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The neuropeptide relaxin-3 and its cognate receptor, relaxin family peptide-3 receptors (RXFP3), have been implicated in modulating learning and memory processes, but their specific roles remain unclear. This study utilized behavioral and molecular approaches to investigate the effects of putatively reversible blockade of RXFP3 in the ventral dentate gyrus (vDG) of the hippocampus on spatial and fear memory formation in rats. Male Wistar rats received bilateral vDG cannula implantation and injections of the RXFP3 antagonist, R3(BΔ23-27)R/I5 (400 ng/0.5 µL per side), or vehicle at specific time points before acquisition, consolidation, or retrieval phases of the Morris water maze and passive avoidance learning tasks. RXFP3 inhibition impaired acquisition in the passive avoidance task but not the spatial learning task. However, both memory consolidation and retrieval were disrupted in both tasks following RXFP3 antagonism. Ventral hippocampal levels of the consolidation-related kinase p70-S6 kinase (p70S6K) were reduced RXFP3 blockade. These findings highlight a key role for ventral hippocampal RXFP3 signaling in the acquisition, consolidation, and retrieval of spatial and emotional memories, extending previous work implicating this neuropeptide system in hippocampal memory processing.

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Abstract Amitriptyline (AMT) was developed for the treatment of chronic and neuropathic pain. There is also evidence it may be useful in the treatment of neurodegenerative disorders. In this regard, the effect of on the experimental model of seizures and memory impairment caused by seizures in rats is investigated in the present study. Seizures in Wistar rats (200-250 g) were induced by pentylenetetrazole (PTZ, 60 mg/kg, intraperitoneally (i.p.)). The anticonvulsant effect of AMT (10 and 20 mg/kg, i.p.) was evaluated in the seizure model. The effect on memory was assessed using passive avoidance (PA) learning and memory test. After behavioral tests, the animals underwent deep anesthesia and were put down painlessly. Animal serum was isolated for oxidant/antioxidant assays (malondialdehyde (MDA), and glutathione peroxidase (GPx)). Intraperitoneal injection of AMT decreased the mean number of myoclonic jerks and generalized tonic-clonic seizure (GTCS) duration and increased the mean latency of myoclonic jerk and GTCS compared to the PTZ group. Moreover, in the PA test, AMT caused a significant increase in retention latency (RL) and total time spent in the light compartment (TLC) compared to the PTZ group. Biochemical tests showed that AMT was able to significantly increase GPx serum levels and significantly reduce MDA serum levels compared to the PTZ group. Overall, this study suggests the potential neuroprotective effects of the AMT drug in a model of memory impairment caused by seizures via the mechanism of inhibition of the oxidative stress pathway.

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Neurotransmitter and neuromodulator neurotensin (NT) has been proved to facilitate spatial and passive avoidance learning after microinjected into the rat central nucleus of amygdala (CeA). These previous studies of our laboratory also revealed that neurotensin-1 receptor (NTS1) is involved in the mentioned actions of NT. Extensive literature confirms the interaction between neurotensinergic and dopaminergic systems, and our research group also suppose that the mesolimbic dopaminergic system (MLDS) is involved in the spatial learning and memory-facilitating effect of NT in the CeA. In the present work, NT and dopamine (DA) interaction has been examined in the Morris water maze and passive avoidance tests. Rats received 100 ng NT, 5 µg dopamine D2 receptor antagonist sulpiride in itself, sulpiride as a pretreatment before NT or vehicle solution into the CeA. NT microinjection significantly decreased target-finding latency in the Morris water maze test and significantly increased entrance latency in the passive avoidance test, as was expected based on our previous findings. The DA D2 receptor antagonist pretreatment was able to inhibit both effects of NT. The results confirm the facilitatory effect of NT on spatial learning and memory and let us conclude that these actions can be exerted via the DA D2 receptors.

