found that OXT directly induced DA release from cultured DA neurons through OXT and V1a receptors. In STX1A KO mice, the atypical social behavior was partially improved by OXT administration, which was inhibited by D1 receptor blockade. In addition, the atypical social behavior in STX1A KO mice was partially improved by facilitation of DAergic signaling with the DA reuptake inhibitor GBR12909. Moreover, the amelioration by GBR12909 was inhibited by OXTR blockade. These results suggest that the reciprocal interaction between the DAergic and OXTergic neuronal systems in the CNS may be important in regulating social behavior.
Navigation using global or local reference frames in rats with medial and lateral entorhinal cortex lesions
JulienPoitreau1ManonButtet1ChristineManrique2BrunoPoucet1FrancescaSargolini1EtienneSave1
doi : 10.1016/j.bbr.2021.113448
Volume 413, 10 September 2021, 113448
The medial (MEC) and the lateral (LEC) regions of the entorhinal cortex send a major input to the hippocampus and have been proposed to play a foremost role in combining spatial and non-spatial attributes of episodic memory. In addition, it has been recently suggested that the MEC is involved in the processing of information in a global reference frame and the LEC in the processing of information in a local reference frame. Whether these putative functions could be generalized to navigation contexts has not been established yet. To address this hypothesis, rats with MEC or LEC NMDA-induced lesions were trained in two versions of a navigation task in the water maze, a global cue condition in which they had to use distal room cues and a local cue condition in which they had to use 3 objects placed in the pool. In the global cue condition, MEC-lesioned rats exhibited slower acquisition and were not able to precisely locate the submerged platform during the probe trial. In contrast LEC-lesioned rats exhibited control-like performance. In the local cue condition, navigational abilities were spared in both lesion groups. In addition when the 3 different objects were replaced by 3 identical objects, all groups maintained their navigation accuracy suggesting that the identity of objects is not crucial for place navigation. Overall, the results indicate that the MEC is necessary for place navigation using a global reference frame. In contrast, navigation using a local reference frame does not require the LEC nor the MEC.
Exercise prevents the impairment of learning and memory in prenatally phthalate-exposed male rats by improving the expression of plasticity-related proteins
Gwo-ChingSunabYi-JuLeecYi-ChingLeedHsien-FuYucDean-ChuanWangce
doi : 10.1016/j.bbr.2021.113444
Volume 413, 10 September 2021, 113444
Regular exercise has been identified to facilitate neuroplasticity that maximize functional outcome after brain injuries. Brain-derived neurotrophic factor (BDNF) has emerged as a key facilitator of neuroplasticity after exercise. The activity-regulated cytoskeleton associated protein (Arc) is induced by BDNF and N-methyl-d-aspartic acid receptor (NMDAR), contributing to functional modification of neuroplasticity in the hippocampus. Meanwhile, early-life exposure to neuroendocrine disruptor di-(2-ethylhexyl)-phthalate (DEHP) is a risk factor for behavioral deficits, but the mechanisms responsible for DEHP-induced neurotoxicity are not well understood. The purpose of this study is to investigate whether hippocampal Arc expression is impaired by DEHP exposure and to examine the protective role of exercise in the prenatally DEHP-exposed male rats. Sprague Dawley dams were fed with vehicle or DEHP during gestation. The male offspring were trained to treadmill running for 5 weeks followed by examination of behavioral and biochemical outcomes. The results showed that DEHP-exposed rats exhibited impairment of spatial learning and memory as well as down-regulations of BDNF, NMDAR, Arc, and synaptophysin. Importantly, aerobic exercise during childhood-adolescence prevented the impairment of learning and memory by recovering the expressions of BDNF, NMDAR, Arc, and synaptophysin. These findings suggest that exercise may provide beneficial effects on ameliorating the impairment of neuroplasticity in the prenatally DEHP-exposed male rats at late adolescence.
