Protective effects of a lactobacilli mixture against Alzheimer's disease-like pathology triggered by Porphyromonas gingivalis.

Porphyromonas gingivalis (P. gingivalis) is one of the pathogens involved in gingival inflammation, which may trigger neuroinflammatory diseases such as Alzheimer's disease (AD). This study aimed to investigate the protective (preventive and treatment) effects of a lactobacilli mixture combining Lactobacillus reuteri PTCC1655, Lactobacillus brevis CD0817, Lacticaseibacillus rhamnosus PTCC1637, and Lactobacillus plantarum PTCC1058 against P.

Maternal linalool treatment protects against radiofrequency wave-induced deteriorations in adolescent rats: A behavioral and electrophysiological study.

Recent years, the rapid advancement of technology has raised concerns. We studied the effects of prenatal exposure to 900 MHz radiofrequency (RF) from mobile phones and the protective effects of linalool on learning and memory, and anxiety in adolescent male and female offspring rats. Pregnant rats were divided into four groups: control, wave, wave + linalool, and linalool.

The synergic effects of presynaptic calcium channel antagonists purified from spiders on memory elimination of glutamate-induced excitotoxicity in the rat hippocampus trisynaptic circuit.

The hippocampus is a complex area of the mammalian brain and is responsible for learning and memory. The trisynaptic circuit engages with explicit memory. Hippocampal neurons express two types of presynaptic voltage-gated calcium channels (VGCCs) comprising N and P/Q-types.

Quercetin-Conjugated Superparamagnetic Iron Oxide Nanoparticles Protect AlCl-Induced Neurotoxicity in a Rat Model of Alzheimer's Disease Antioxidant Genes, APP Gene, and miRNA-101.

Alzheimer's disease (AD) is a neurodegenerative disease with cognitive impairment. Oxidative stress in neurons is considered as a reason for development of AD. Antioxidant agents such as quercetin slow down AD progression, but the usage of this flavonoid has limitations because of its low bioavailability.

The effects of lactobacilli (L. rhamnosus, L. reuteri, L. Plantarum) on LPS-induced memory impairment and changes in CaMKII-α and TNF-α genes expression in the hippocampus of rat.

In recent years, some investigations have focused on the relationship between gut microbiota and brain function in healthy and disease conditions. Moreover, changes in the gut microbiome may affect memory, behavior, and cognition. This study aimed to evaluate the effect of lactobacilli on passive avoidance learning, hippocampal CaMKII-α, and TNF-α genes expression in one experimental model of neuroinflammtion.

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.

The role of nucleus accumbens shell on acquisition and retrieval stages of morphine state dependent learning.

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.

Agmatine attenuates methamphetamine-induced passive avoidance learning and memory and CaMKII-α gene expression deteriorations in hippocampus of rat.

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.

Portulaca oleracea L. prevents lipopolysaccharide-induced passive avoidance learning and memory and TNF-α impairments in hippocampus of rat.

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.

Nurr1 and PPARγ protect PC12 cells against MPP(+) toxicity: involvement of selective genes, anti-inflammatory, ROS generation, and antimitochondrial impairment.

Parkinson's disease (PD) can degenerate dopaminergic (DA) neurons in midbrain, substantia-nigra pars compacta. Alleviation of its symptoms and protection of normal neurons against degeneration are the main aspects of researches to establish novel therapeutic strategies. PPARγ as a member of PPARs have shown neuroprotection in a number of neurodegenerative disorders such as Alzheimer's disease and PD.

Omega-3 fatty acids prevent LPS-induced passive avoidance learning and memory and CaMKII-α gene expression impairments in hippocampus of rat.

Background: Neuroinflammation is considered to be a major factor in several neurodegenerative diseases. Recently, the polyunsaturated fatty acid omega-3 has been shown to have anti-inflammatory effects and might play an effective role in improving memory impairment due to inflammation. In order to test this, we stimulated neuroinflammation in an animal model and induced memory dysfunction as measured by reduced retention of passive avoidance learning (PAL) and altered expression of CaMKII-α, a gene known to be crucial for memory formation.

Alteration in messenger RNA neurotrophin 4 and tyrosine kinase receptors B expression levels following spinal cord injury.

Background: Neurotrophins as polypeptide growth factors have important roles during nervous system development and are involved in neuronal differentiation and survival and spinal cord reorganization. Neurotrophins have been recognized as factors which are involved in the development of damaged axons and increase the axon growth ability and neuroplasticity. Spinal cord injury (SCI) is associated with numerous physiological damages, leading to neuron death, axon extended destruction healthy and intact neurons demyelination, inflammation, cell death and severe motor/sensory defects.

Role of hippocampal CA1 area gap junction channels on morphine state-dependent learning.

Morphine produces a state dependent learning. The hippocampus is involved in this kind of learning. Gap junctions (GJs) are involved in some of the effects of morphine and exist in different areas of the hippocampus.

Copines-1, -2, -3, -6 and -7 show different calcium-dependent intracellular membrane translocation and targeting.

The copines are a family of C2- and von Willebrand factor A-domain-containing proteins that have been proposed to respond to increases in intracellular calcium by translocating to the plasma membrane. The copines have been reported to interact with a range of cell signalling and cytoskeletal proteins, which may therefore be targeted to the membrane following increases in cellular calcium. However, neither the function of the copines, nor their actual movement to the plasma membrane, has been fully established in mammalian cells.

Orexin-1 receptor mediates long-term potentiation in the dentate gyrus area of freely moving rats.

Orexin neurons, localized in the lateral hypothalamus area, synthesize two neuropeptides called orexin A and orexin B and send their axons to hippocampal formation including dentate gyrus (DG). Orexin A and orexin B act as endogenous ligands for two G-protein coupled receptors called orexin-1 and orexin-2 receptors (OX1R and OX2R). In the dentate gyrus (DG) region, OX1R, which has high affinity for orexin A, is expressed.

The effect of antagonization of orexin 1 receptors in CA1 and dentate gyrus regions on memory processing in passive avoidance task.

The hippocampal formation plays an essential role in associative learning like passive avoidance (PA) learning. It has been shown; orexin-containing terminals and orexin receptors densely are distributed in the hippocampal formation. We have previously demonstrated that antagonization of orexin 1 receptor (OX1R) in CA1 region of hippocampus and dentate gyrus (DG) impaired spatial memory processing.

Effect of the GABAergic system on memory formation and state-dependent learning induced by morphine in rats.

In the present study, the effects of intraperitoneal injections of GABA(A) receptor agonist and antagonist on memory formation and morphine state-dependent learning were investigated in rats. Pre-training administration of morphine (1-15 mg/kg) in a step-down passive avoidance task induced state-dependent learning with impaired memory retrieval on the test day. The impairment of memory was restored after the pre-test administration of the same dose of morphine.