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Mainly found in brussels sprouts, broccoli, and black mustard seeds, sinigrin (2-propenyl glucosinolate) has enjoyed some attention currently for its effects on health and disease prevention. The present research design is aimed at investigating the effects of sinigrin on inflammation, oxidative stress (OS) and memory. Randomly, six groups of male Wistar rats were categorized into the control and experimental groups. The experimental groups were treated with sinigrin (10 and 20 mg/kg, orally). The control positive group was given the pentylenetetrazole (PTZ) treatment and the control negative one was given normal saline. All groups were kindled by the sub-threshold dose (35 mg/kg, i.p.) of PTZ for 12 times in one month. When the kindling procedure was done, the seizure behaviors and the behavioral function were evaluated. For cognitive parameters, the shuttle box test was employed. When the experiment was terminated, the rats were euthanized and their blood serum as well as brain samples were isolated for respective measuring of OS and gene expression parameters. The treatment with sinigrin significantly delayed the appearance of the seizure symptoms in comparison to that of the PTZ group. It also significantly increased the memory parameters like retention latency and the total time having been spent in the light compartment in the epileptic rats. In addition, sinigrin increased the superoxide dismutase and catalase levels. Treatment with sinigrin suppressed the Il1b and Nlrp3 gene expression at hippocampal level. In sum, sinigrin prevents inflammation, OS and memory impairment against the PTZ-kindling epilepsy in rats.

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AIMS: To characterize exercise fatigue, metabolic phenotype and cognitive and mood deficits correlated with brain neuroinflammatory and gut microbiome changes in a chronic Gulf War Illness (GWI) mouse model. The latter have been described in an accompanying paper [1]. MAIN METHODS: Adult male C57Bl/6N mice were exposed for 28 days (5 days/week) to pyridostigmine bromide: 6.5 mg/kg, b.i.d., P.O. (GW1) or 8.7 mg/kg, q.d., P.O. (GW2); topical permethrin (1.3 mg/kg in 100% DMSO) and N,N-diethyl-meta-toluamide (DEET 33% in 70% EtOH) and restraint stress (5 min). Exercise, metabolic and behavioral endpoints were compared to sham stress control (CON/S). KEY FINDINGS: Relative to CON/S, GW2 presented persistent exercise intolerance (through post-treatment (PT) day 161), deficient associative learning/memory, and transient insulin insensitivity. In contrast to GW2, GW1 showed deficient long-term object recognition memory, milder associative learning/memory deficit, and behavioral despair. SIGNIFICANCE: Our findings demonstrate that GW chemicals dose-dependently determine the presentation of exercise fatigue and severity/type of cognitive/mood-deficient phenotypes that show persistence. Our comprehensive mouse model of GWI recapitulates the major multiple symptom domains characterizing GWI, including fatigue and cognitive impairment that can be used to more efficiently develop diagnostic tests and curative treatments for ill Gulf War veterans.

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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.

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Prenatal and early postnatal are the most sensitive and high-risk periods to expose to electromagnetic fields (EMFs). This study aimed to investigate the effect of prenatal and early postnatal exposure to 900 MHz radiofrequency waves (RFWs) emitted from a base transceiver station antenna on passive avoidance learning and memory (PALM) and hippocampus histomorphology. Female Sprague Dawley rats (190-230 g) were paired with males. The mated rats, confirmed by observing a vaginal plug, were divided into two groups; control and exposed. The control group (n = 7) was not exposed to RFW. The exposed group was divided into three subgroups (n = 8); exposed Ⅰ, exposed during the gestational period (fetal life), and exposed Ⅱ and Ⅲ (postnatal exposure), exposed to RFW during the first 21 days of life, for 2 h/d and 4 h/d, respectively. PALM was evaluated by a shuttle box in 45-day-old pups. Learning and memory of animals were demonstrated as the duration of remaining within the light area, which is called the lighting time. Histological sections were prepared from brain tissues and stained with hematoxylin and eosin. An impairment in the PALM performance was noticed in all exposed subgroups (Ⅰ, Ⅱ, and Ⅲ) (p < 0.05). Learning (short-term memory) and retention (long-term memory) behaviors were more affected in exposed subgroup Ⅰ (prenatal exposed) compared to other postnatal exposed subgroups (Ⅱ and Ⅲ). Also, a mild decrease in the density of pyramidal cells was observed in the hippocampus of exposed subgroups (Ⅰ and Ⅲ). Prenatal and early postnatal exposure to 900 MHz RFW adversely affected PALM performance and hippocampus tissue in rat pups with more impact for prenatal period exposure.

