Efficacy of Black Mulberry Mouthwash for Prevention of Chemotherapy-Induced Oral Mucositis: A Double-Blind Randomized Clinical Trial.

Oral mucositis is a common side effect of cancer chemotherapy. Traditionally, black mulberry or L. (M.

Investigating the Co-administration of Ghrelin and Nicotine Into the Medial Septum and Its Influencing on Morphine Amnestic Effect.

Introduction: Evidence indicates that medial septum nicotinic receptors regulate cognitive processes. Ghrelin is a gut hormone that regulates energy homeostasis. Ghrelin is also produced in the brain and is involved in cognitive function.

Memory impairment was ameliorated by corticolimbic microinjections of arachidonylcyclopropylamide (ACPA) and miRNA-regulated lentiviral particles in a streptozotocin-induced Alzheimer's rat model.

The present study aimed to investigate the effect of corticolimbic cannabinoid CB1 receptors activity on memory impairment in the intracerebroventricular (ICV)-streptozotocin (STZ) animal model of Alzheimer's like-disease. This study also assessed whether the corticolimbic overexpression of miRNA-137 or -let-7a could increase the endocannabinoids by inhibiting the monoglyceride lipase (MAGL) to ameliorate STZ response. The results showed that ICV microinjection of STZ (3 mg/kg/10 μl) impaired passive avoidance memory retrieval.

Addictive drugs modify neurogenesis, synaptogenesis and synaptic plasticity to impair memory formation through neurotransmitter imbalances and signaling dysfunction.

Drug abuse changes neurophysiological functions at multiple cellular and molecular levels in the addicted brain. Well-supported scientific evidence suggests that drugs negatively affect memory formation, decision-making and inhibition, and emotional and cognitive behaviors. The mesocorticolimbic brain regions are involved in reward-related learning and habitual drug-seeking/taking behaviors to develop physiological and psychological dependence on the drugs.

Ameliorating effect offluoxetine 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.

Basolateral amygdala cannabinoid CB1 receptors mediate the antinociceptive activity of harmaline in adolescent male mice.

Evidence suggests a clear role for the amygdala endocannabinoid system in pain processing. Harmaline has been also known as the main nociceptive agent extracted from the Peganum harmala plant. In this study, the role of basolateral amygdala (BLA) cannabinoid CB1 receptors in pain sensitivity of harmaline-treated mice were assessed using tail-flick and hot plate methods in adolescent male NMRI mice.

Activation of VTA/CeA/mPFC cannabinoid CB1 receptors induced conditioned drug effects via interacting with hippocampal CAMKII-CREB-BDNF signaling pathway in rats.

The present study intended to investigate whether the activation of cannabinoid CB1 receptors of the ventral tegmental area (VTA), the central amygdala (CeA) and the medial prefrontal cortex (mPFC) could induce conditioned place preference or aversion (CPP or CPA) in adult male Wistar rats. The involvement of hippocampal signaling pathway of Ca/calmodulin-dependent protein kinase II (CaMKII)/cAMP response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) was also examined following a 3-day schedule of conditioning with the injection of arachidonylcyclopropylamide (ACPA; a selective cannabinoid CB1 receptors agonist) into the targeted sites. The results showed that intra-VTA injection of the higher dose of ACPA (5 ng/rat) caused a significant CPP associating with the increased hippocampal level of the phosphorylated (p)-CAMKII/CAMKII.

Ventral tegmental area serotonin 5-HT receptors and corticolimbic cFos/BDNF/GFAP signaling pathways mediate dextromethorphan/morphine anti-allodynia.

Aims: The present study examined the role of ventral tegmental area (VTA) serotonergic 5HT receptors in dextromethorphan/morphine-induced anti-allodynia and the possible changes of corticolimbic cFos, brain-derived neurotrophic factor (BDNF), and glial fibrillary acidic protein (GFAP) following the treatments.

Materials And Methods: The VTA cannulation and the chronic constriction of the sciatic nerve were performed in male Wistar rats. Flexion withdrawal thresholds to mechanical stimulation in the hind-limb were determined using von Frey hairs.

Harmaline potentiates morphine-induced antinociception via affecting the ventral hippocampal GABA-A receptors in mice.

