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Repeated Amphetamine Exposure Blunted Angiotensin II-Induced Responses Mediated by AT Receptors.
Discov Med
January 2025
Department of Pharmacology "Otto Orsingher", Institute of Experimental Pharmacology of Córdoba (IFEC-CONICET), Faculty of Chemical Sciences, National University of Córdoba, X5000 Córdoba, Argentina.
Background: Angiotensin II, is critical in regulating the sympathetic and neuroendocrine systems through angiotensin II type 1 receptors (AT-R). Angiotensin II intracerebral administration increases water and sodium intake, as well as renal sodium excretion. Previously, our group has shown that AT-R is involved in behavioral and neurochemical sensitization induced by amphetamine.
View Article and Find Full Text PDFCharacterising a New Sheep Model of Parkinson's Disease Using Unilateral Intracerebral Injection of 6-Hydroxydopamine Into the Substantia Nigra.
Eur J Neurosci
January 2025
Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
New therapeutic agents developed for treating neurological disorders are often tested successfully on rodents. Testing in an appropriate large animal model where there is longer lifespan and comparable brain size to humans should improve translational success and is frequently expected by regulatory bodies. In this project, we aimed to establish a novel sheep model of Parkinson's disease as a large-brained experimental model for translational research.
View Article and Find Full Text PDFEsketamine Provides Neuroprotection After Intracerebral Hemorrhage in Mice via the NTF3/PI3K/AKT Pathway.
CNS Neurosci Ther
December 2024
Department of Anesthesiology, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, China.
Background: Esketamine (ESK), a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) receptors, modulates neurotransmitter signaling in the central nervous system. However, the specific mechanisms and therapeutic potential of ESK for intracerebral hemorrhage (ICH) remain unclear. This study aimed to investigate whether ESK promotes nerve repair and improves neurological outcomes in an experimental model of ICH.
View Article and Find Full Text PDFProgress on the Mechanisms and Neuroprotective Benefits of Dexmedetomidine in Brain Diseases.
Brain Behav
November 2024
Department of Neurosurgery, Jiangnan University Medical Center, Wuxi, China.
Introduction: Dexmedetomidine, a highly specific α2 agonist, has been extensively utilized in clinical sedation and surgical anesthesia since its introduction in 2000 due to its excellent sympatholytic, sedative, and analgesic effects. This review aimed to identify new approaches for the treatment of patients with brain disorders by thoroughly describing the mechanism of action of dexmedetomidine and examining its neuroprotective effects from the standpoints of basic and clinical research.
Methods: The PubMed and Web of Science databases were searched using the keywords dexmedetomidine and related brain diseases, although relevant articles from the last decade were included for detailed summarization and analysis.
Jujuboside A Regulates Calcium Homeostasis and Structural Plasticity to Alleviate Depression-Like Behavior via Shh Signaling in Immature Neurons.
Drug Des Devel Ther
October 2024
Science & Technology Innovation Center, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, People's Republic of China.
Article Synopsis
- Depression is a major global health issue linked to neuronal dysfunction and calcium imbalances, and Jujuboside A (JuA) shows promise as a potential antidepressant due to its anti-anxiety and anti-insomnia effects.
- In a study with rats subjected to a depression model, JuA improved depressive behaviors, boosted neurotransmitter levels, and enhanced synaptic connections while also affecting immature neurons and calcium homeostasis.
- The antidepressant effects of JuA were linked to increased expression of key signaling proteins and were significantly reduced when Sonic hedgehog (Shh) signaling was inhibited, indicating Shh plays a vital role in JuA's mechanisms.
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