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Fluoxetine, a common antidepressant drug, is widely used for mental disorders therapy in adolescents. Previous animal experiments have indicated that exposure to fluoxetine during adolescence leads to persistent behavioral changes and neuroplasticity in the hippocampal formation and cortex which may continue until adulthood. Therefore, in the present experimental study, we examined the effects of chronic fluoxetine exposure (5 mg/kg/day, gavage) throughout adolescence (postnatal day 21-60) on passive avoidance learning and memory, pain sensitivity, and brain-derived neurotrophic factor (BDNF) level in the prefrontal cortex of young adult male and female rats. Passive avoidance learning, memory, and nociception were assessed by the shuttle box and hot plate tests respectively. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was applied to estimate the BDNF mRNA expression. Our data showed that chronic administration of fluoxetine had an increasing effect on passive avoidance memory in female animals. As well as, chronic fluoxetine treatment decreased latency of response to thermal stimulus in male and female rats. The mRNA expression of BDNF in the prefrontal cortex significantly increased in fluoxetine- exposed female rats. In conclusion, chronic fluoxetine treatment has sex-dependent effects on passive avoidance memory and BDNF mRNA expression, but the pain threshold decreases in both sexes. Therefore, passive avoidance memory, pain sensitivity, and the BDNF level are influenced by the manipulation of the serotonergic system.

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Objective: Metabolic syndrome (MetS) and insufficient vitamin D levels are globally increasing phenomena which are correlated with cognitive impairment. This study investigated the interactive effect of aerobic training with vitamin D supplementation on memory deficit in rats with metabolic syndrome induced by ovariectomy.Methods: A total of forty Wistar rats weighing 240-255 gr were randomly matched on their body weight and divided into ovariectomy (OVX, n = 32) and sham-operated (SHAM; n = 8) groups. OV group was then divided into vitamin D supplementation (OVX + Vit D; 10000 IU/kg/week, for 8 weeks, n = 8), aerobic training (OVX + AT; n = 8), aerobic training and vitamin D supplementation (OVX + AT + Vit D; 10000 IU/kg/week, for 8 weeks, n = 8), and vehicle control group receiving sesame oil (OVX + Ses Oil; n = 8). After the end of intervention, passive avoidance learning and memory were assessed in step through passive avoidance paradigm. Obtained data were analyzed by ANOVA and post hoc Tukey test.Results: After 8 weeks of aerobic training and vitamin D supplementation, step through dark compartment latency (STL) was significantly higher and total time spent in that compartment (TSD) was lower in OVX + AT + Vit D compared to the other counterpart groups.Conclusion: Vitamin D supplementation combined with 8-week aerobic training alleviates cognitive impairment metabolic syndrome induced by ovariectomy.

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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.

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AIM: In the present study, the effect of transient inactivation of the shell subregion of the nucleus accumbens (NAC shell) by lidocaine on the acquisition and retrieval stages of passive avoidance learning (PAL) and memory and morphine state-dependent learning (SDL) in male wistar rats was investigated. METHODOLOGY: Adult male wistar rats weighing (220-250 g) were used. Lidocaine hydrochloride was bilaterally injected into the shell area of the nucleus accumbens 5 min before of subcutaneous morphine administration. RESULTS: pre-training and pre-test infusion of lidocaine into the NAC shell significantly impaired PAL and memory. Furthermore, Pre-training administration of morphine (5 mg/kg, s.c.) in a step-through passive avoidance task induced state-dependent learning with impaired memory retrieval on the test day. The impairment of memory was restored after pre-test administration of the same dose of morphine. This phenomenon has been named as morphine state dependent learning (SDL). Moreover, Pre-training and pre-test inactivation of the NAC shell impaired morphine SDL. CONCLUSIONS: The results suggest the role of NAC shell as a common structure in the PAL and morphine SDL. It is suggested that NAC shell as a common area plays a critical role in the acquisition and retrieval stages of PAL and also morphine SDL.