Morphine is one of the most effective medications for treatment of pain, but its side effects limit its use. Therefore, identification of new strategies that can enhance morphine-induced antinociception and/or reduce its side effects will help to develop therapeutic approaches for pain relief. Considering antinociceptive efficacy of harmaline and also highlighted the important role of GABA-A receptors in the pain perception, this research aimed to determine whether the ventral hippocampal (vHip) GABA-A receptors are involved in the possible harmaline-induced enhancement of morphine antinociception.

Morphine improved stress-induced amnesia and anxiety through interacting with the ventral hippocampal endocannabinoid system in rats.

The present study aimed to investigate the possible role of the ventral hippocampal (VH) cannabinoid CB1 receptors in the improving effect of morphine on stress-induced memory formation impairment and anxiety. A step-through type passive avoidance task and a hole-board test were used to measure memory formation and anxiety-like exploratory behavior, respectively. The results showed that the exposure to 10-min stress immediately after the successful training phase impaired memory formation and also produced anxiogenic-like exploratory behaviour in adult male Wistar rats.

Expression analysis of hippocampal and amygdala CREB-BDNF signaling pathway in nicotine-induced reward under stress in rats.

Extensive research has shown that individuals are more sensitive to develop addiction and drug taking under stress state. The present study includes an expression analysis to identify the possible role of hippocampal and amygdala CREB (cAMP response element-binding protein) and BDNF (Brain-derived neurotrophic factor) activation in nicotine-induced conditioned place preference (CPP) under exposure to acute or sub-chronic stress. Using western-blot technique, CREB phosphorylation was shown to increase in the hippocampus and the amygdala following nicotine-induced CPP.

Arbutin reduces cognitive deficit and oxidative stress in animal model of Alzheimer's disease.

Recent evidences have shown the beneficial effects of natural products for treating of Alzheimer's disease (AD). Arbutin is derived from and exerts a wide range of pharmacological activities including anti-inflammatory and anti-oxidant effects. The present study was designed to examine the protective effects of arbutin on streptozotocin (STZ)-induced neurotoxicity in rats.

The involvement of ventral hippocampal microglial cells, but not cannabinoid CB1 receptors, in morphine-induced analgesia in rats.

It is well known that glial cells are involved in pain processing. The purpose of the present study was to investigate the possible involvement of the ventral hippocampal (VH) glial cells in morphine-induced analgesia. A tail-flick apparatus was used to measure pain sensitivity in male Wistar rats that were bilaterally cannulated in the VH by stereotaxic surgery.

The blockade of 5-HT receptors in the ventral tegmental area inhibited morphine/dextromethorphan-induced analgesia in pain rat models.

The aim of the present study was to determine the involvement of the VTA 5-HT receptors in analgesia induced by the co-administration of morphine and dextromethorphan (DM). Male Wistar rats were bilaterally cannulated in the VTA by the stereotaxic instrument. The tail-flick and formalin tests were performed to assess nociception in the acute and tonic pain conditions respectively.

Medial Prefrontal Cortical Cannabinoid CB1 Receptors Mediate Morphine-Dextromethorphan Cross State-Dependent Memory: The Involvement of BDNF/cFOS Signaling Pathways.

The present study set out to assess the possible role of the medial prefrontal cortex (mPFC) cannabinoid CB1 receptors and BDNF/cFOS signaling pathways in morphine-dextromethorphan (DXM) cross state-dependent memory (SDM) using male Wistar rats. Changes on the levels of BDNF and cFOS proteins in the PFC were examined by Western blot analysis. Present results revealed that levels of BDNF and cFOS proteins were significantly increased in the animals that were trained in the passive avoidance apparatus.

The basolateral amygdala dopaminergic system contributes to the improving effect of nicotine on stress-induced memory impairment in rats.

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.

Brain nicotinic acetylcholine receptors are involved in stress-induced potentiation of nicotine reward in rats.

The aim of the present study was to examine the possible role of nicotinic acetylcholine receptors of the dorsal hippocampus (CA1 regions), the medial prefrontal cortex or the basolateral amygdala in the effect of acute or sub-chronic stress on nicotine-induced conditioned place preference. Our results indicated that subcutaneous administration of nicotine (0.2 mg/kg) induced significant conditioned place preference.

