Passive Avoidance Learning Task Research Articles

Effects of Different Auditory Environments on Behavior, Learning Ability, and Fearfulness in 4-Week-Old Laying Hen Chicks.

Environmental enrichment can improve animal welfare. As a method of environmental enrichment, the effect of different auditory stimulations on the behavior response and welfare of laying hen chicks has yet to be investigated. Therefore, this study was aimed at exploring the impact of various auditory exposures on the behavior, learning ability, and fear response of 4-week-old laying hen chicks. A total of 600 1-day-old chicks were randomly assigned to five different groups: C (control group), LM (Mozart's String Quartets, 65 to 75 dB), LN (recorded ventilation fans and machinery, 65 to 75 dB), HN (recorded ventilation fans and machinery, 85 to 95 dB), and HM (Mozart's String Quartets, 85 to 95 dB). The experiment was conducted from day 1 until the end of the experiment on day 28. Groups LM and LN were exposed to music and noise stimulation ranging from 65 to 75 dB. Groups HN and HM, meanwhile, received noise and music stimulation ranging from 85 to 95 dB. The control group (C) did not receive any additional auditory stimuli. During the experimental period, continuous behavioral recordings were made of each group of chicks from day 22 to day 28. On day 21, the PAL (one-trial passive avoidance learning) task was conducted. On days 23 and 24, OF (open field) and TI (tonic immobility) tests were performed, and the levels of serum CORT (corticosterone) and DA (dopamine) were measured. The results indicated that exposure to music and noise at intensities ranging from 85 to 95 dB could reduce comforting, preening, PAL avoidance rate, the total number of steps and grid crossings of OF, and the concentration of DA in 4 WOA chicks (p < 0.05), increase the freezing times of OF (p < 0.05); 65 to 75 dB of noise stimulation could reduce preening and total number steps of OF in 4 WOA chicks (p < 0.05), increase the freezing times of OF (p < 0.05); and 65 to 75 dB of music exposure could reduce the concentration of CORT in 4 WOA chicks (p < 0.05). Therefore, 65 to 75 dB of music exposure could produce positive effects on chicks and showed relatively low CORT level, whereas 85 to 95 dB of music and noise exposure could reduce comforting and preening behavior, impair learning ability, and increase the fear responses of chicks.

Latent profiles of substance use, early life stress, and attention/externalizing problems and their association with neural correlates of reinforcement learning in adolescents.

Adolescent substance use, externalizing and attention problems, and early life stress (ELS) commonly co-occur. These psychopathologies show overlapping neural dysfunction in the form of reduced recruitment of reward processing neuro-circuitries. However, it is unclear to what extent these psychopathologies show common v. different neural dysfunctions as a function of symptom profiles, as no studies have directly compared neural dysfunctions associated with each of these psychopathologies to each other. In study 1, a latent profile analysis (LPA) was conducted in a sample of 266 adolescents (aged 13-18, 41.7% female, 58.3% male) from a residential youth care facility and the surrounding community to investigate substance use, externalizing and attention problems, and ELS psychopathologies and their co-presentation. In study 2, we examined a subsample of 174 participants who completed the Passive Avoidance learning task during functional magnetic resonance imaging to examine differential and/or common reward processing neuro-circuitry dysfunctions associated with symptom profiles based on these co-presentations. In study 1, LPA identified profiles of substance use plus rule-breaking behaviors, attention-deficit hyperactivity disorder, and ELS. In study 2, the substance use/rule-breaking profile was associated with reduced recruitment of reward processing and attentional neuro-circuitries during the Passive Avoidance task (p < 0.05, corrected for multiple comparisons). Findings indicate that there is reduced responsivity of striato-cortical regions when receiving outcomes on an instrumental learning task within a profile of adolescents with substance use and rule-breaking behaviors. Mitigating reward processing dysfunction specifically may represent a potential intervention target for substance-use psychopathologies accompanied by rule-breaking behaviors.