Anxiolytic effect of chronic intake of supplemental magnesium chloride in rat
MonserratMac?as-CarballoSergioRosas-NavarroMar?a LeonorL?pez-MerazLuisBeltran-ParrazalConsueloMorgado-Valle
doi : 10.1016/j.bbr.2021.113460
Volume 413, 10 September 2021, 113460
Evidence suggest that magnesium dietary supplementation has several health benefits including lowering blood pressure, reducing insulin resistance, and improving symptoms of depression, anxiety, and migraine. Here, we aimed to study the effect of chronic magnesium supplementation on anxiety-like behavior in rats by supplementing with magnesium their drinking water for 30 days. Anxiety-like behavior was induced by subcutaneous injection of veratrin 30 min before performing elevated plus maze and open field tests to measure anxiety levels and locomotion, respectively. We quantify the concentration of magnesium in plasma and cerebrospinal fluid. We used diazepam to compare the efficacy of magnesium supplementation as an anxiolytic agent. Our results show that rats supplemented with magnesium had a statistically significant decrease in anxiety levels with not effects on locomotion and a statistically significant increase in concentration of magnesium in plasma and cerebrospinal fluid. However, the anxiolytic effect of magnesium supplementation washes-out in 12 days. We discuss the advantages of using supplemental magnesium as anxiolytic.
Legumain knockout improves repeated corticosterone injection-induced depression-like emotional and cognitive deficits
WenxinZhangXueqingChaiXiaolinLiXiaoyueTanZhuoYang
doi : 10.1016/j.bbr.2021.113464
Volume 413, 10 September 2021, 113464
Emotional and cognitive impairment has been recognized as a central feature of depression, which is closely related to hyperfunction of the hypothalamic-pituitary-adrenal (HPA) axis caused by down-regulation of glucocorticoid receptor (GR) expression in patients. A decrease in GR expression can cause pathological changes and lead to the impairment of synaptic plasticity. Legumain, a lysosomal cysteine protease, plays an important role in neurological diseases. It is reported that legumain activates the MAPK signaling pathway, which modifies the GR. Therefore, we hypothesize that regulation of the GR by legumain plays a crucial role in the pathological process of depression. The relationships between legumain, GR, synaptic plasticity and emotional and cognitive deficits were explored in this study. The results demonstrated that repeated corticosterone (CORT) injections (3 weeks) induced emotional and cognitive deficits in mice, based on behavioral experiments and the detection of synaptic plasticity. Furthermore, CORT injections decreased the expression of hippocampal synapse-related proteins, cell density and dendritic spine density in the hippocampus, accompanied by increased protein expression in the MAPK signaling pathway and decreased expression of the GR. In conclusion, our results demonstrated that legumain knockout up-regulated expression of the GR by reducing protein expression in the MAPK signaling pathway, thereby improving hippocampal synaptic plasticity as well as the emotional and cognitive impairment of model mice. This suggests that legumain may be an effective therapeutic target for emotional and cognitive deficits.
Engrailed 2 deficiency and chronic stress alter avoidance and motivation behaviors
Mimi L.PhanaTonia T.LiuaMallory S.VollbrechtbMark H.MansouraIvanaNikodijevicaNikitaJadavaNeeharikaPatibandaaJennyDangaGopnaShekaranaRobert C.ReisleraWon S.KimaXiaofengZhoubEmanuelDiCicco-BloombBenjamin A.Samuelsa
doi : 10.1016/j.bbr.2021.113466
Volume 413, 10 September 2021, 113466
Autism spectrum disorder (ASD) is a pervasive neurodevelopmental disorder characterized by impairments in social interaction, cognition, and communication, as well as the presence of repetitive or stereotyped behaviors and interests. ASD is most often studied as a neurodevelopmental disease, but it is a lifelong disorder. Adults with ASD experience more stressful life events and greater perceived stress, and frequently have comorbid mood disorders such as anxiety and depression. It remains unclear whether adult exposure to chronic stress can exacerbate the behavioral and neurodevelopmental phenotypes associated with ASD. To address this issue, we first investigated whether adult male and female Engrailed-2 deficient (En2-KO, En2?/?) mice, which display behavioral disturbances in avoidance tasks and dysregulated monoaminergic neurotransmitter levels, also display impairments in instrumental behaviors associated with motivation, such as the progressive ratio task. We then exposed adult En2-KO mice to chronic environmental stress (CSDS, chronic social defeat stress), to determine if stress exacerbated the behavioral and neuroanatomical effects of En2 deletion. En2?/? mice showed impaired instrumental acquisition and significantly lower breakpoints in a progressive ratio test, demonstrating En2 deficiency decreases motivation to exert effort for reward. Furthermore, adult CSDS exposure increased avoidance behaviors in En2-KO mice. Interestingly, adult CSDS exposure also exacerbated the deleterious effects of En2 deficiency on forebrain-projecting monoaminergic fibers. Our findings thus suggest that adult exposure to stress may exacerbate behavioral and neuroanatomical phenotypes associated with developmental effects of genetic En2 deficiency.
