A5075385695- Neuroscience and Neuropharmacology Research
- Neuropeptides and Animal Physiology
- Neuroinflammation and Neurodegeneration Mechanisms
- Memory and Neural Mechanisms
- Neurological Disease Mechanisms and Treatments
- Receptor Mechanisms and Signaling
- Alkaloids: synthesis and pharmacology
- Alzheimer's disease research and treatments
- Neural dynamics and brain function
- Stress Responses and Cortisol
- Tryptophan and brain disorders
- Biochemical Analysis and Sensing Techniques
- Metabolomics and Mass Spectrometry Studies
- Nicotinic Acetylcholine Receptors Study
- Apelin-related biomedical research
- Adipose Tissue and Metabolism
- Regulation of Appetite and Obesity
- Hormonal Regulation and Hypertension
- Ion channel regulation and function
- RNA Interference and Gene Delivery
- Neuroscience of respiration and sleep
- Phosphodiesterase function and regulation
- Lipid Membrane Structure and Behavior
- Phytochemistry and Biological Activities
- Neurogenesis and neuroplasticity mechanisms
Kitasato University
2018-2025
Tokyo University of Science
2013-2024
Abstract Aim We previously reported that oxytocin, a peptide hormone, can reverse the β‐amyloid (25–35) (Aβ 25–35 )‐induced impairments of murine hippocampal synaptic plasticity. In this study, we examined effects oxytocin on Aβ ‐induced impairment cognitive behavior in order to investigate potential as clinical treatment tool for Alzheimer's disease (AD). Methods The Y‐maze and Morris water maze (MWM) tests were performed. Since intracerebroventricular (ICV) administration is both invasive...
QO58 (5-(2,6-dichloro-5-fluoropyridin-3-yl)-3-phenyl-2-(trifluoromethyl)-1H-[1,5-a] pyrimidin-7-one) is currently used as a specific activator of the Kv7 (KCNQ) family K+ channels. Here, we report an unexpected potentiating effect this drug on nicotinic acetylcholine receptors. We recorded whole-cell responses to rapid application nicotine with Cs+-based pipette solution in intracardiac ganglion neurons freshly dissociated from rat heart. Nicotine-induced inward currents were...
Glucagon‐like peptide‐1 (GLP‐1) is derived from the processing of proglucagon in intestinal L‐cells and releases insulin pancreatic β‐cells as an incretin. The GLP‐1 receptor has been proposed a possible therapeutic target for treatment Alzheimer's disease, which neuroinflammation critical pathogenesis. present study investigates whether (7–36) amide, active fragment GLP‐1, protected against synaptic impairments induced by inflammation‐related injurious agents (lipopolysaccharide [LPS],...
Abstract Glucagon-like peptide 2 (GLP-2) is derived from the proglucagon gene expressed in intestines, pancreas and brain. Our previous study showed that GLP-2 improved lipopolysaccharide-induced memory impairments. The current was designed to further investigated potential of impairment induced by intracerebroventricular administration streptozotocin (ICV-STZ) mice, which have been used as an animal model sporadic Alzheimer’s disease (AD). STZ administered on alternate days (Day-1 Day-3)...
Abstract Glucose is the sole neural fuel for brain and essential cognitive function. Abnormalities in glucose tolerance may be associated with impairments Experimental obese model mice can generated by an intraperitoneal injection of monosodium glutamate ( MSG ; 2 mg/g) once a day 5 days from 1 after birth. ‐treated have been shown to develop intolerance exhibit chronic neuroendocrine dysfunction marked malfunctions at 28–29 weeks old. Although hippocampal synaptic plasticity impaired mice,...