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Methamphetamine (METH) abuse is one the most worldwide problems with wide-ranging effects on the central nervous system (CNS). Chronic METH abuse can associate with cognitive abnormalities and neurodegenerative changes in the brain. Agmatine, a cationic polyamine, has been proposed as a neuromodulator that modulates many effects of abused drugs. The aim of this study was to determine if agmatine can decrease the impairment effect of METH on memory and hippocampal CaMKII-α gene expression, a gene that plays a major role in memory. Male wistar rats (200-220 g) were allocated into 7 groups, including 5 groups of saline, METH (1, 2 mg/kg), Agmatine (5, 10 mg/kg) and 2 groups of agmatine (5, 10 mg/kg) with higher doses of METH (2 mg/kg) for 5 consecutive days (n = 8 in each group). All injections were done intraperitoneally and agmatine was administrated 10 min before METH treatment. Furthermore, Passive avoidance learning (PAL) test was assessed on the 5th day. Retention test was done 24 h after training and the rats were sacrificed immediately. Hippocampi were removed and stored at -80 °C. Finally, hippocampal CaMKII-α gene expression was measured using Quantitative Real-time PCR. Our data showed that chronic METH dose-dependently impaired PAL retrieval, as it decreased step-through latency (STL) and increased time spent in the dark compartment (TDC). While Agmatine with a higher dose (10 mg/kg) significantly decreased impairment effect of METH (2 mg/kg) on PAL and memory. Also, molecular results revealed that METH (2 mg/kg) markedly decreased hippocampal CaMKII-α gene expression while agmatine (10 mg/kg) co-adminstration prevented it. Taken together, the results propose that agmatine may provide a potential therapy for learning and memory deficits induced by METH.

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Stress seems to be an important risk factor in the beginning and continuing stages of cigarette tobacco smoking in humans. Considering that both of nicotine administration and stress exposure affect cognitive functions including memory formation, the aim of the present study was 1) to evaluate the effect of subcutaneous (s.c.) administration of nicotine on memory formation under stress and 2) to assess the possible role of the basolateral amygdala (BLA) dopamine D1 and D2 receptors in the effect of nicotine on stress-induced memory retrieval impairment. Adult male wistar rats were bilaterally implanted in the BLA. A step-through type passive avoidance task was used to measure memory retrieval. To induce acute stress, the animals were placed on an elevated platform. The results showed that pre-test exposure to 20 and 30 min stress, but not 10 min, impaired memory retrieval. Nicotine administration (0.05 mg/kg, s.c.) improved stress-induced memory retrieval impairment. The activation of the BLA dopamine receptors via bilateral microinjection of apomorphine (0.025-0.4 µg/rat), a non-selective dopamine receptor agonist, potentiated the effect of nicotine on stress-induced memory retrieval impairment. Interestingly, intra-BLA microinjection of SCH23390 (a selective dopamine D1 receptor antagonist; 0.02-0.5 µg/rat) or sulpiride (a selective dopamine D2 receptor antagonist; 0.02-0.5 µg/rat) dose-dependently inhibited nicotine-induced improvement of the stress amnesic effect. Taken together, it can be concluded that stress-induced impairment of memory retrieval can be improved by nicotine administration. Moreover, the dopaminergic neurotransmission in the BLA through D1 and D2 receptors mediates the improving effect of nicotine on stress-induced memory retrieval impairment.

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The aim of the present study was to compare the effects of artificial sweeteners (aspartame, saccharin, and sucralose) on rat brain. Twenty-four adult male Sprague-Dawley rats were included in the study. The control group (n = 6) received regular tap water, whereas other groups received aspartame (3 mg/kg/day, n = 6,) or saccharin (3 mg/kg/day, n = 6) or sucralose (1.5 mg/kg/day, n = 6) in the drinking water. Following 6 weeks, the passive avoidance learning (PAL) test was performed to evaluate the neurobehavioral effects of sweeteners. The brains were assessed for lipid peroxides, neuron count, and Glial fibrillary acidic protein (GFAP) immunohistochemistry. Our results demonstrated that chronic intake of sweeteners significantly impaired PAL performance in all groups. Hippocampal CA1-CA3 areas revealed significantly lower neuronal count in aspartame and increased GFAP expression in all groups. Brain lipid peroxides were significantly higher in all groups. Our findings suggest that long-term consumption of artificial sweeteners may have harmful effects on cognition and hippocampal integrity in rats.