Royal jelly improves learning and memory deficits in an amyloid β-induced model of Alzheimer's disease in male rats: Involvement of oxidative stress.

Alzheimer's disease (AD) as the commonest type of dementia is associated with the cognitive function failure. Oxidative stress performs an essential role in the progression of AD. Royal jelly (RJ) is a natural product of bees with antioxidant and anti-inflammatory properties. The present research aimed to investigate the possible protective effect of RJ on learning and memory in a rat model of Aβ-induced AD. Forty male adult Wistar rats were equally distributed into five groups: control, sham-operated, Aβ (receiving intracerebroventricular (ICV) injection of amyloid beta (Aβ1-40)), Aβ + RJ 50mg/kg, and Aβ + RJ 100mg/kg. RJ was administered daily post-surgery by oral gavage for four weeks. Behavioral learning and memory were examined using the novel object recognition (NOR) and passive avoidance learning (PAL) tests. Also, oxidative stress markers, such as malondialdehyde (MDA), total oxidant status (TOS) and total antioxidant capacity (TAC), were assessed in the hippocampus. Aβ reduced step-through latency (STLr) and increased time spent in the dark compartment (TDC) in the PAL task and also decreased discrimination index in the NOR test. Administration of RJ ameliorated the Aβ-related memory impairment in both NOR and PAL tasks. Aβ decreased TAC and increased MDA and TOS levels in the hippocampus, whereas RJ administration reversed these Aβ-induced alterations. Our results indicated that RJ has the potential to ameliorate learning and memory impairment in the Aβ model of AD via attenuating oxidative stress.

The effects of polyvinyl alcohol-coated selenium nanoparticles on memory impairment in rats.

Some mineral elements exert beneficial neuroprotection, especially in the form of nanoparticles. The aim of the present study was to evaluate the effects of selenium nanoparticles (SeNPs) and polyvinyl alcohol (PVA)-coated SeNPs (PVA-SeNPs) on Alzheimer's disease (AD) in a rat model of AD. Twenty-eight rats were randomly divided into four groups of seven rats: control, Alz, Alz + Se, and Alz + Se-PV groups. PVA-SeNPs and SeNPs were chemically synthesized and orally administrated (0.4mg/kg) to the AD rats for one month. AD was induced by an intracerebroventricular (ICV) injection of streptozotocin (STZ). The memory function was assessed by the novel object recognition (NOR) and passive avoidance learning (PAL) tests. The expression of hippocampal brain-derived neurotrophic factor (BDNF) and stress oxidative markers (MDA and TAC), and the number of amyloid-beta (Aβ) plaques were assessed using ELISA kits, biochemical methods, and Congo red staining, respectively. The results of the behavioral tests showed that the discrimination index in the NOR test increased in the Alz + PVA-SeNPs group compared to the Alz group. Memory performance in the PAL task improved in the PVA-SeNPs and SeNPs groups compared to the Alz group. The level of the BDNF in both of the Alz treatment groups (PVA-SeNPs and SeNPs) showed a significant increase compared to the Alz group. MDA levels and Aβ plaques decreased in both NPs-treated Alz groups, while TAC levels decreased in all Alz groups. PVA-SeNPs were more effective than SeNPs in the improvement of the cognition deficit. The results suggest that PVA-SeNPs improve the cognition and memory deficit induced by an ICV injection of STZ through a decrease in the number of Aβ plaques and malondialdehyde levels and an increase in the BDNF levels.

The effect of minocycline on beta-amyloid-induced memory and learning deficit in male rats: A behavioral, biochemical, and histological study