Neuromodulatory effects of the dorsal hippocampal endocannabinoid system in dextromethorphan/morphine-induced amnesia.

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.

Divergent pathway of lipid profile components for cardiovascular disease and mortality events: Results of over a decade follow-up among Iranian population.

Background: Data regarding the impact of different lipid measures on cardiovascular diseases (CVD) and mortality events is not consistent. We aimed to evaluate the relationship between different lipid parameters and incident CVD and mortality events in an Iranian population over a median follow-up of 11.9 years.

Basolateral amygdala CB1 cannabinoid receptors are involved in cross state-dependent memory retrieval between morphine and ethanol.

Ethanol and morphine are largely co-abused and affect memory formation. The present study intended to investigate the involvement of cannabinoid CB1 receptors of the basolateral amygdala (BLA) in cross state-dependent memory retrieval between morphine and ethanol. Adult male Wistar rats received bilateral cannulation of the BLA, and memory retrieval was measured in step-through type passive avoidance apparatus.

Activation of cannabinoid CB1 receptors in the ventral hippocampus improved stress-induced amnesia in rat.

The ventral hippocampus (VH) has a high distribution of cannabinoid CB1 receptors which are important in modulating stress responses. Stress exposure activates the hypothalamic-pituitary-adrenal axis (HPA) which can impact hippocampal formation to change hippocampus-based memories. The purpose of the present study was to determine the possible role of the VH cannabinoid CB1 receptors in stress-induced amnesia using a step-through passive avoidance procedure in male Wistar rats.

Activation of the dorsal hippocampal nicotinic acetylcholine receptors improves tamoxifen-induced memory retrieval impairment in adult female rats.

Tamoxifen (TAM), a selective estrogen receptor modulator, has frequently been used in the treatment of breast cancer. In view of the fact that cognitive deficits in women who receive adjuvant chemotherapy for breast cancer is a common health problem, using female animal models for investigating the cognitive effects of TAM administration may improve our knowledge of TAM therapy. Therefore, the present study assessed the role of dorsal hippocampal cholinergic nicotinic receptors (nAChRs) in the effect of TAM administration on memory retrieval in ovariectomized (OVX) and non-OVX female rats using a passive avoidance learning task.

Role of hippocampal and prefrontal cortical signaling pathways in dextromethorphan effect on morphine-induced memory impairment in rats.

Evidence suggests that dextromethorphan (DM), an NMDA receptor antagonist, induces memory impairment. Considering that DM is widely used in cough-treating medications, and the co-abuse of DM with morphine has recently been reported, the aims of the present study was (1) to investigate whether there is a functional interaction between morphine and DM in passive avoidance learning and (2) to assess the possible role of the hippocampal and prefrontal cortical (PFC) signaling pathways in the effects of the drugs on memory formation. Our findings indicated that post-training or pre-test administration of morphine (2 and 6 mg/kg) or DM (10-30 mg/kg) impaired memory consolidation and retrieval which was associated with the attenuation of the levels of phosphorylated Ca(2+)/calmodulin-dependent protein kinase II (p-CAMKII) and cAMP responsive element-binding protein (p-CREB) in the targeted sites.

Inhibition of microglia in the basolateral amygdala enhanced morphine-induced antinociception: Possible role of GABAA receptors.

In clinical medicine, morphine is widely used to relieve many types of pain, but it has several side effects such as the development of tolerance and dependence. In order to decrease the side effects of morphine administration for the treatment of pain, the combination of minocycline as a glial inhibitor and morphine has been suggested in previous studies. It is important to understand which synaptic mechanisms are involved in the potentiative effect of minocycline on morphine antinociception.

μ-Opioid and N-methyl-D-aspartate receptors in the amygdala contribute to minocycline-induced potentiation of morphine analgesia in rats.

The aim of the present study was to investigate the role of the amygdala in the potentiative effect of minocycline, a semisynthetic tetracycline antibiotic, on morphine analgesia in male Wistar rats. We also examined the involvement of the amygdala μ-opioid and N-methyl-D-aspartate (NMDA) receptors in the minocycline-induced potentiation of morphine analgesia. Intraperitoneal administration of morphine (3-9 mg/kg) induced analgesia in a tail-flick test.