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BACKGROUND: Pulpal pain is one of the most common and severe orofacial pain conditions with considerable adverse effects on physiological processes including learning and memory. Regular exercise is known to be effective on cognitive function as well as pain processing in the central nervous system. Here, the possible effects of regular exercise on pulpal pain response as well as pain-induced changes in learning and memory efficiency in rats were investigated. METHODS: Twenty-four male Wistar rats were randomly assigned to the control, capsaicin, exercise, and exercise plus capsaicin groups. Rats in exercise groups were forced to run on a treadmill with a moderate exercise protocol for 4 weeks. Capsaicin was used to induce dental pulp pain. Passive avoidance learning and memory performance was assessed by using a shuttle box apparatus. RESULTS: According to the results, regular exercise could decrease the time course of capsaicin-induced pulpal pain (P < 0.001). Moreover, in capsaicin-treated rats, passive avoidance acquisition was impaired as compared to the control (P < 0.05) and exercise (P < 0.001) groups. Additionally, regular exercise before capsaicin injection could attenuate capsaicin-induced memory impairments (P < 0.05). CONCLUSIONS: Taken together, the present data showed that regular exercise has inhibitory effects on capsaicin-induced pulpal pain as well as pain-induced cognitive dysfunction in rats.

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There is an extensive evidence concerning basolateral amygdala (BLA) function to hippocampal memory processing. However, few researches have addressed the orexinergic system roles in this modulation. Then, the present study aims at investigating the action of orexin 1 and 2 receptors in BLA on passive avoidance (PA) learning. Wistar male rats (n=79) were trained to avoid foot shock in one type of PA task. The rats were injected bilaterally into BLA, a selective orexin 1 receptor antagonist, SB-334867-A (3, 6, 12µg/0.5µl), and an orexin 2 receptor antagonist, TCS-OX2-29 (2.5, 5, 10µg/0.5µl), after training or before retrieval of the inhibitory avoidance task. Control rats received dimethyl sulfoxide at the same volume. The amount of learning was assessed 24h later. The time of the first entrance to the dark compartment and the total time spending in the light compartment were measured as criteria for the avoidance memory. The results showed that consolidation and retrieval were significantly impaired by SB-334867-A administration into BLA in 3, 6 and 12µg/0.5µl. However, TCS-OX2-29 in 2.5µg/0.5µl could not influence neither consolidation nor retrieval. The TCS-OX2-29 administration into BLA impaired memory retrieval in 5 and 10µg/0/5µl but not the consolidation. It gives the impression that orexinergic system of the BLA plays an important role in regulation of memory processing and learning in the rats.

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Dextromethorphan which is an active ingredient in many cough medicines has been previously shown to potentiate amnesic effect of morphine in rats. However, the effect of dextromethorphan, that is also a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, in combination with morphine on hippocampus-based long term memory has not been well characterized. The aim of the present study was to assess the possible role of endocannabinoid system of the dorsal hippocampus in dextromethorphan /morphine-induced amnesia. Our results showed that intraperitoneal (i.p.) injection of morphine (5mg/kg) or dextromethorphan (5-15mg/kg) before testing the passive avoidance learning induced amnesia. Combination of ineffective doses of dextromethorphan (7.5mg/kg, i.p.) and morphine (2mg/kg, i.p.) also produced amnesia, suggesting the enhancing effects of the drugs. To assess the effect of the activation or inhibition of the dorsal hippocampal cannabinoid CB1 receptors on this amnesia, ACPA or AM251 as selective receptor agonists or antagonists were respectively injected into the CA1 regions before systemic injection of dextromethorphan and morphine. Interestingly, intra-CA1 microinjection of ACPA (0.5-1ng/rat) improved the amnesic effect of dextromethorphan /morphine combination. The microinjection of AM251 into the CA1 region enhanced the response of the combination of dextromethorphan /morphine in inducing amnesia. Moreover, Intra-CA1 microinjection of AM251 inhibited the improving effect of ACPA on dextromethorphan /morphine-induced amnesia. It is important to note that intra-CA1 microinjection of the same doses of the agonist or antagonist by itself had no effects on memory formation. Thus, it can be concluded that the dorsal hippocampal endocannabinoid system, via CB1 receptor-dependent mechanism, may be involved in morphine/dextromethorphan -induced amnesia.