ObjectivesMinocycline hydrochloride is a semi-synthetic, second-generation tetracycline with neuroprotective, neurorestorative, anti-amyloidogenic, anti-inflammatory, antioxidant, and anti-apoptotic properties. The present study was designed to investigate the potential protective effects of minocycline against beta-amyloid (Aβ)-induced Alzheimer’s disease (AD), recognition memory decline, and the possible involved anti-apoptotic mechanisms. MethodsThe rats were treated with minocycline (50 and 100 mg/kg/day; P.O.) after AD induction for 30 days. Behavioral functions were assessed by employing standard behavioral tests, including novel object recognition (NOR) and passive avoidance learning (PAL) tasks. Then, total antioxidant capacity (TAC) and total oxidant status (TOS) were measured in blood serum using ELISA kits. Apoptosis and the number of Aβ plaques were examined by the TUNEL and Congo red staining, respectively. ResultsTreatment of Aβ rats with minocycline improved memory deficit in the PAL task and a decline in recognition memory in the NOR test. Minocycline at 50 and 100 mg/kg significantly reduced the TOS levels and increased the TAC levels (P < 0.0001). Also, minocycline at 50 and 100 mg/kg reduced the apoptotic index in the hippocampus of Aβ rats. After Congo red staining, the minocycline group showed improved cell morphology and markedly fewer Aβ plaques. ConclusionsMinocycline reduced memory and learning deficit in behavioral experiments after Aβ injection, which may be due to its anti-inflammatory and anti-apoptotic effects.

Ameliorating effect of fluoxetine on tamoxifen-induced memory loss: The role of corticolimbic NMDA receptors and CREB/BDNF/cFos signaling pathways in rats

Tamoxifen-induced cognitive dysfunction may lead to fluoxetine consumption in patients with breast cancer. Since the brain mechanisms are unclear in tamoxifen/fluoxetine therapy, the blockade effect of hippocampal/amygdala/prefrontal cortical NMDA receptors was examined in fluoxetine/tamoxifen-induced memory retrieval. We also assessed the corticolimbic signaling pathways in memory retrieval under the drug treatment in adult male Wistar rats. Using the Western blot technique, the expression levels of the cAMP response element-binding protein (CREB), brain-derived neurotrophic factor (BDNF), and cFos were evaluated in the corticolimbic regions. The results showed that pre-test administration of fluoxetine (3 and 5 mg/kg, i.p.) improved tamoxifen-induced memory impairment in the passive avoidance learning task. Pre-test bilateral microinjection of D-AP5, a selective NMDA receptor antagonist, into the dorsal hippocampal CA1 regions and the central amygdala (CeA), but not the medial prefrontal cortex (mPFC), inhibited the improving effect of fluoxetine on tamoxifen response. It is important to note that the microinjection of D-AP5 into the different sites by itself did not affect memory retrieval. Memory retrieval increased the signaling pathway of pCREB/CREB/BDNF/cFos in the corticolimbic regions. Tamoxifen-induced memory impairment decreased the hippocampal/PFC BDNF level and the amygdala level of pCREB/CREB/cFos. The improving effect of fluoxetine on tamoxifen significantly increased the hippocampal/PFC expression levels of BDNF, the PFC/amygdala expression levels of cFos, and the ratio of pCREB/CREB in all targeted areas. Thus, NMDA receptors’ activity in the different corticolimbic regions mediates fluoxetine/tamoxifen memory retrieval. The corticolimbic synaptic plasticity changes likely accompany the improving effect of fluoxetine on tamoxifen response.

Post-Weaning Treatment with Probiotic Inhibited Stress-Induced Amnesia in Adulthood Rats: The Mediation of GABAergic System and BDNF/c-Fos Signaling Pathways.