Fragmented day-night cycle induces period lengthening, lowered anxiety, and anhedonia in male mice
Melissa E.S.RichardsonabDesireeBrownaDanielleHonoreaAndisaLabossierea
doi : 10.1016/j.bbr.2021.113453
Volume 413, 10 September 2021, 113453
Light exposure at night disrupts circadian-regulated biological functions, including mood. However, the consequence of fragmenting the night period and distributing it across the 24-hr period is less understood. Here we show that fragmenting an 8 -h and 6 -h night into equally distributed 2 -h periods throughout the 24-hr day results in period lengthening of the circadian rhythm in mice. Furthermore, mice exhibited less anxiety, which indicates increased risk-taking behavior, and a lack of pleasure-seeking, known as anhedonia. The successive alley and open field tests were used to assess anxiety, while the sucrose preference test was used to assess anhedonia. Analysis of depressive-like behaviors with the forced swim and tail suspension tests were not observed. After two weeks in 12 h light – 12 h dark, mice exposed to the fragmented night recovered and exhibited normal behaviors for both anxiety and anhedonia. Our results are congruent with published studies that describe the detrimental effects of constant light conditions on circadian rhythms and mood. These findings unveil the negative impact that fragmenting the day-night cycle has on circadian rhythms and mood.
Social impairments in mice lacking the voltage-gated potassium channel Kv3.1
SarahBeeaAmandaRinglandaLaurenceCoutellierab
doi : 10.1016/j.bbr.2021.113468
Volume 413, 10 September 2021, 113468
Parvalbumin (PV)-expressing neurons have been implicated in the pathology of autism spectrum disorders (ASD). Loss of PV expression and/or reduced number of PV-expressing neurons have been reported not only in genetic and environmental rodent models of ASD, but also in post-mortem analyses of brain tissues from ASD vs. healthy control human subjects. PV-expressing neurons play a pivotal role in the maintenance of the balance between excitation and inhibition within neural circuits in part because of their fast-spiking properties. Their high firing rate is mostly regulated by the voltage-gated potassium channel Kv3.1. It is yet unknown whether disturbances in the electrophysiological properties of PV-expressing neurons per se can lead to behavioral disturbances. We assessed locomotor activity, social interaction, recognition and memory, and stereotypic behaviors in Kv3.1 wild-type (WT) and knockout (KO) mice. We then used Western Blot analyses to measure the impact of Kv3.1 deficiency on markers of GABA transmission (PV and GAD67) and neural circuit activity (Egr1). Deficiency in Kv3.1 channel is sufficient to induce social deficits, hyperactivity and stereotypic behaviors. These behavioral changes were independent of changes in GAD67 levels and associated with increased levels of PV protein in the prefrontal cortex and striatum. These findings reveal that a loss of PV expression is not a necessary factor to induce an ASD-like phenotype in mice and support the need for further investigation to fully understand the contribution of PV-expressing neurons to ASD pathology.