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The present study was designed to investigate the involvement of the muscarinic cholinergic receptors in the basolateral amygdala (BLA) in memory retrieval. Also, the possible relationship between the BLA muscarinic cholinergic and the NMDA receptor systems was evaluated in the inhibitory avoidance learning. Male Wistar rats were bilaterally cannulated into the BLAs and memory retrieval was measured in a step-through type inhibitory avoidance apparatus. Intra-BLA microinjection of different doses of a non-selective muscarinic receptor antagonist, scopolamine (0.5-1µg/rat, intra-BLA), 5min before the testing phase dose-dependently induced amnesia. Pre-test intra-BLA microinjection of different doses of NMDA (0.005-0.05µg/rat) reversed scopolamine-induced amnesia and improved memory retrieval. In addition, different doses of a selective NMDA receptor antagonist, D-AP5 (0.001-0.005µg/rat, intra-BLA) potentiated the response of an ineffective dose of scopolamine (0.5µg/rat) to inhibit memory retrieval. It should be considered that pre-test intra-BLA microinjection of the same doses of NMDA or D-AP5 by themselves had no effect on memory retrieval. Similar to ANOVA analysis, our cubic interpolation analysis also predicted that the activation or inactivation of the NMDA receptors by different doses of drugs can affect the scopolamine response. On the other hand, pre-test intra-BLA microinjection of D-AP5 inhibited the reversal effect of NMDA on scopolamine-induced amnesia. It can be concluded that the BLA cholinergic system, via muscarinic receptors, has a critical role in memory retrieval. Our results also suggest that a cooperative interaction between the BLA NMDA and muscarinic acetylcholine receptors modulates memory formation of inhibitory avoidance task in rats.

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Previously we reported that prenatal morphine exposure during embryonic days 5-8 can cause cognitive deficits of one-trial passive avoidance learning (PAL) in one-day old chicks. Because protein kinase C (PKC) has been associated with memory capacity, we investigated the effects of prenatal morphine exposure on PKC isoforms expression in the left intermediate medial mesopallium (IMM) of chick brain at a time when memory tests were performed at 30, 120 and 360min respectively following training in PAL paradigm. We found that the level of PKCα in the membrane fractions in left IMM was decreased but that in the cytosol fractions showed a increased trend in prenatally morphine-exposed chicks with impaired long-term memory (120 and 360min). Moreover, the translocation of PKC δ from cytosol to membrane in left IMM was shown in prenatal morphine group which had significantly impaired long-term memory at 360min after training. Furthermore, there were no statistical differences between the two groups regarding the expressions of PKCα and PKC δ in the membrane fraction, although their levels in the cytosol fraction of prenatal morphine group which showed impaired intermediate-term memory at 30min after training, were quite different from that of prenatal saline group. Taken together, these results indicate that PKCα and PKC δ in the left IMM are differentially involved in the impairments of long-term memory induced by prenatal morphine exposure. Neither PKCα nor PKC δ in left IMM may be associated with the disruption of intermediate-term memory of chicks prenatally exposed to morphine.

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There is a growing body of evidence that neuroinflammation can impair memory. It has been indicated that Portulaca oleracea Linn. (POL), possess anti-inflammatory activity and might improve memory disruption caused by inflammation. In this study the effect of pre-treatment with the hydro-alcoholic extract of POL on memory retrieval investigated in lipopolysaccharide (LPS) treated rats. Male Wistar rats (200-220g) received either a control diet or a diet containing of POL (400mg/kg, p.o.) for 14days. Then, they received injections of either saline or LPS (1mg/kg, i.p.). In all the experimental groups, 4h following the last injection, passive avoidance learning (PAL) and memory test was performed. The retention test was done 24h after the training and then the animals were sacrificed. Hippocampal TNF-α levels measured using ELISA as one criteria of LPS-induced neuroinflammation. The results indicated that LPS significantly impaired PAL and memory and increased TNF-α levels in hippocampus tissue. Pre-treatment with POL improved memory in control rats and prevented memory and TNF-α deterioration in LPS treated rats. Taken together, the results of this study suggest that the hydro-alcoholic extract of POL may improve memory deficits in LPS treated rats, possibly via inhibition of TNF-α and anti-inflammatory activity.

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