The current study aimed to examine the effect of post-weaning treatment with probiotics on memory formation under stress during the adult period in male Wistar rats. Considering GABA is a potential mediator between probiotics and the host, the present study also investigated the involvement of the GABAergic system in the probiotic response. The hippocampal and prefrontal cortical (PFC) expression levels of BDNF and c-Fos were also assessed to show whether the treatments affect the memory-related signaling pathway. Three weeks after birth, the post-weaning rats were fed with probiotic water (PW) or tap water (TW) for 2, 3, 4, or 5weeks. Exposure to acute stress impaired memory formation in a passive avoidance learning task. Feeding the post-weaning animals with probiotic strains (3, 4, or 5weeks) inhibited stress-induced amnesia of the adult period. Post-training intracerebroventricular (ICV) microinjection of muscimol improved stress-induced amnesia in the animals fed with TW. ICV microinjection of muscimol inhibited probiotic treatment's significant effect on the stress response in the memory task. The expression levels of BDNF and c-Fos in the PFC and the hippocampus were significantly decreased in the stress animal group. The levels of BDNF and c-Fos were increased in the PW/stress animal group. The muscimol response was compounded with the decreased levels of BDNF and c-Fos in the PFC and the hippocampus. Thus, the GABA-A receptor mechanism may mediate the inhibitory effect of this probiotic mixture on stress-induced amnesia, which may be associated with the PFC and hippocampal BDNF/c-Fos signaling changes.

Protective effects of L-carnitine against valproic acid-induced memory impairment and anxiety-like behavior in adult rat

This study was designed to explore the effects of valproic acid (VPA) on spatial and passive avoidance learning and memory as well as to assess the protective effects of L-Carnitine (LC) against VPA-induced memory deficit in the rat. Male Wistar rats received VPA (300 mg/kg/daily by i.p. injection), or LC (50 mg/kg/ daily by i.p. injection), or co-treatment with VPA and LC for 28 days. Following 28 days, Elevated Plus-Maze (EPM), Morris Water Maze (MWM), and Passive Avoidance Learning (PAL) tasks were used to evaluate the anxiety-like behavior and spatial and passive learning and memory, respectively. Our results showed that VPA has no effect on memory acquisition (in both MWM and PAL) but induced reference memory impairment. We demonstrated that treatment with LC partially ameliorated the impairment in the retrieval of reference memory and passive avoidance learning. Moreover, VPA increased anxiety-like behavior, which was partially reversed by the administration of LC. In conclusion, these results show that LC is effective in counteracting the anxiety-like behavior and reference memory impairment caused by VPA. Therefore, LC may serve as a possible therapeutic agent for VPA-induced memory change.

Prenatal Exposure to Classical Music Improves Learning and Memory in Adult Rats

Abstract. Background: Exposure to music during pregnancy enhances brain development and improves learning in neonatal rats. Methods: In these experiments, we examined the effects of exposure to silence, hard rock, classical, and rap music in utero plus 60 days postpartum on learning and memory in adult Wistar rats. Passive avoidance learning (PAL) was assessed at age 60 days, and a retention test was done 24 hours after training. Elevated plus maze (EPM) was also used as a standard behavioral task for assessing the effects of music therapy on anxiety. Furthermore, we measured serum corticosterone levels and adrenal weight at the end of experiments to show the possible effect of stress on the rats’ behavior. Results: Hard rock music impaired acquisition, increasing the number of trials to acquisition in PAL task. Hard rock music also impaired the retrieval process by decreasing step-through latency and increasing time spent in the dark compartment during the retention trial. Further, in the hard rock group, there were increases in serum corticosterone and adrenal weight of rats. Classical music, in turn, improved acquisition learning and retention memory and decreased serum corticosterone levels compared to the silence group. Rats’ exposure to rap music did not show any significant change in acquisition and retrieval processes compared to the silence group. In the EPM task, classical music exposure had anxiolytic-like effects revealed in an increase in the number of entries into open arms and time spent in the open arms. However, in this task, hard rock music induced an anxiogenic effect. Conclusions: Prenatal and postnatal exposure to music improves PAL and memory in adult rats. The effects of music therapy with classical music might be related to stress reduction by lowering corticosterone as a stress biomarker or anxiolytic effects; this deserves further examination.

Effect of prenatal different auditory environment on learning ability and fearfulness in chicks.