Acute effects of high-intensity interval training and moderate-intensity continuous exercise on BDNF and irisin levels and neurocognitive performance in late middle-aged and older adults
Chia-LiangTsaiaChien-YuPanbYu-TingTsengcdFu-ChenChenbYu-ChuanChangaTsai-ChiaoWanga
doi : 10.1016/j.bbr.2021.113472
Volume 413, 10 September 2021, 113472
The purposes of the present study were (1) to explore and compare the acute effects of high-intensity interval training (HIIT) and moderate-intensity continuous exercise (MICE) on neurocognitive performance and molecular biomarkers in late middle-aged and older adults, and (2) to examine the relationships of HIIT/MICE exercise-induced neurocognitive changes with changes in circulating irisin and BDNF levels elicited by different acute exercise modes. Using a within-subject design, twenty-one participants completed an acute bout of 30 min of HIIT, MICE, or a non-exercise-intervention (REST) session in a counterbalanced order. The neuropsychological [i.e., accuracy rate (AR) and reaction time (RT)] and neurophysiological [i.e., event-related potential (ERP) P3 latency and amplitude] indices were simultaneously measured when the participants performed a working memory task at baseline and after an intervention mode. Blood samples were also taken before and after the intervention mode. The results showed that, although ARs were significantly increased only via the MICE intervention mode, the acute HIIT and MICE interventions improved RT performance and increased ERP P3 amplitudes in the late middle-aged and older adults under consideration. Serum BDNF levels were significantly increased with the acute HIIT and MICE interventions, and significant irisin level increases were only observed following the HIIT intervention. However, changes in the levels of Irisin and BDNF pre- and post-intervention were not correlated with changes in neurocognitive performance, with the exception of the correlation between the changes in irisin levels and RTs with acute exercise in the MICE intervention mode. The present findings suggested similar beneficial effects on neurocognitive performance (i.e., RTs and ERP P3 amplitudes) and peripheral BDNF levels following MICE and HIIT interventions in the middle-aged and older adults. In terms of ARs and irisin, the two acute exercise modes appear to induce divergent effects. Irisin may play a potential facilitating role in the neuropsychological (e.g., RT) performance of working memory in such a group. However, the mechanisms remain to be determined.
Estrous cycle modulates the anxiogenic effects of caffeine in the elevated plus maze and light/dark box in female rats
GabrielGuillén-RuizaJonathanCueto-EscobedobFabiolaHern?ndez-L?pezcLina E.Rivera-AburtodEmma V.Herrera-HuertaeJuan FranciscoRodr?guez-Landadf
doi : 10.1016/j.bbr.2021.113469
Volume 413, 10 September 2021, 113469
Caffeine is a commonly used stimulant of the central nervous system that reduces fatigue, increases alertness, and exerts positive effects on emotion through actions on various brain structures. High doses of caffeine can cause headaches, heart palpitations, hyperactivity, and anxiety symptoms. Consequently, reducing the consumption of stimulant substances, such as sugar and caffeine, is proposed to ameliorate symptoms of premenstrual syndrome in women. The administration of steroid hormones has been suggested to modulate the effects of caffeine, but unknown is whether endogenous hormone variations during the estrous cycle modulate the pharmacological effects of caffeine. The present study evaluated the effects of caffeine (10, 20, and 40 mg/kg) during metestrus-diestrus and proestrus-estrus of the ovarian cycle in rats on anxiety-like behavior using the elevated plus maze and light/dark box. During metestrus-diestrus, all doses of caffeine increased anxiety-like behavior, indicated by the main variables in both behavioral tests (i.e., higher Anxiety Index and lower percent time spent on the open arms in the elevated plus maze and less time spent in the light compartment in the light/dark box). During proestrus-estrus, only 20 and 40 mg/kg caffeine increased these parameters of anxiety-like behavior, albeit only slightly. In conclusion, caffeine increased anxiety-like behaviors in metestrus-diestrus, with an attenuation of these effects of lower doses of caffeine in proestrus-estrus. These effects that were observed in metestrus-diestrus and proestrus-estrus may be associated with low and high concentrations of steroid hormones, respectively, that naturally occur during these phases of the ovarian cycle.
