A chronic deprivation of brain cholinergic functions in rats caused by intracerebroventricular injection of neurotoxin AF64A increases the escape latency in Morris water maze test as compared to control sham-operated animals. Measurements and analysis of rat movement tracks using an original computerized "Behavioral Vision" system revealed the ability of 17 beta-Estradiol and its synthetic isomer J-861 (both administered daily in per os dose 0.2 mg/kg during 7 days before and 10 days after a single intracerebroventricular injection of AF64A) to improve learning of the animals. Directivity of search trajectories was estimated by a novel index of track straightness. The introduction of an index of "passive swimming" made it possible to reveal episodes of immobility in water-maze behavior of AF64A-injected animals. Unlike J-861, 17 beta-Estradiol almost completely eliminated these episodes. The newly developed indices (especially straightness) seem to be very useful in differentiating learning ability of rats from a decrease in their mobility in the Morris water-maze test, in particular, in case of the estrogens under study.
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Metab Brain Dis
January 2025
Division of Applied Biomedical Science and Biotechnology, School of Health Science, IMU University, No. 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
Alzheimer's disease (AD) consists of two main pathologies, which are the deposition of amyloid plaque as well as tau protein aggregation. Evidence suggests that not everyone who carries the AD-causing genes displays AD-related symptoms; they might never acquire AD as well. These individuals are referred to as non-demented individuals with AD neuropathology (NDAN).
View Article and Find Full Text PDFFront Cardiovasc Med
December 2024
Department of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
MicroPubl Biol
December 2024
Laboratory of Physiology, Department of Medicine, University of Patras, Pátrai, West Greece, Greece.
Cholinergic transmission fundamentally modulates information processing in the brain via muscarinic receptors. Using electrophysiological recordings of population spikes from the CA1 region, we found that the muscarinic receptor agonist carbachol (CCh, 1 μM) enhances the basal excitation level in the dorsal but not ventral hippocampus. Using a frequency stimulation protocol, we found that CCh transforms depression of neuronal output into facilitation (at 3-30 Hz) in the ventral hippocampus while only lessening depression in the dorsal hippocampus, suggesting that muscarinic transmission boosts basal neuronal activation in the dorsal hippocampus and strongly facilitates the output of the ventral hippocampus in a frequency-dependent manner.
View Article and Find Full Text PDFCurr Top Med Chem
December 2024
Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, NH#19 Delhi Mathura Highway, Chaumuhan, Mathura-(281406), UP, India.
Alzheimer's Disease (AD), a prevalent neurodegenerative disorder, poses a significant global health challenge with complicated pathogenesis. Pathological characteristics of AD include increasing loss of cholinergic neurons, oxidative stress, mitochondrial dysfunction, and amyloid beta accumulation. Due to the limited availability of effective therapeutic options with only symptomatic relief and their severe adverse effects, there is a significant need to search and explore new agents for the management of AD.
View Article and Find Full Text PDFJ Ethnopharmacol
January 2025
School of Basic Medical Sciences, Shanxi University of Chinese Medicine, Jinzhong, Shanxi, 030619; Shanxi Provincial Key Laboratory of TCM Encephalopathy; National International Joint Research Center for Molecular Traditional Chinese Medicine. Electronic address:
Ethnopharmacological Relevance: Dihuang Drink (DHD), formulated by Liu Hejian during the Yuan Dynasty, is listed as one of the first ancient classical prescriptions by the National Medical Products Administration of China. It is commonly used for the prevention and treatment of Alzheimer's disease (AD). This study further investigates the therapeutic effects and potential mechanisms of DHD in AD.
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