ObjectiveEarly environmental enrichment in life can improve cognition in animals. The effect of prenatal auditory stimulation on learning ability and fear level in chick embryos remained unexplored. Therefore, this study investigated the effect of prenatal auditory stimulation on the learning ability and fear level of chicks.MethodsA total of 450 fertilized eggs were randomly divided into 5 groups, including control group (C), low-sound intensity music group (LM), low-sound intensity noise group (LN), high-sound intensity noise group (HN) and high-sound intensity music group (HM). From the 10th day of embryonic development until hatching, group LM and group LN received 65 to 75 dB of music and noise stimulation. Group HN and group HM received 85 to 95 dB of noise and music stimulation, and group C received no additional sound. At the end of incubation, the one-trial passive avoidance learning (PAL) task and tonic immobility (TI) tests were carried out, and the serum corticosterone (CORT) and serotonin (5-HT) concentrations were determined.ResultsThe results showed that compared with the group C, 65 to 75 dB of music and noise stimulation did not affect the PAL avoidance rate (p>0.05), duration of TI (p>0.05) and the concentration of CORT (p>0.05) and 5-HT (p>0.05) in chicks. However, 85 to 95 dB of music and noise stimulation could reduce duration of TI (p<0.05) and the concentration of CORT (p<0.05), but no significant effect was observed on the concentration of 5-HT (p>0.05) and PAL avoidance rate (p>0.05).ConclusionTherefore, the prenatal auditory stimulation of 85 to 95 dB can effectively reduce the fear level of chicks while it does not affect the learning ability.

Different forms of childhood maltreatment have different impacts on the neural systems involved in the representation of reinforcement value

BackgroundThe current study aimed to address two gaps in the literature on child maltreatment, reinforcement processing and psychopathology. First, the extent to which compromised reinforcement processing might be particularly associated with either neglect or abuse. Second, the extent to which maltreatment-related compromised reinforcement processing might be associated with particular symptom sets (depression, conduct problems, anxiety) or symptomatology more generally. MethodsA sample of adolescents (N = 142) aged between 14 and 18 years with varying levels of prior maltreatment participated in this fMRI study. They were scanned while performing a passive avoidance learning task, where the participant learns to respond to stimuli that engender reward and avoid responding to stimuli that engender punishment. Maltreatment (abuse and neglect) levels were assessed with the Childhood Trauma Questionnaire (CTQ). ResultsWe found that: (i) level of neglect, but not abuse, was negatively associated with differential BOLD responses to reward-punishment within the striatum and medial frontal cortex; and (ii) differential reward-punishment responses within these neglect-associated regions were particularly negatively associated with level of conduct problems. ConclusionOur findings demonstrate the adverse neurodevelopmental impact of childhood maltreatment, particularly neglect, on reinforcement processing. Moreover, they suggest a neurodevelopmental route by which neglect might increase the risk for conduct problems.

Cannabidiol Attenuates MK-801-Induced Cognitive Symptoms of Schizophrenia in the Passive Avoidance Test in Mice.

Schizophrenia is a chronic mental disorder that disturbs feelings and behavior. The symptoms of schizophrenia fall into three categories: positive, negative, and cognitive. Cognitive symptoms are characterized by memory loss or attentional deficits, and are especially difficult to treat. Thus, there is intense research into the development of new treatments for schizophrenia-related responses. One of the possible strategies is connected with cannabidiol (CBD), a cannabinoid compound. This research focuses on the role of CBD in different stages of memory (acquisition, consolidation, retrieval) connected with fear conditioning in the passive avoidance (PA) learning task in mice, as well as in the memory impairment typical of cognitive symptoms of schizophrenia. Memory impairment was provoked by an acute injection of the N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (animal model of schizophrenia). Our results revealed that an acute injection of CBD (30 mg/kg; intraperitoneally (i.p.) improved all phases of long-term fear memory in the PA test in mice. Moreover, the acute injection of non-effective doses of CBD (1 or 5 mg/kg; i.p.) attenuated the memory impairment provoked by MK-801 (0.6 mg/kg; i.p.) in the consolidation and retrieval stages of fear memory, but not in the acquisition of memory. The present findings confirm that CBD has a positive influence on memory and learning processes in mice, and reveals that this cannabinoid compound is able to attenuate memory impairment connected with hypofunction of glutamate transmission in a murine model of schizophrenia.