Systemic administration of N-acetylcysteine during the extinction period and on the reinstatement day decreased the maintenance of morphine rewarding properties in the rats
Seyedeh-NajmehKatebiaAnahitaTorkaman-BoutorabiabNasimVousooghiabcEsmailRiahidAbbasHaghparaste
doi : 10.1016/j.bbr.2021.113451
Volume 413, 10 September 2021, 113451
Many animal studies and early clinical trials suggested that N-acetylcysteine (NAC) may benefit addiction treatment. The present study tried to evaluate whether chronic administration of systemic NAC during the extinction period and acute administration of systemic NAC on the reinstatement day could reduce the maintenance of the morphine rewarding properties in the conditioned place preference (CPP) paradigm in the rats. Ninety-six adult male Wistar rats (190?220 g) were examined with morphine (7 mg/kg; sc) and saline (1 mL/kg; sc) during the 3-day conditioning phase in the CPP paradigm. After the acquisition of morphine CPP, different doses of NAC were daily administered during the extinction period (5, 10, 25, and 50 mg/kg; ip), or 30 min before the CPP test on the reinstatement day (2, 5, 10, 25, and 50 mg/kg; ip). Conditioning score and locomotor activity were recorded by the video tracking system and Ethovision software after acquisition on the post-conditioning day, the extinction period, and reinstatement day. Daily NAC administration in high doses (25 and 50 mg/kg; ip) reduced extinction-responding compared with the vehicle-control group during the extinction period. Although a single injection of NAC in doses 10, 25, 50 mg/kg decreased the reinstatement of morphine-induced CPP, two lower doses (2 and 5 mg/kg) could not significantly reduce the CPP scores. These are the first data suggesting that NAC's application during the extinction period could attenuate the morphine reward-associated behaviors in the rats. Moreover, NAC could inhibit the reinstatement of morphine CPP, which adds to the growing appreciation that the NAC may have potential therapeutic use in combating morphine dependence. It can be consistent with the hypothesis of the involvement of the glutamatergic system in the pathophysiology of addiction.
Alpha neural oscillation of females in the luteal phase is sensitive to high risk during sequential risk decisions
JiajiaXiea1YangLua1JianhuaLibWeidongZhanga
doi : 10.1016/j.bbr.2021.113427
Volume 413, 10 September 2021, 113427
Risk taking is a non-negligible component in decision-making. Previous behavioral studies have demonstrated that female's risk decisions vary along with their menstrual cycle phases. However, little is known how females’ neural processes of risk stimuli change in different menstrual cycle phases. To address this, the present study adopted a sequential economic risk-taking task and EEG technique. Thirty eligible female participants completed the task twice with EEG recordings, once in the late follicular phase and once in the midluteal phase, separately. We found that the risk stimuli induced an evident frontal N1 in the early time window of 90?180 ms. The results on N1 showed no significant difference between two phases for low- and medium-risk stimuli; whereas, for high-risk stimuli, females in midluteal phase exhibited a significantly larger N1 than that in late follicular phase. Further, by exploiting time-frequency transformation, we observed a pronounced low alpha (?8 Hz) activity in frontal area from stimuli onset to 175 ms. The results indicated that, only for high-risk stimuli, the alpha power was significantly greater in midluteal phase than that in late follicular phase. Our neural results demonstrated a stronger early neural response to high-risk stimuli of females in midluteal phase, which suggests women are more sensitive to high risk in midluteal than in late follicular phase.
Combination of MAP6 deficit, maternal separation and MK801 in female mice: A 3-hit animal model of neurodevelopmental disorder with cognitive deficits
SolennPercelayThomasFreretNicoleTurnbullValentineBouet1MichelBoulouard1
doi : 10.1016/j.bbr.2021.113473
Volume 413, 10 September 2021, 113473
Schizophrenia is a major psychiatric disease still lacking efficient treatment, particularly for cognitive deficits. To go further in research of new treatments that would encompass all the symptoms associated with this pathology, preclinical animal models need to be improved. To date, the aetiology of schizophrenia is unknown, but there is increasing evidence to highlight its multifactorial nature. We built a new neurodevelopmental mouse model gathering a triple factor combination (3-M): a genetic factor (partial deletion of MAP6 gene), an early stress (maternal separation) and a late pharmacological factor (MK801 administration, 0.05?mg/kg, i.p., daily for 5 days). The effects of each factor and of their combination were investigated on several behaviours including cognitive functions.