Effects of vanillic acid on Aβ1-40-induced oxidative stress and learning and memory deficit in male rats

Alzheimer's disease (AD) is a neurodegenerative disease, in which the accumulation of β-amyloid (Aβ) peptide in the extracellular space causes a progressive reduction in cognitive performance. Aβ stimulates active oxygen species generation leading to oxidative stress and neural cell death. Vanillic Acid (VA) is the oxidant form of vanillin widely found in vanilla beans. VA has many properties, such as suppressing apoptosis and eliminating the harmful effects of oxidative stress in animal models. The VA effects on impaired learning and memory in Aβ rats were assessed. Forty adults male Wistar rats were assigned to the following five groups in random: the control, sham (received saline (vehicle) via intracerebroventricular (ICV) injection), Aβ (received Aβ1–40 via ICV injection), VA (50 mg/kg by oral gavage once a day through four weeks), and Aβ + VA (50 mg/kg) groups. Open field test, novel object recognition (NOR) test, Morris water maze (MWM) test, and passive avoidance learning (PAL) task were performed, and finally, we determined the malondialdehyde (MDA), total antioxidant capacity (TAC) and total oxidant status (TOS) levels. Aβ decreased the cognitive memory in NOR, spatial memory in MWM, and passive avoidance memory in PAL tests. In contrast, VA improved learning and memory in the treated group. Aβ significantly increased MDA and TOS and decreased TAC levels, whereas VA treatment significantly reversed TAC, TOS and MDA levels. In conclusion, VA decreased the Aβ effects on learning and memory by suppressing oxidative stress and can be regarded as a neuroprotective substance in AD.

Electrophysiological, Behavioral and Molecular Study of Vitamin E and Ginkgo biloba in a Rat Model of Alzheimer’s Disease

Background and objectives: Alzheimer's disease (AD) is characterized by progressive cognitive decline. Oxidative stress plays a central role in the pathogenesis of AD. It has been proposed that administration of antioxidants affect cognitive processes, such as learning and memory. This study investigated the protective effects of vitamin E and Ginkgo biloba extract (as antioxidants) on learning and memory, hippocampal plasticity, and apoptotic marker proteins in a rat model of AD. Methods: The hyroalcoholic extract of Gingko biloba leaves wasprepared using maceration method. Male Wistar rats were randomly divided into six groups: control, sham received intra-hippocampal injection (I.H.P) of vehicle, AD model that received intra-hippocampal injection of the beta-amyloid (Aβ), AD+ vitamin E (200 mg/kg, i.p.), AD+ G. biloba (100 mg/kg/p.o.), and AD+ vitamin E (200 mg/kg, i.p.)+ G. biloba (100 mg/kg/p.o.). At the end of the treatments, the rats were subjected to the passive avoidance learning (PAL) test. The field long wterm potentials (LTP) were recorded in the hippocampal dentate gyrus. Hippocampal expressions of Bax and Bcl-2 (as pro-apoptotic, as anti-apoptotic) proteins were measured by western blot method. Results: Treatment with G. biloba and vitamin E improved the Aβ-induced memory impairment in the PAL task. Vitamin E and/or G. biloba extract enhanced the population spike amplitude evoked potentials of the LTP components, vitamin E and/or G. biloba extract increased Bcl-2 expression and decreased Bax expression in the hippocampus. Conclusion: Ginkgo biloba and vitamin E could suppress the expression of apoptosis markers and improved hippocampal LTP impairment and the memory deficit induced by Aβ.

Chronic NaHS treatment improves spatial and passive avoidance learning and memory and anxiety-like behavior and decreases oxidative stress in rats fed with a high-fat diet

Cognitive function is impaired by increased consumption of a high-fat diet (HFD). Also, HFD consumption can alter hydrogen sulfide (H2S) metabolism. H2S is an important signaling molecule with antioxidant effects that regulates multiple functions in the brain. In the present study, we investigated the effect of sodium hydrosulfide (NaHS, an H2S donor) on cognitive impairment and oxidative stress changes induced by HFD consumption. Following 11 weeks of HFD regimes in Wistar rats, elevated plus-maze (EPM), Morris water maze (MWM), and passive avoidance learning (PAL) tasks were used to evaluate the anxiety-like behavior and spatial and passive learning and memory, respectively. Daily intraperitoneal injection of NaHS was done during the dietary regimen. Serum and hippocampal oxidative stress biomarkers (malondialdehyde (MDA), total antioxidant capacity (TAC), and total oxidant status (TOS)) were measured. We demonstrated that treatment with NaHS ameliorated the impairment in the retrieval of reference memory and passive avoidance learning. Moreover, HFD increased anxiety-like behavior, which was reversed by the administration of NaHS. Additionally, the increase in MDA and TOS and the decrease in TAC induced by HFD in the serum and hippocampus were significantly reduced following administration of NaHS. These results indicate that NaHS could significantly ameliorate HFD-induced spatial and passive learning and memory impairment and anxiety-like behavior, at least in part, via its antioxidant activities. Therefore, the administration of NaHS can provide a therapeutic approach for HFD-induced memory impairment.

Reward and Punishment Sensitivity in Borderline and Avoidant Personality Disorders.

The authors compared self-reported and behavioral responses to reward and punishment in individuals diagnosed with borderline personality disorder (BPD) or avoidant personality disorder (APD) relative to a healthy comparison (HC) group. As predicted, self-reported sensitivity to reward was significantly higher in the BPD group than in the APD and HC groups. Also as predicted, self-reported sensitivity to punishment was significantly elevated in both disordered groups but significantly higher in APD than in BPD. These hypothesized patterns were also evident in responses to behavioral tasks: Participants with BPD made more errors of commission and fewer errors of omission than HC participants on a passive avoidance learning task, and participants with APD showed greater reactivity to losses than other participants on a probabilistic reversal learning task. Results help characterize differences between these two disorders.

Alcohol Use Disorder, But Not Cannabis Use Disorder, Symptomatology in Adolescents Is Associated With Reduced Differential Responsiveness to Reward Versus Punishment Feedback During Instrumental Learning

BackgroundThe two most commonly used illegal substances by adolescents in the United States are alcohol and cannabis. Alcohol use disorder (AUD) and cannabis use disorder (CUD) have been associated with dysfunction in decision-making processes in adolescents. One potential mechanism for these impairments is thought to be related to abnormalities in reward and punishment processing. However, very little work has directly examined potential differential relationships between AUD and CUD symptom severity and neural dysfunction during decision making in adolescents. MethodsIn the current study, 154 youths participated in a passive avoidance learning task during functional magnetic resonance imaging to investigate the relationship between relative severity of AUD/CUD and dysfunction in processing reward and punishment feedback. ResultsIncreasing Alcohol Use Disorder Identification Test scores were associated with reduced neural differentiation between reward and punishment feedback within regions of striatum, posterior cingulate cortex, and parietal cortex. However, increasing Cannabis Use Disorder Identification Test scores were not associated with any neural dysfunction during the passive avoidance task. ConclusionsThese data expand on emerging literature that relative severity of AUD is associated with reduced responsivity to rewards in adolescents and that there are differential associations between AUD and CUD symptoms and neurocircuitry dysfunction in the developing adolescent brain.

The protective and therapeutic effects of vinpocetine, a PDE1 inhibitor, on oxidative stress and learning and memory impairment induced by an intracerebroventricular (ICV) injection of amyloid beta (aβ) peptide

Alzheimer’s disease (AD) is a neurodegenerative disease leading to cognitive and memory impairment. This study aimed at investigating the therapeutic and preserving effects of vinpocetine on amyloid beta (Aβ)-induced rat model of AD. Sixty male adult Wistar rats were randomly divided into 6 groups (n = 10 per group) as follows: 1; control, 2; sham, 3; Aβ, 4; pre-treatment (vinpocetine + Aβ): oral gavage administration of vinpocetine at 4 mg/kg for 30 days followed by intracerebroventricular (ICV) injection of Aβ, 5; treatment (Aβ + vinpocetine): Aβ ICV injection followed by vinpocetine administration for 30 days, 6; pre-treatment + treatment (vinpocetine + Aβ + vinpocetine): vinpocetine administration for 30 days before and 30 days after AD induction. Following treatments, the animals’ learning and memory were investigated using passive avoidance learning (PAL) task, Morris water maze (MWM), and novel object recognition (NOR) tests. The results demonstrated that Aβ significantly enhanced escape latency and the distance traveled in the MWM, decreased step-through latency, and increased time spent in the dark compartment in PAL. Vinpocetine ameliorated the Aβ-infused memory deficits in both MWM and PAL tests. Administration of vinpocetine in the Aβ rats increased the discrimination index of the NOR test. It also significantly diminished the nitric oxide and malondialdehyde levels and restored the reduced glutathione (GSH) levels. Vinpocetine can improve memory and learning impairment following Aβ infusion due to its different properties, including antioxidant effects, which indicates that vinpocetine administration can lead to the amelioration of cognitive dysfunction in AD.

Lidocaine Reversible Inactivation of the Central Nucleus of Amygdala Impairs Acquisition, Consolidation, and Retrieval of Morphine State-Dependent Learning in Rat

Background/Aims: Morphine causes state-dependent learning that its mechanism and brain-related structures are not fully understood. This study aimed to determine whether lidocaine reversible inactivation of the central nucleus of the amygdala (CeA) could affect acquisition, consolidation, and retrieval of morphine state-dependent learning. Methods: One hundred twenty male Wistar rats were allocated into 15 experimental groups. Subcutaneous administration of morphine (5 mg/kg) induced morphine state-dependent learning. Intra-CeA injection of Lidocaine hydrochloride was performed 5 min before each morphine session for transient inactivation of the CeA. The step-through latency and the time spent in the dark compartment were measured using passive avoidance learning task. Results: Our results showed that pretraining, posttraining, and pretest inhibition of the CeA severely impaired acquisition, consolidation, and retrieval of morphine state-dependent learning. Conclusion: These data revealed the involvement of the CeA in different stages of memory and morphine state-dependent learning.

Effect of Crataegus extract supplementation on diabetes induced memory deficits and serum biochemical parameters in male rats

This study was undertaken to investigate the Crataegus extract (CE) eff ;ects on diabetes-induced memory deficit in passive avoidance learning (PAL), blood glucose, and lipid profile panel. Male Wistar rats were divided into five groups: Control (CTRL); Diabetic (DM); and Diabetic animals treated with three doses of CE (100, 300 and 1000 mg/kg) (DM + CE). Streptozotocin (STZ)-induced diabetic rats (50 mg/kg, ip) were orally administrated with CE once a day for 2 weeks. After 2 weeks, PAL task was used to evaluate the passive avoidance learning and memory. At the end of experiment, the level of plasma glucose, triglycerides (TG), cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were determined. Our results showed that the step-through latency (STLr) in diabetic animals was less than the control group (P = 0.0009). Crataegus (300 mg) increased STLr in diabetic animals (P = 0.0418). Diabetic animals spent more time in the dark compartment (TDC) (P = 0.0009). Crataegus (300 and 1000 mg) decreased TDC in diabetic animals (P = 0.0175). Crataegus (100 and 300 mg) decreased blood glucose in diabetic animals (P < 0.001). TG and Cholesterol concentration increased in diabetic animals in comparison with control (P < 0.05). CE (100 and 300 mg) reduced the cholesterol concentration in diabetic animals (P < 0.001). There was no significant difference in the case of LDL among the experimental groups (P > 0.05). CE (1000 mg) increased HDL in diabetic animals (P < 0.05). Our findings demonstrated that CE had the hypolipidemic and hypoglycemic effects and lead to memory improvement in STZ-induced diabetes.